Flu drugs may help ward off the low-grade inflammation and related cognitive decline that can come with HIV infection, an early study suggests.

Upwards of 24% of people with HIV experience some degree of cognitive impairment that interferes with functions like attention, concentration and multitasking. These declines are often mild but can worsen quality of life, and they can happen even when a person consistently takes HIV medications that suppress the virus.

Understanding why this impairment emerges and how to prevent it is especially relevant as the population of people with HIV grows older.

"This is very important," study co-author Mohamed Abdel-Mohsen, an associate professor of medicine in the division of infectious diseases at Northwestern University Feinberg School of Medicine. "Despite the fact that people living with HIV live longer, so the lifespan is preserved, the 'health span' is not as preserved."

The new study, published Friday (June 5) in the journal Med, pinpoints a potential driver of this decline along with a strategy to reverse it. The scientists used mouse experiments and blood samples from HIV patients, so the work is at an early stage, but it could open the door to future treatments.

"Not only do they describe a mechanism, but they then report in animal models that this mechanism is something that potentially could be targeted by an intervention," said Dr. Alan Winston, a professor of HIV and genitourinary medicine at Imperial College and a consultant physician at St. Mary's Hospital in London. "That's really what's novel," said Winston, who was not involved in the study.

Anti-inflammatory sugars

HIV treatments are now so effective that people with the chronic viral infection can live nearly as long as people without HIV, provided they consistently take the medicines. In 2022 in the U.S., more than half of people living with HIV were over 50 years old, and that figure is expected to grow.

HIV treatment, called antiretroviral therapy (ART), suppresses the virus so that it can't multiply. This prevents the disease from progressing to AIDS while also driving down transmission rates, making the virus unable to spread via sex. But while ART wards off many symptoms of HIV/AIDS and extends an infected person's lifespan, it does not make the chronic infection completely benign. People with HIV still show various signs of accelerated aging, including earlier cognitive decline, in some cases.

"Before we had antiretroviral therapy, we saw profound effects of HIV in the brain," Winston noted. HIV-associated dementia is now rare, because its rates declined as the use of ART increased.

But some percentage of people still develop milder cognitive impairments, and "it can actually have quite a big impact on concentrating at work, for instance, and undertaking daily activities," he said. People have a higher risk of impairment when they've had a big gap between contracting HIV and starting ART, and interruptions in treatment can also raise the risk. However, the underlying cause of the impairments isn't fully understood, Winston said.

To unpack that mechanism, Abdel-Mohsen and colleagues investigated a clue that's recently emerged in the medical literature: sugar molecules called glycans.

These sugars are found throughout the body, including in the bloodstream, where they bind to proteins and fats. In circulation, they tag certain immune molecules to keep inflammation in check. But with age, the concentration of these inflammation-controlling glycans declines: This decline is fairly steady for males, while it has a sudden dip around menopause for females, Abdel-Mohsen said.

Scientists have previously explored how this decline might contribute to age-related diseases, including cancer, while Abdel-Mohsen and colleagues have investigated its relationship to HIV. In a 2024 study comparing people with and without HIV, they found that those with the infection show age-related shifts in their glycans at younger ages than usual. These shifts come with an increase in enzymes known to degrade the sugars, as well as increases in inflammation.

"While it's low-grade [inflammation], it's still damaging because it's continuous," Abdel-Mohsen said. "It's chronic; it doesn't get resolved."

Potential treatment?

In their latest study, the researchers wanted to see if they could connect the dots between the glycan loss, inflammation and cognitive decline.

They analyzed blood samples from more than 100 people with HIV who contributed data to the AIDS Clinical Trials Group, a global research network. All the individuals were taking ART and either had signs of cognitive impairment or did not, according to various assessments. The group with impairments showed greater losses in two glycans that help control inflammation: sialic acid and galactose. In particular, these losses were most pronounced in women, and they correlated with the degree of cognitive decline seen in a given person.

It's not clear why this pattern was more pronounced in women, and that remains a question for future study, Abdel-Mohsen noted. That said, it's known that glycans dip around menopause and that key immune cells bear estrogen receptors, so it's possible that estrogen levels play a role, he suggested. Winston wondered if the timing of diagnosis might also be relevant, since women tend to get diagnosed later than men and may therefore start ART later.

After studying the blood samples, the team used two models of HIV infection in lab mice. One enabled them to study the glycan changes and inflammation triggered by HIV, while the second let them examine signs of cognitive decline. They again found that infection was tied to a loss of glycans and increase in inflammation, as well as worse performance on cognitive tests.

Next, they set out to see if they could reverse those effects.

A class of drugs called sialidase inhibitors work by blocking the effects of enzymes that split sialic acid, one of the key inflammation-quenching glycans. These drugs include Tamiflu, because flu viruses rely on sialic acid to infect cells and spread through the body. The team found that, at least in mice, these flu drugs helped preserve sialic acid, prevent inflammation and improve cognition.

We saw that "this class of inhibitor could reduce inflammation caused by viral infection … and even more importantly, preserve cognition and and prevent memory deficits," Abdel-Mohsen said.

Abdel-Mohsen considers this work "proof-of-concept" that glycans may play a role in HIV-related cognitive decline, pointing to potential treatments. The end goal isn't necessarily to use flu drugs to treat cognitive impairment in HIV, but rather to identify compounds that could "either prevent the glycans from being degraded or just replace them," he said.

One limitation of the current study is that its definition of cognitive impairment was limited, Winston noted. It relied on cognitive test scores — how well participants solved various puzzles — and a standard "scoring" system that's used to assess a handful of cognitive functions. Including details of patients' symptoms and challenges they experience in daily life would have made the meaning of those scores more tangible, Winston said, and he would hope to see that in future work.

In the long run, Winston could see this research leading to a "precision medicine" approach in which patients' glycan levels are checked, and if they're low, they could get a treatment to address that. It's likely that different factors drive cognitive impairment in different people with HIV, so matching patients with the right treatment is imperative, he said.

And in theory, it may be that the loss of glycans also drives other issues seen in aging adults with HIV, such as increased rates of cardiovascular disease. If that's the case, the same treatments may serve multiple functions. "It will be definitely fantastic to study and see how targeting this mechanism could impact the multiple comorbidities," Abdel-Mohsen said.

This article is for informational purposes only and is not meant to offer medical advice.

A 63-year-old man known as the Oslo patient is "likely cured" of HIV after a stem-cell transplant remodeled his entire immune system.

Prior to this case, a handful of other HIV patients who received similar transplants had entered long-term remission from the infection. In those cases, the donated cells came from people unrelated to the patients, but in the Oslo patient's case, the transplanted cells came from his brother. His sibling happened to carry a genetic mutation that made him resistant to HIV, doctors reported Monday (April 13) in the journal Nature Microbiology.

The mutation, called CCR5 delta 32, disables a protein on the surface of immune cells that HIV often exploits to trigger infection. The patient's brother carried two copies of this mutation, which effectively locks the virus out of cells that would normally be its prime targets.

"A sibling has a 25% probability of being a match for a transplant, and the frequency of CCR5Δ32/Δ32 is around 1%" in northern European populations, study co-author Dr. Anders Eivind Myhre, a hematologist at Oslo University Hospital, where the patient was treated, told Live Science in an email. "So it is an unlikely scenario, and we were not aware of the donor's CCR5 status before the transplant."

"Like winning the lottery twice"

The Oslo patient had been diagnosed with HIV in 2006, at age 44. In 2010, he started antiretroviral therapy (ART), which suppresses the virus's ability to replicate in the body and thus prevents the infection from progressing to AIDS. The treatment drove the HIV in the man's blood down to undetectable levels, which also stops the virus from being transmitted through sex. The patient has maintained this level of "viral suppression" from August 2010 to the present.

However, in 2017, the patient became fatigued, and his blood cell counts plummeted. The next year, he was diagnosed with a type of bone marrow cancer called myelodysplastic syndrome, in which new blood cells made in the bone marrow fail to mature. Initially, the patient responded well to a drug for the condition and entered remission, but he later relapsed, prompting his doctors to seek a bone marrow transplant instead.

Also known as hematopoietic stem cell transplants, bone marrow transplants involve infusing healthy, blood-making stem cells into the body to replace diseased ones. These new stem cells multiply and give rise to new red and white blood cells, ultimately remodeling the patient's blood supply and immune system.

At that point, the patient was referred to Myhre's care at Oslo University Hospital, and the team there searched for a bone marrow donor who happened to carry the coveted CCR5 delta 32 mutation. They were aware of similar cases where patients with HIV and blood cancer had received transplants with the mutation and then entered long-term remission from both their conditions. (More recently, there have been a few reported cases of remission without CCR5 delta 32, or with only one copy.)

Unfortunately, the team's search failed to turn up a compatible donor with double CCR5 delta 32, so the patient's 60-year-old brother donated his bone marrow instead, to at least treat the cancer. But on the day of the procedure, the medical team discovered that the sibling happened to have two copies of CCR5 delta 32.

The patient has said "he feels like he has won the lottery twice," study co-author Dr. Marius Trøseid, a group leader, professor and infectious-disease specialist at Oslo University Hospital, told Live Science. "He was cured for his bone marrow disease, which could be fatal, and he's also now cured for HIV, most likely."

Following the transplant, the patient did experience a complication known as graft-versus-host disease. This happens when the transplanted cells give rise to new immune cells that then see the patient's body as "foreign" and attack the tissues. But he was treated for this complication with an immune-modulating medicine, and over time, the new immune system successfully took over.

Two years out, the new cells had completely replaced the patient's original immune cells in the blood, bone marrow and gut, the study authors found in a thorough analysis.

"Most likely, it's a cure"

Trøseid was asked to evaluate the Oslo patient's case following the transplant, when a question emerged about whether he could safely stop ART. Tests confirmed that the patient's immune system had been completely transformed, leaving no trace of HIV in the blood. The team collected 65 million CD4 T cells — the primary targets of HIV infection — and found that none carried virus capable of replicating.

So, 24 months after his transplant, the patient was cleared to stop ART. Since then, there's been no sign of viral rebound — and Trøseid and colleagues have been on the lookout.

They thoroughly analyzed lymph tissues in the patient's gastrointestinal tract, which serve as the main hiding place for HIV in the body, and found no trace of the virus. They also ran tests with the patient's immune cells, and found that they responded well to common viruses, like the "mono" virus and influenza viruses, but did not react to HIV.

"So they function well, but they do not recognize HIV," Trøseid said. "It seems like his new immune system has never met HIV and does not recognize it."

Taken together, these analyses suggest the Oslo patient's case represents a "likely cure," Trøseid noted, though conservatively, scientists prefer to label such cases "sustained remission" from HIV. There's no consensus as to when a given patient can officially be declared cured, but from a practical standpoint, the Oslo patient no longer needs to take daily medications to keep the virus at bay.

"What will happen when some of these cure cases reach very old age and the immune system starts to decline a bit for other reasons? We don't know," he added. "I think we will just need to see. But most likely, it's a cure."

Trøseid thinks the myriad tests they ran in this study could be useful benchmarks for future transplants, to help doctors judge when a patient is in long-term remission. Studying these patients could also help reveal new and better strategies for controlling the virus, which are still needed.

"It's one of several stepping stones on the way to a functional cure," Trøseid said of studying these transplant cases. A functional cure would sustainably suppress HIV in the body without needing to completely eliminate it, as the latter would be a more difficult feat to achieve.

ART is very effective at stopping viral replication, disease progression and transmission, but it must be taken consistently for life. This presents logistical and monetary challenges for many people with HIV, some of whom also struggle to access ART due to the stigma that comes with acknowledging an HIV diagnosis. And while bone marrow transplants offer one route to long-term remission, the harsh procedures carry a lot of risks and are generally administered only to patients who need them for another serious condition, like cancer.

"The number of people living with HIV worldwide is more than 30 million, so it's also not feasible" to give them all transplants, Trøseid said. "We need to find other strategies to cure or control the virus."

Trøseid noted that recent trials suggest that engineered antibodies may be a promising solution for controlling the virus without ART. And in Europe, an international consortium called EU2Cure has formed to help spur the development of these and other potential HIV cures.

"Hopefully, we can move the threshold a little bit with each trial," he said, "and eventually, get a functional cure where a large fraction of people can live for a longer time without taking meds."

This article is for informational purposes only and is not meant to offer medical advice.

In a single year, the secretary of Health and Human Services (HHS), Robert F. Kennedy Jr. (RFK Jr.), has done such comprehensive damage to the extraordinarily successful HIV prevention program as to leave the country almost defenseless against a brewing HIV pandemic, right when elimination seemed possible.

These unprecedented actions have stunned and frightened many who work in the field. But I know from past personal experience that strong science promoted by strong advocacy can return us to the path of HIV elimination.

I saw the AIDS epidemic play out firsthand. In my final year of medical school in 1983, I did a month-long practice internship at the San Francisco General Hospital AIDS ward, the first in the country. The cause of acquired immunodeficiency syndrome (AIDS) was unknown. No test or treatment existed, and the modes of transmission were controversial.

Gay men were the primary risk group. The number diagnosed with AIDS was exploding exponentially, and everyone died slow, lingering, excruciating deaths. Patients were blinded and emaciated, vomiting and asphyxiating and covered with sores, often abandoned by neighbors, family and friends out of the terror of contagion.

Stonewall had come and gone, Harvey Milk had been assassinated, and now fundamentalist preachers thundered from the pulpit that AIDS was God's justified vengeance on sinners.

Then there was the soft-spoken, low-expenditure, laissez-faire approach, with the implication that AIDS was nature's way of culling out undesirables.

Soon after my time on the AIDS ward, the cause of AIDS was identified: human immunodeficiency virus (HIV).

Supported by science, AIDS activists refused to accept that HIV was an inevitable death sentence and launched a hard-hitting campaign demanding research on treatments. Within years, there was a proliferating alphabet soup of anti-HIV medications, which ultimately ensured that most of those infected could live near-normal life spans.

Success produced a paradox: Increased years of potential infectivity meant an expanding epidemic. In 2010, I was working for the CDC on HIV prevention in Kenya, with a tiny role in an ongoing giant multi-national study examining whether it was possible to use anti-HIV treatment to stop HIV transmission. In a meeting room in the local public hospital, I was speaking to a group of health care workers who were going to carry out this study and others.

Almost all were women. They were being paid the standard princely salary of about $300 a month. They were our study workers because they came from the community most at risk. One-in-four women in their age group were HIV infected. Access to anti-HIV medication was fiscally and logistically limited. Only a third of those who needed treatment actually received it. That meant an unknown number of the women to whom I was speaking were ultimately going to die the same death as those in the San Francisco AIDS ward. But they went out to the villages and did the hard work to enroll study subjects and bring home the data.

Because of these women and others across the globe, the resulting 2016 scientific publication became one of the most cited and influential studies in medicine. For the first time, it demonstrated that HIV transmission was not inevitable. It could be stopped cold through anti-HIV treatment. Zero transmission — IF appropriate treatment is received.

Fast forward a decade, and RFK Jr., is an HIV skeptic, suggesting that a conspiracy of persons with personal ambitions had diverted attention away from other potential causes of AIDS, such as a "toxin." He's also claimed, without evidence, that anti-HIV medications were based on "phony, crooked" studies that killed people.

In 2025, five of the 11 branches of the CDC's Division of HIV Prevention were abolished and the employees laid off. All the CDC's HIV websites were taken down. After being restored by court order, the web page on treatment now contains the header, "This page does not reflect biological reality and therefore the Administration and this Department rejects it." A similar header appeared on the HIV prevalence page, but some brave CDC soul managed to insert an explanation why the data was frozen in 2023: "the branches that produced HIV incidence estimates... were eliminated." RFK Jr. cancelled $759 million in HIV research grants, and proposed that responsibility for HIV be transferred from the CDC and all other agencies to a new Administration for a Healthy America under his direct control, with a funding reduction of 80%. Pending that reorganization, a half-billion dollars in budget cuts from HIV treatment were put before Congress.

All this came at the moment when the tools to end the HIV epidemic seemed to be in our hands. New cases had been cut by more than 90%, and maternal-to-child transmission had been eliminated completely.

Now, instead of having resources to finish the job, states are implementing or considering a host of expenditure reduction measures: treatment waiting lists, reduced formulary options, work requirements, low income requirements, an end to reimbursement for the lab assays needed to know if the medications were working.

Similar cutbacks are happening globally, as the U.S. withdrew assistance from international HIV prevention. With our domestic defenses being stripped away and an increased threat of foreign exposures, viral spread will obviously accelerate to infect far more than the current 1-in-300 Americans. Those new cases will infect others. Inevitably, HIV will escape from its risk groups to create a generalized pandemic in the U.S.

1983 redux?

Thanks to almost 50 years of hard work by AIDS activists in San Francisco, village health workers in Kenya, laboratorians across the world, along with so many others, the choices now seem clear: With appropriate treatment, we can bring the HIV epidemic to a halt before it becomes a pandemic, allow the infected to live near normal lives, and provide great cost-savings for society. Or, with lack of treatment, we can have uncontrolled transmission, a spreading epidemic that becomes a pandemic, tormented deaths for individuals, and great costs for society.

In this choice, perhaps the term "1983" should take on the same resonance for health that George Orwell once gave the term "1984" for politics. For HIV, do we really want to return to the hopelessness of 1983? Or do we defy inevitability, use strong advocacy backed by strong science to restore our defenses, stop the HIV resurgence before it starts, and put an end to the epidemic before it becomes a pandemic?

Opinion on Live Science gives you insight on the most important issues in science that affect you and the world around you today, written by experts and leading scientists in their field.

A vaccine designed using "DNA origami" activated more of the key immune cells needed to fight HIV than did traditional vaccines built upon protein scaffolds, a new mouse study found.

"DNA origami" refers to a precisely engineered, three-dimensional scaffold made of folded DNA that can hold and display viral antigens — bits of viruses that the immune system can recognize and attack.

The new mouse study's results, published Feb. 5 in the journal Science, suggest a "potential breakthrough" that could "transform the way we think about active immunotherapies and vaccine design," study co-author Mark Bathe, a professor of biological engineering at MIT, said in a statement.

Why could this origami approach be transformational? The answer may lie in how the DNA-based vaccines are seen by the immune system, compared to traditional vaccines.

How the DNA origami vaccine works

Conventionally, vaccines have relied on weakened or killed viruses to rouse immune cells to make antibodies against proteins found on that virus's surface. By binding to the proteins, the antibodies block the virus from invading human cells and flag the germ for destruction by other immune cells.

This process imparts immunity by prompting the body to make "memory B cells," which linger and get activated much faster if the same pathogen is encountered again.

But nowadays, rather than using whole viruses, many vaccines use only the surface antigens attached to synthetic, virus-like particles. These nanostructures mimic the size and geometry of viruses but cannot cause infection.

Most virus-like particles used today are built using protein scaffolds that the immune system sees as "foreign," so they trigger an "off-target" antibody response against the scaffold itself. In some contexts, this may dilute the responses against the antigen, previous studies suggest.

In the new study, scientists replaced the protein scaffolds with a DNA-based scaffold and, by doing so, sharply reduced those off-target responses. This new vaccine design produced up to three times more of the important memory B cells than state-of-the-art protein nanoparticle vaccines did.

John Moore, an HIV researcher at Weill Cornell Medicine who was not involved in the work, described the study as "elegant." It clearly demonstrates how eliminating scaffold-related immune responses pushes the immune response "in the right direction," he told Live Science.

He cautioned, however, that it remains to be seen whether the same degree of immune focusing will occur in humans.

An edge on the competition?

HIV evades the immune system by constantly reshaping its surface proteins so that antibodies that work against one strain often fail against others. That is why HIV vaccine design has been "incredibly challenging," said Adam Wheatley, an immunologist at the University of Melbourne who was not involved in the study.

What the vaccine needs to produce are "broadly neutralizing antibodies" against the virus, he said. These antibodies lock onto parts of the virus that barely change from strain to strain.

One example of such an antibody is called VRC01, which has been identified in a small number of people living with HIV whose bodies produce broad antibody responses. VRC01 targets a vulnerable region on HIV's outer envelope called the CD4-binding site. This is the "key" the virus uses to enter human immune cells, and it doesn't differ much between strains.

The challenge is that B cells that are capable of producing VRC01-like antibodies are extraordinarily rare in the human body, said Raiees Andrabi, an immunologist at the University of Pennsylvania who was not involved in the work. Activating those elusive cells "becomes an engineering problem," he told Live Science.

To target these rare B cells, the researchers carefully engineered the vaccine using an HIV antigen on the DNA scaffolding. Developed about a decade ago, the antigen they used mimics the CD4-binding site and selectively binds the rare B cells' receptors, thus initiating the production of broadly neutralizing antibodies.

The researchers got the idea to combine the antigen with DNA origami after testing the origami approach in an experimental COVID-19 vaccine. They'd found that the immune system showed virtually no response to the DNA scaffold.

"This property seemed especially useful for a case like HIV, where the B cells of interest are exceptionally rare," first study author Anna Romanov, an immunology researcher at MIT, said in the statement.

They hypothesized that delivering the antigen on a silent scaffold could reduce the competition with other irrelevant B cells, thereby boosting the "on-target" response against HIV. And in the study, they found the silent-scaffold approach had indeed amplified the B cells that produce broadly neutralizing antibodies. (That said, they have not yet assessed how many broadly neutralizing antibodies actually get made; that should be addressed in future work.)

"We were all surprised" that DNA origami outperformed the standard virus-like particles used in eliciting the desired B cell responses, Bathe said.

In general, it's unclear how bad it is for the body to generate an immune response against the scaffold, Wheatley said. But in the case of HIV, the desired B cells are so rare that even a modest off-target response seems to undermine the response against the target antigen.

The road ahead

The engineering of the DNA-origami vaccine was not straightforward; early versions produced weak immune responses. That was partly because, after injection, those vaccines failed to reach specialized immune cells inside the lymph nodes, where B cells train.

To correct this, the team redesigned the DNA particles to pack the HIV antigens more precisely and tightly. This enabled them to be carried into the right regions within the lymph nodes. The researchers also added a molecule to help activate T cells — immune cells help the critical immune response grow. This T-cell recruitment happens naturally with protein-scaffold vaccines.

"I think it is quite striking how efficiently they modified their DNA scaffold in a number of ways to get it to work," Wheatley said. "I guess the major utility of it is [that] it's really tunable."

Beyond HIV, the study authors suggest that DNA origami could be applied to make vaccines against other rapidly mutating viruses, such as influenza, where the effectiveness of the vaccine might be improved by focusing the immune response it triggers.

However, it remains to be seen how well this technique will translate to humans. HIV vaccination is "very difficult" and might have multiple components to help develop the immune response over time, Andrabi explained, adding, "It's not just going to be one or two shots."

However, he said, "they have figured out the first step."

Around the world, some 40 million people are living with HIV. And though progress in treatment means the infection isn't the death sentence it once was, researchers have never been able to bring about a cure. Instead, HIV-positive people must take a cocktail of antiretroviral drugs for the rest of their lives.

But in 2025, researchers reported a breakthrough that suggests that a "functional" cure for HIV — a way to keep HIV under control long-term without constant treatment — may indeed be possible. In two independent trials using infusions of engineered antibodies, some participants remained healthy without taking antiretrovirals, long after the interventions ended.

In one of the trials — the FRESH trial, led by virologist Thumbi Ndung'u of the University of KwaZulu-Natal and the Africa Health Research Institute in South Africa — four of 20 participants maintained undetectable levels of HIV for a median of 1.5 years without taking antiretrovirals. In the other, the RIO trial set in the United Kingdom and Denmark and led by Sarah Fidler, a clinical doctor and HIV research expert at Imperial College London, six of 34 HIV-positive participants have maintained viral control for at least two years.

These landmark proof-of-concept trials show that the immune system can be harnessed to fight HIV. Researchers are now looking to conduct larger, more representative trials to see whether antibodies can be optimized to work for more people.

"I do think that this kind of treatment has the opportunity to really shift the dial," Fidler says, "because they are long-acting drugs" — with effects that can persist even after they're no longer in the body. "So far, we haven't seen anything that works like that."

People with HIV can live long, healthy lives if they take antiretrovirals. But their lifespans are still generally shorter than those of people without the virus. And for many, daily pills or even the newer, bimonthly injections present significant financial, practical and social challenges, including stigma. "Probably for the last about 15 or 20 years, there's been this real push to go, 'How can we do better?'" says Fidler.

The dream, she says, is "what people call curing HIV, or a remission in HIV." But that has presented a huge challenge because HIV is a master of disguise. The virus evolves so quickly after infection that the body can't produce new antibodies quickly enough to recognize and neutralize it.

And some HIV hides out in cells in an inactive state, invisible to the immune system. These evasion tactics have outwitted a long succession of cure attempts. Aside from a handful of exceptional stem-cell transplants, interventions have consistently fallen short of a complete cure — one that fully clears HIV from the body.

A functional cure would be the next best thing. And that's where a rare phenomenon offers hope: Some individuals with long-term HIV do eventually produce antibodies that can neutralize the virus, though too late to fully shake it. These potent antibodies target critical, rarely changing parts of HIV proteins in the outer viral membrane; these proteins are used by the virus to infect cells. The antibodies, able to recognize a broad range of virus strains, are termed broadly neutralizing.

Scientists are now racing to find the most potent broadly neutralizing antibodies and engineer them into a functional cure. FRESH and RIO are arguably the most promising attempts yet.

In the FRESH trial, scientists chose two antibodies that, combined, were likely to be effective against HIV strains known as HIV-1 clade C, which is dominant in sub-Saharan Africa. The trial enrolled young women from a high-prevalence community as part of a broader social empowerment program. The program had started the women on HIV treatment within three days of their infection several years earlier.

The RIO trial, meanwhile, chose two well-studied antibodies shown to be broadly effective. Its participants were predominantly white men around age 40 who also had gone on antiretroviral drugs soon after infection. Most had HIV-1 clade B, which is more prevalent in Europe.

By pairing antibodies, the researchers aimed to decrease the likelihood that HIV would develop resistance — a common challenge in antibody treatments — since the virus would need multiple mutations to evade both.

Participants in both trials were given an injection of the antibodies, which were modified to last around six months in the body. Then their treatment with antiviral medications was paused. The hope was that the antibodies would work with the immune system to kill active HIV particles, keeping the virus in check. If the effect didn't last, HIV levels would rise after the antibodies had been broken down, and the participants would resume antiretroviral treatment.

Excitingly, however, findings in both trials suggested that, in some people, the interventions prompted an ongoing, independent immune response, which researchers likened to the effect of a vaccine.

In the RIO trial, 22 of the 34 people receiving broadly neutralizing antibodies had not experienced a viral rebound by 20 weeks. At this point, they were given another antibody shot. Beyond 96 weeks — long after the antibodies had disappeared — six still had viral levels low enough to remain off antiviral medications.

An additional 34 participants included in the study as controls received only a saline infusion and mostly had to resume treatment in four to six weeks; all but three were back on treatment within 20 weeks.

A similar pattern was observed in FRESH (although, because it was mostly a safety study, this trial did not include control participants). Six of the 20 participants retained viral suppression for 48 weeks after the antibody infusion, and of those, four remained off treatment for more than a year. Two and a half years after the intervention, one remains off antiretroviral medication. Two others also maintained viral control but eventually chose to go back on treatment for personal and logistical reasons.

It's unknown when the virus might rebound, so the researchers are cautious about calling participants in remission functionally cured. However, the antibodies clearly seem to coax the immune system to fight the virus. Attached to infected cells, they signal to immune cells to come in and kill.

And importantly, researchers believe that this immune response to the antibodies may also stimulate immune cells called CD8+ T cells, which then hunt down HIV-infected cells. This could create an "immune memory" that helps the body control HIV even after the antibodies are gone.

The response resembles the immune control seen in a tiny group (fewer than 1%) of individuals with HIV, known as elite controllers. These individuals suppress HIV without the help of antiretrovirals, confining it mostly to small reservoirs. That the trials helped some participants do something similar is exciting, says Joel Blankson, an infectious diseases expert at Johns Hopkins Medicine, who coauthored an article about natural HIV controllers in the 2024 Annual Review of Immunology. "It might teach us how to be able to do this much more effectively, and we might be able to get a higher percentage of people in remission."

One thing scientists do know is that the likelihood of achieving sustained control is higher if people start antiretroviral treatment soon after infection, when their immune systems are still intact and their viral reservoirs small.

But post-treatment control can occur even in people who started taking antiretrovirals a long time after they were initially infected: a group known as chronically infected patients. "It just happens less often," Blankson says. "So it's possible the strategies that are involved in these studies will also apply to patients who are chronically infected."

A particularly promising finding of the RIO trial was that the antibodies also affected dormant HIV hiding out in some cells. These reservoirs are how the virus rebounds when people stop treatment, and antibodies aren't thought to touch them. Researchers speculate that the T cells boosted by the antibodies can recognize and kill latently infected cells that display even trace amounts of HIV on their surface.

The FRESH intervention, meanwhile, targeted the stubborn HIV reservoirs more directly through incorporating another drug, called vesatolimod. It's designed to stimulate immune cells to respond to the HIV threat, and hopefully to "shock" dormant HIV particles out of hiding. Once that happens, the immune system, with the help of the antibodies, can recognize and kill them.

The results of FRESH are exciting, Ndung'u says, "because it might indicate that this regimen worked, to an extent. Because this was a small study, it's difficult to, obviously, make very hard conclusions." His team is still investigating the data.

This article originally appeared in Knowable Magazine, a nonprofit publication dedicated to making scientific knowledge accessible to all. Sign up for Knowable Magazine’s newsletter.

New HIV vaccines have shown promise in studies with lab animals and human volunteers, pointing to a potential way of preventing the lifelong viral disease.

These experimental vaccines are built upon mRNA technology and several triggered potent immune responses in these early tests, while also causing few side effects.

Scientists described the new vaccines in a pair of studies published Wednesday (July 30) in the journal Science Translational Medicine. The first study tested a few vaccines in rabbits and monkeys, and the promising results of that work led to further development of the shots and the subsequent human trial. The trial included over 100 healthy human volunteers and tested three vaccines similar to those tested in animals.

The effort "marks significant progress in the global effort to develop a safe and effective HIV vaccine that prevents infection," said Seth Cheetham, director of the Australian mRNA Cancer Vaccine Centre and deputy director of the BASE mRNA manufacturing facility at the University of Queensland.

"While drugs for HIV treatment and prevention have transformed the lives of people living with HIV, an effective vaccine is still urgently needed," Cheetham, who was not involved in the work, told Science Media Exchange.

Over the past decade, the annual rate of new human immunodeficiency virus (HIV) infections has fallen significantly, according to the World Health Organization, but, each year, many hundreds of thousands still occur. Globally, an estimated 1.3 million people acquired HIV in 2024, including about 120,000 children. An HIV vaccine could be transformative if, in just a few doses, it could raise the immune system's ability to block the virus from taking hold in the first place.

Related: Nearly 3 million extra deaths by 2030 could result from HIV funding cuts, study suggests

Currently, preventive medications for HIV must be taken on an ongoing basis — either daily, every other month or twice yearly. This can pose a particular challenge in areas with limited health care resources and infrastructure. Many scientists think a vaccine will be the key to ending the HIV/AIDS epidemic worldwide, because such a tool could efficiently stymie new infections and curb further spread of the disease.

But crafting an HIV vaccine is very challenging. The virus expertly evades the immune system by donning disguises, and it mutates rapidly, constantly switching up its look. Ideally, HIV vaccines will trigger the production of elusive "broadly neutralizing antibodies" — proteins that target relatively immutable bits of the virus that look similar across many strains and can block infections, thus offering wide-ranging protection.

Scientists are exploring different strategies to trigger that protection. On that front, the researchers behind the new studies turned to messenger RNA (mRNA), a molecule that serves as instructions for cells to make proteins. They designed their experimental vaccines to carry directions for a complex of proteins found on the surface of HIV. Called the "envelope trimer," this complex enables the virus to grab the surface of human immune cells and invade those cells.

Once injected into the body, the vaccines prompt cells to build one of two versions of the envelope trimer: one that exits the cell and floats away, and another that stays bound to the surface of the cell. The free-floating version has been targeted in prior HIV vaccines studies, but previously hasn't produced adequate neutralizing antibodies, the study authors noted.

They think this is because, on the surface of a real HIV particle, the base of the trimer is embedded inside the virus and thus hidden from view. They anticipated that the latter version of the trimer — the one that stays stuck to the cell — would trigger better neutralizing responses that take aim at other parts of the complex, rather than the base.

That turned out to be the case in both the animal study and the early clinical trial.

For the human trial, the researchers recruited 108 healthy people ages 18 to 55, split them into three groups, and gave each group one of three mRNA vaccines. One vaccine encoded a free-floating trimer, while the latter two encoded different bound versions of the structure. Each participant received three doses of their assigned vaccine: one at the initial visit, another two months later, and a final dose six months after the first.

As in the animal tests, the bound trimers elicited stronger signs of protection than the free-floating trimer did. The bound-trimer vaccines produced neutralizing antibodies in 80% of those vaccinated, while the free-floating-trimer vaccine triggered the same response in only 4% of the recipients.

Related: In a 1st, HIV vaccine triggers rare and elusive antibodies in humans

The bound-trimer vaccines also "generated strong memory responses, meaning the body would be better prepared to fight off HIV even long after vaccination," Cheetham noted. This would be thanks to antibody-producing memory B cells, which persist for a long time to help mount quick immune responses against germs they've encountered in the past, either through infection or vaccination.

The human trial was primarily designed to look at the safety of the vaccines, and they were "well tolerated overall." They triggered mostly mild and transient side effects, such as fatigue, achiness, headache, chills, nausea and injection-site pain. However, hives, also called urticaria, were seen in seven participants, which the authors noted was "a far higher frequency than reported with COVID-19 mRNA vaccines." Several of the affected individuals experienced the skin reaction for months.

"While most adverse reactions were mild and treatable, several people experienced a skin reaction," Cheetham said. "If these side effects can be reduced in next-generation versions and the results hold up in larger real-world studies in the community, mRNA vaccines could be a transformative tool in the fight against HIV."

The trial had several other limitations. First, it was open-label, meaning the researchers and vaccine recipients knew which shots were being given, which can potentially bias the results. In addition, the vaccines were not specifically designed to make broadly neutralizing antibodies that can handle many strains but rather neutralizing antibodies that can tackle only select strains.

Nonetheless, the trial results provide insight into the safety and efficacy of mRNA vaccines that code for HIV envelope trimers, the researchers noted. It should inform future efforts to refine these vaccines so they trigger more broadly protective antibody responses.

This article is for informational purposes only and is not meant to offer medical advice.

Human immunodeficiency virus (HIV) is a germ that causes a lifelong infection that slowly weakens the immune system. Though the infection is lifelong, medicines can keep the virus in check and help people reach lifespans of near-normal length.

However, when people don't have access to those medicines, HIV infections progress to an advanced stage called acquired immunodeficiency syndrome (AIDS), which is fatal within about three years if not treated. When a person has AIDS, most of their key, disease-fighting immune cells are lost. This loss of immune protection leaves the person vulnerable to deadly infections and cancers.

Although an HIV diagnosis was once a death sentence, scientists have developed treatments that suppress the virus and enable people to live long lives without transmitting the disease to others. Additionally, there are now effective preventive medications that can dramatically reduce the risk of getting HIV in the first place.

There is not yet a widespread cure for HIV/AIDS, although a handful of people have been cured of the infection or are in long-term remission thanks to special stem-cell transplants, specially cell transplants from people who have genes that make them resistant to the virus. Scientists are exploring potential avenues for a cure, which could someday mean that people who contract HIV could be rid of the infection rather than having to take medication for life to manage the disease.

HIV/AIDS remains a major public health threat worldwide, with an estimated 39.9 million people living with the disease at the end of 2023. Around 630,000 people died from illnesses related to AIDS the same year; by weakening the immune system, AIDS opens the door to these fatal diseases.

Everything you need to know about HIV

Glossary

• Antiretroviral therapy (ART) – Combinations of medications that lower the amount of HIV in a person's blood. These drugs, given as pills or shots, prevent the viral infection from progressing to AIDS and dramatically lower a person's risk of complications and of transmitting the virus to others.
• Pre-exposure prophylaxis (PrEP) – Medicines that people at risk of being exposed to HIV take to prevent the infection.
• Viral load – The amount of HIV in a person's blood. This is measured in terms of the number of HIV RNA molecules — the virus's genetic material — found in a milliliter of blood. It's an important way to measure how well ART is working.
• Viral suppression – When a person's viral load falls to 200 copies/mL or lower. Viral suppression is the goal of ART, as it both lowers a person's likelihood of spreading the virus and extends their lifespan by preventing the infection from progressing to AIDS.
• CD4 T lymphocyte – A type of white blood cell that helps coordinate the actions of other immune cells to fight infections. HIV infects CD4 cells and uses them to multiply while the virus depletes the number of CD4 cells in the body.

HIV/AIDS pictures

Discover more about HIV

• We could end the AIDS epidemic in less than a decade. Here's how.
• In a 1st, HIV vaccine triggers rare and elusive antibodies in humans
• Nearly 3 million extra deaths by 2030 could result from HIV funding cuts, study suggests

Editor's note: This story was first published on March 26, 2025.

We could see up to 10.8 million more HIV cases than anticipated in the next five years if planned cuts to international HIV funding take place.

This surge in infections in low- and middle-income countries would contribute up to 2.9 million more HIV-related deaths by 2030.

These disturbing figures come from a new modeling study published March 26 in the journal The Lancet HIV. The researchers wanted to analyze the potential impact of cuts to international funding for HIV/AIDS programs, which work to prevent both transmission and deaths related to the infection.

As of February 2025, the five top donors of this funding — the United States, United Kingdom, France, Germany and the Netherlands — have all announced significant cuts to foreign aid that threaten HIV programs worldwide. The study predicts how these cuts would impact low- and middle-income countries (LMICs), which since 2015 have relied on international sources for 40% of their HIV program funding.

"These findings are a sobering reminder that progress in the fight against HIV is not guaranteed — it is the result of sustained political will and investment," said Dr. Ali Zumla, a professor of infectious diseases and international health at University College London who was not involved in the research.

But equally, "the projected surge in new infections and deaths is not an inevitability; it is a consequence of choices being made today," Zumla told Live Science in an email. "If these funding cuts move forward, we risk unraveling decades of hard-won progress, leaving millions vulnerable and pushing global HIV goals further out of reach."

Related: We could end the AIDS epidemic in less than a decade. Here's how.

Unprecedented cuts to aid

As of 2023, five donors have supplied more than 90% of the international funding for HIV programs, with the United States providing over 72% of the total. Specific populations at high risk of HIV — including people who inject drugs, men who have sex with men, female sex workers and their clients, and transgender and gender diverse people — particularly rely on these international funding sources for access to HIV prevention and testing.

Much of the U.S. funding comes from the President's Emergency Plan for AIDS Relief (PEPFAR), which is largely implemented by the Agency for International Development (USAID). However, PEPFAR and USAID were hit by an unprecedented funding pause and staffing reduction in January, following an executive order from President Donald Trump.

PEPFAR later received a temporary waiver to continue some services, including those for antiretroviral therapy (ART), the drugs that keep HIV from progressing to AIDS. These treatments must be taken consistently or the virus will rebound.

"The widespread rollout and uptake of antiretroviral therapy funded by international sources has been one of the most important factors reducing AIDS related deaths in lower income settings," said Justin Parkhurst, an associate professor of global health policy at the London School of Economics and Political Science who was not involved in the study. ART also cuts the number of new infections by suppressing the virus in people living with HIV, thus preventing transmission, he told Live Science in an email.

However, despite the waiver, PEPFAR's services still haven't resumed as normal, given the waiver didn't trigger immediate funding to eligible programs and many clinics had already shuttered by the time it was issued. Even now, PEPFAR's future after the waiver's expiration remains uncertain.

Following the U.S., the next top four donors for international HIV funding are the U.K., France, Germany and the Netherlands. However, as of February 2025, each of these donors has also announced major cuts in foreign aid spending — "and more might follow," the study authors wrote.

Based on the projected cuts being made by the top five donors, the researchers used a mathematical model to predict the rates of new HIV cases and deaths. They focused their model on 26 LMICs, which together receive 49% of international HIV aid, overall, and 54% of PEPFAR aid. They then used the data from these 26 countries to extrapolate to all LMICs worldwide.

Cuts could "undo nearly all progress achieved since 2000"

The researchers considered several scenarios in their model. The first — the "status quo" — served as a baseline, projecting the rates of cases and deaths if recent levels of HIV spending were maintained between 2025 and 2030, rather than cut. In this scenario, more than 1.8 million new infections and over 720,000 HIV-related deaths occurred in LMICs.

In the worst-case scenario the team considered, all PEPFAR funding was indefinitely stopped on Jan. 20, 2025, and no alternative funding sources emerged to fill that gap. Simultaneously, other, non-PEPFAR sources of international funding were also reduced. That scenario led to an estimated 10.8 million more cases and 2.9 million more deaths than the status quo.

Related: Single-shot HIV treatment suppresses virus 10,000-fold for months, animal study finds

This suggests that "the number of new infections in 2026 could return to 2010 levels, and by 2030 the number of new infections could surpass historical estimates," the study authors wrote. "In the worst-case scenario, if PEPFAR funding were ceased entirely and no equivalent mechanism replaced it, surges in HIV incidence could potentially undo nearly all progress achieved since 2000."

This worst-case scenario would hit sub-Saharan Africa (SSA) particularly hard — out of eight SSA countries included in the analysis, six receive over 40% of their HIV funding through PEPFAR. Children in the region could see a nearly three-fold increase in HIV infections, the authors predicted.

And outside of SSA, other vulnerable populations, such as sex workers, would be much harder hit by such cuts than the general population, showing up to a six-fold higher increase in cases than other demographics, the data suggested.

The team also looked at a less extreme scenario, modeling what would happen if new funding sources filled the gap left by PEPFAR. In this scenario, they assumed that the gap could be partially filled by 2026 and then fully filled by 2027. If that mitigation were to happen, the number of extra cases drops to 4.4 million and the extra deaths to 770,000 over the course of five years.

So while filling the gap left by PEPFAR would help substantially, that sudden loss of funding would still have devastating impacts, the study suggests.

"Modelling reveals the potential for severe consequences following abrupt stopping, with no notice, of international support aimed at stopping AIDS as a global public health threat," Dr. Catherine Hankins, a professor of global and public health at McGill University in Canada who was not involved in the study, told Live Science in an email.

Cuts could be felt for decades to come

According to the study authors, even if the PEPFAR gap could be filled within two years, the ripple effects would be felt for decades to come. They estimated that it would take 20 to 30 extra years of 2024-level funding to end AIDS as a public health threat.

Ambitious goals set by UNAIDS have aimed to end the threat by 2030. And historic HIV trends suggested that many of the LMICs featured in the new paper could have hit their targets by about 2036, if funding continued at past levels, the authors wrote.

"This study indicates that an abrupt termination of programmes has serious risks to human life," Parkhurst said. "Even for those who believe the US or other governments should reduce foreign aid spending in this area, there can be planning around how to do so without producing serious harm to millions of people around the world who have come to rely on the treatment."

The study suggests that, if that abrupt stop could be avoided, many lives could be spared.

The researchers looked at what would happen if PEPFAR was reinstated or "equivalently recovered" and estimated that there could be 70,000 to 1.73 million extra cases and 5,000 to 61,000 extra deaths, compared to status quo. Those estimates assume that other international funding will still be reduced, but that countries will be able to make up for some of the lost funds domestically.

The new study has some limitations, as "there is inherent uncertainty in global modelling," said study co-first author Rowan Martin-Hughes, a senior research officer at the Burnet Institute in Australia.

The "most important" limitation is that there is uncertainty in the HIV fiscal space, although the authors covered some of that unpredictability by looking at a range of possible outcomes, Martin-Hughes told Live Science in an email. There are also gaps in the global reporting of financial data that could affect their model, and the 26 featured countries might not be fully representative of the overall impacts of funding cuts, he added.

However, "overall, we think most sources of uncertainty are likely to result in underestimating rather than overestimating the real effects of immediate and severe funding cuts to HIV programmes globally, especially in the sub-Saharan African region," he said.

In light of the impending cuts, "it is paramount now to track AIDS mortality and HIV incidence while urgently reversing the cuts, mitigating the effects, and creating new funding strategies to prevent further suffering," Hankins said.

Martin-Hughes agreed.

"Governments, donors, and stakeholders must collaborate on feasible mitigation strategies to preserve HIV prevention, testing, and treatment services to avoid a resurgence in the HIV epidemic," he said. "In doing so, the global community can secure both the immediate and long-term stability of resilient health systems so integral to saving lives through HIV epidemic control."

Global investment, especially from the U.S., has put targets for the elimination of HIV transmission within reach, he said. "But all of that progress is vulnerable, and could be wiped out within a few years if there are dramatic and unmanaged cuts to HIV services."

Smoking, being exposed to toxic chemicals or radiation, and carrying mutations in certain genes are some of the best-known risk factors for cancer. But another cause of cancer isn't discussed as often: viruses.

So which viruses can cause cancer, and how do they do it?

There are at least seven viruses that are known to contribute to the development of cancer in humans, either directly or indirectly. These include human papillomaviruses (HPV), hepatitis B virus (HBV), hepatitis C virus (HCV), Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus, human T-cell lymphotropic virus and Merkel cell polyomavirus. In addition, human immunodeficiency virus (HIV) raises the risk of cancer in part by opening the door for cancer-driving viruses to invade the body.

It's important to note, however, that only a small percentage of people who are infected with these viruses go on to develop cancer — in other words, catching one of these viruses doesn't guarantee that you'll develop cancer. For example, over 90% of adults worldwide have been infected with EBV at some point in their lives, but only 1% of cancers are associated with EBV, the virus behind "mono."

Related: What's the oldest known case of cancer in humans?

Cases driven by all these viruses do add up, though. An estimate based on 2012 infection numbers suggested that viral infections may contribute to more than 1.4 million cancer cases worldwide that year, representing about 10% of all cancer cases.

"For a long time, many people in the field were very skeptical that any virus has caused cancer in people," Dr. Jay Berzofsky, a senior investigator at the National Cancer Institute, told Live Science. "And then, once there were some discovered, more people jumped on that bandwagon and found more."

Berzofsky explained that viruses can have carcinogenic, or cancer-causing effects through both direct and indirect mechanisms, and each virus can cause cancer through a unique route.

Direct mechanisms

One of the best-known viruses that can cause cancer is HPV, a family of viruses that is responsible for more than 37,000 new cancer cases in the U.S. each year. The virus is known for its association with cervical cancer, but it can also cause anal, oropharyngeal (back of the throat), penile, vaginal and vulvar cancers.

Certain HPV viruses promote cancer by transforming normal, healthy cells into abnormal, tumorous cells. This happens because HPV manufactures certain proteins, called E6 and E7 oncoproteins, that inactivate the natural tumor suppressor systems of healthy cells.

"That allows the abnormal cells to grow uncontrolled," Dr. Harrys Torres, a professor of infectious diseases at the University of Texas MD Anderson Cancer Center, told Live Science.

There are more than 200 types of HPV, but only 12 have been strongly associated with cancers. The HPV vaccine, which is recommended for all children between the ages of 11 and 12, protects against these high-risk forms of the virus that could lead to cancer. People can get the shot up to age 26 if they didn't previously receive all their recommended doses.

Other viruses that can directly cause cancer, like EBV and human T-cell lymphotropic virus, exert their effects through different cellular and genetic mechanisms. However, the result is ultimately similar: cancerous cells start to replicate aggressively and evade the body's natural defense systems.

Many factors influence whether infection with these viruses lead to cancer. In the case of HPV and EBV, certain strains have more cancer-causing potential than others. People with weakened immune systems are also at greater risk of developing virus-related cancers. And external factors, such as existing mutations or exposure to environmental carcinogens, can multiply the likelihood of tumor growth.

Related: New self-swab HPV test is an alternative to Pap smears. Here's how it works.

Indirect mechanisms

Viruses can cause cancer through more indirect mechanisms, too. Both HBV and HCV illustrate this. HBV and HCV infect the liver, which in the case of chronic infections, leads to long-term inflammation and cirrhosis, or scarring of the liver.

"Anything that causes chronic inflammation can potentially increase the risk of cancer," Berzofsky said.

As the body tries to repair the extensive damage from HBV or HCV by making new liver cells, there's a chance that some of those cells will mutate and become cancerous. HCV is also associated with non-Hodgkin's lymphoma, a cancer of the lymphatic system, possibly because the constant stimulation of the immune system caused by the virus spurs the development of cancerous cells.

HIV can also raise the risk of cancer developing through indirect mechanisms. That's because uncontrolled HIV infections cause chronic inflammation and weakens the immune system, which makes the body more susceptible to the other viruses directly associated with cancer.

Prevention is key

Although the ways these viruses can cause cancer can be complex and layered, Torres said there are methods for preventing and treating some of these infections.

There are vaccines against HPV and HBV, both of which are highly effective. For example, recent data found absolutely no new cases of cervical cancer in a large cohort of young women in Scotland who had received the HPV vaccine between the ages of 12 and 13.

Both HIV and HBV spread through multiple bodily fluids, such as blood and semen, while HCV primarily spreads through just blood. Using condoms and never sharing needles can help reduce the risk of contracting the infections, and preventative medicines called PrEP are also available for HIV. Note that these viruses can also spread to fetuses and newborns during pregnancy, childbirth or breastfeeding, so pregnant people are advised to get tested for the infections.

Antiviral treatments can also keep conditions like HIV and chronic HBV at bay, making them less likely to cause cancer. And HCV infections are curable with antivirals.

Torres is hopeful that vaccination, prevention and treatment of these viruses can help decrease the global cancer burden.

"It's a work in progress," he said. "We're trying to do as much as we can."

Researchers have developed an experimental HIV treatment that sustains itself in the body, with the goal of controlling virus levels for the long term after a single dose.

So far, the new treatment has been tested in monkeys, not people. But in the monkeys, it dramatically suppressed HIV for at least seven months. If the drug is approved for people someday, its protection might last years, said Adrian Wildfire, a virologist and drug development scientist who was not involved in the research.

"I suspect you'll see some decline in function [of the treatment] after five to seven years," Wildfire told Live Science. That represents a big jump from current treatment options.

About 40 million people worldwide are living with HIV, but only about three-quarters of them are currently receiving antiretroviral therapy, the standard treatment. A smaller percentage are virally suppressed, meaning the amount of HIV in their body has declined to extremely low levels.

Related: We could end the AIDS epidemic in less than a decade. Here's how.

Some people face difficulties obtaining an HIV diagnosis and therapy prescription; others may struggle to afford medication, tolerate its side effects, or remember to take the daily pills many treatment regimens require to keep the virus at bay. Some existing long-acting shots last weeks or months, but people typically need to reach suppression with pills before qualifying for the shots.

Complicating the challenge, the virus also evolves very quickly, meaning it can become resistant to treatments, especially if doses are missed. Without treatment, HIV rapidly destroys a key class of immune cell in the body, leaving the person vulnerable to cancers and infectious diseases. At this stage, the infection has progressed to acquired immunodeficiency syndrome (AIDS).

To overcome some of the issues with existing antiretrovirals, a group of researchers developed a new type of treatment: an engineered form of the virus that can outcompete HIV in the body.

In a study published Aug. 9 in the journal Science, the researchers used genetic engineering to create a version of HIV called a therapeutic interfering particle (TIP). This virus-like particle is designed not to harm its host, but it still replicates quickly. The idea is that, when injected into a person with HIV, the harmless TIP takes over, occupying and protecting cells that the virus would otherwise destroy.

To test that theory, the researchers developed a version of their TIP that resembled simian immunodeficiency virus (SIV), an HIV-like pathogen that infects monkeys. They injected it into six rhesus macaques (Macaca mulatta). After 24 hours, they infected the macaques with an aggressive virus with features of both SIV and HIV and tracked levels of infection for about seven months.

They found that the macaques that received TIPs had 10,000 times lower levels of virus than four infected monkeys that hadn't received the shot. The TIP-injected monkeys also had stronger immune responses and no evidence of inflammation. The untreated monkeys had quickly developed severe illnesses.

Related: People on HIV meds have 'almost zero' chance of spreading virus via sex once levels are low

As designed, the TIPs continued to replicate in the macaques' bodies throughout the entire study period, hinting that long-lasting treatment may be possible.

"These primate studies show the promise of a single-dose TIP intervention and are a strong indicator of efficacy in human trials," senior study author Leor Weinberger, a professor of pharmaceutical chemistry, biochemistry and biophysics at the University of California, San Francisco, said in a statement.

The researchers also applied their TIPs to lab mice with human immune cells and to blood cells from people living with HIV. In both cases, the TIPs outcompeted HIV and suppressed the infection.

"You're reducing viral replication a lot, which could allow people to live with fewer symptoms because far fewer of their T cells are being destroyed," Wildfire told Live Science. But he doesn't think the treatment will last indefinitely.

Because of their similarity to unmodified viruses, TIPs stimulate various immune cells in the body that can eventually become exhausted by this. This opens the door for more TIPs and HIV to enter cells — but since HIV continually evolves, this exhaustion could theoretically allow HIV to gain a foothold over TIPs.

"So what's the outlook on this? Relatively positive in the short term, but I think more work is needed in the long run," Wildfire said.

The researchers have not yet tested whether this new treatment could replace antiretroviral drugs for people who are already living with well-controlled HIV. Their next step is to test this idea in macaques, after which they hope to embark on human clinical trials. The end goal is to offer new options for HIV treatment so people won't have to take medications continually for the rest of their lives.

Ever wonder why some people build muscle more easily than others or why freckles come out in the sun? Send us your questions about how the human body works to community@livescience.com with the subject line "Health Desk Q," and you may see your question answered on the website!

Editor's note: Following the publication of this article, Sweden reported the first known case of clade 1 mpox outside of Africa on Aug. 15. 

The mounting mpox outbreak in Africa constitutes a public health emergency of international concern, the World Health Organization (WHO) declared Wednesday (Aug. 14).

The declaration hinged on advice from an emergency committee that the WHO assembled to discuss an unprecedented surge of mpox in the Democratic Republic of the Congo (DRC), which has now spilled into adjacent countries. Mpox cases were already rising in the DRC in 2023, but now they've skyrocketed — more than 14,000 cases have been reported so far in 2024, exceeding last year's total count.

"In the view of all members, it was unanimous that the current outbreak of mpox is an extraordinary event," Dr. Dimie Ogoina, a physician-scientist and the chair of the 15-member emergency committee, said during a virtual news conference on Wednesday. One big factor in the decision was that "we're having the highest number of cases ever reported in the DRC," he said.

Based on the available data, children in the DRC have been the "worst impacted" by the country's outbreak, Ogoina said. That seems to be the case in Burundi, as well, but not in Nigeria and South Africa, where so far young adults have been most impacted. That said, health officials don't yet understand the full extent of the emergency in the DRC or elsewhere in Africa.

Related: 'Mpox' is the new name for monkeypox, the WHO says

"What we have in Africa is actually the tip of the iceberg," Ogoina said, citing major gaps in diagnostic testing. "We don't have the full picture of this burden of mpox."

Mpox poses a particularly high risk in Africa due to the continent's high burden of HIV infections, a percentage of which are undiagnosed or undertreated. People living with HIV, and especially those with advanced disease, face a higher risk of severe illness and death from mpox, Ogoina said.

Another factor in the committee's decision was the fact that a new branch of the mpox virus family tree, called clade 1b, has emerged. It was first spotted in the DRC last year and has since spread to bordering countries where mpox had not previously been reported. These countries include Burundi, Kenya, Rwanda and Uganda.

"But we are not dealing with one outbreak of one clade," WHO Director-General Dr. Tedros Adhanom Ghebreyesus said in his opening remarks to the emergency committee. "We are dealing with several outbreaks of different clades in different countries with different modes of transmission and different levels of risk."

There are two major clades of mpox, known as clade 1 and clade 2, and the former carries a higher risk of severe disease and death than the latter. Clade 1 viruses have never been detected beyond countries where mpox regularly spreads. (The mpox outbreak that spread to many countries, including the U.S., in 2022 was driven by a clade 2 virus.)

This year, two offshoots of clade 1 — called 1a and 1b — have been circulating in various African countries, and both are spreading in the DRC. In addition, clade 2 viruses have been spreading in several countries, such as Cameroon, Nigeria and South Africa.

The picture of how mpox is spreading is complex. The main mode of transmission is through close physical contact, which drives spread in households, for instance, said Maria Van Kerkhove, the WHO's acting interim director of Epidemic and Pandemic Preparedness and Prevention (EPPP). The virus, and especially clade 1b, is also spreading through sexual networks. To a lesser extent, transmission from contact with infected animals or their bodily fluids is also driving cases, she added.

In the DRC and Burundi, there's evidence that mpox is spreading through community networks, Dr. Abou Salam Gueye, the emergency director for the WHO African Region, said at the news conference. But in some other countries that have reported fewer cases, such as Kenya, Uganda and Côte d’Ivoire, it's suspected that these cases have been isolated events, he said.

The WHO is now working to increase the availability of mpox vaccines in Africa by securing deals with manufacturers and donations from countries with existing stockpiles. They're working with the makers of vaccines called MVA-BN (which is marketed as Jynneos in the U.S.) and LC16, which is produced by the government of Japan, according to Tim Nguyen, head of the Unit for High Impact Events within the EPPP department.

"Vaccines are one intervention that can be utilized," Van Kerkhov said. But there's also work that needs to be done around communicating people's risk of mpox and precautions that can be taken to prevent the disease, she added.

In addition, more studies need to be undertaken to understand how the virus' transmission dynamics differ in different settings and how illnesses from mpox progress, and as Ogoina noted, gaps in testing need to be closed, she said.

Without swift action, mpox could spread to additional African countries and also beyond the continent.

As such, "mpox requires a coordinated response, not only in Africa, but globally," Ogoina said. "Collectively, all parties involved can work to improve surveillance, diagnosis, and other public health responses that are needed to nip this challenge in the bud."

This article is for informational purposes only and is not meant to offer medical advice.

Ever wonder why some people build muscle more easily than others or why freckles come out in the sun? Send us your questions about how the human body works to community@livescience.com with the subject line "Health Desk Q," and you may see your question answered on the website!

A large clinical trial in South Africa and Uganda has shown that a twice-yearly injection of a new pre-exposure prophylaxis drug gives young women total protection from HIV infection.

The trial tested whether the six-month injection of lenacapavir would provide better protection against HIV infection than two other drugs, both daily pills. All three medications are pre-exposure prophylaxis (or PrEP) drugs.

Physician-scientist Linda-Gail Bekker, principal investigator for the South African part of the study, tells Nadine Dreyer what makes this breakthrough so significant and what to expect next.

Related: We could end the AIDS epidemic in less than a decade. Here's how. 

Tell us about the trial and what it set out to achieve

The Purpose 1 trial with 5,000 participants took place at three sites in Uganda and 25 sites in South Africa to test the efficacy of lenacapavir and two other drugs.

Lenacapavir (Len LA) is a fusion capside inhibitor. It interferes with the HIV capsid, a protein shell that protects HIV's genetic material and enzymes needed for replication. It is administered just under the skin, once every six months.

The randomized controlled trial, sponsored by the drug developers Gilead Sciences, tested several things.

The first was whether a six-monthly injection of lenacapavir was safe and would provide better protection against HIV infection as PrEP for women between the ages of 16 and 25 years than Truvada F/TDF, a daily PrEP pill in wide use that has been available for more than a decade.

Secondly, the trial also tested whether Descovy F/TAF, a newer daily pill, was as effective as F/TDF. The newer F/TAF has superior pharmacokinetic properties to F/TDF. Pharmacokinetic refers to the movement of a drug into, through, and out of the body. F/TAF is a smaller pill and is in use among men and transgender women in high-income countries.

Related: How are people cured of HIV? Here's everything you need to know

The trial had three arms. Young women were randomly assigned to one of the arms in a 2:2:1 ratio (Len LA: F/TAF oral: F/TDF oral) in a double blinded fashion. This means neither the participants nor the researchers knew which treatment participants were receiving until the clinical trial was over.

In eastern and southern Africa, young women are the population who bear the brunt of new HIV infections. They also find a daily PrEP regimen challenging to maintain, for a number of social and structural reasons.

During the randomized phase of the trial none of the 2,134 women who received lenacapavir contracted HIV. There was 100% efficiency.

By comparison, 16 of the 1,068 women (or 1.5%) who took Truvada (F/TDF) and 39 of 2,136 (1.8%) who received Descovy (F/TAF) contracted the HIV virus.

The results at a recent independent data safety monitoring board review led to the recommendation that the trial's "blinded" phase should be stopped and all participants should be offered a choice of PrEP.

This board is an independent committee of experts who are put in place at the start of a clinical trial. They see the unblinded data at stipulated times during the trial to monitor progress and safety. They ensure that a trial does not continue if there is harm or a clear benefit in one arm over others.

What is the significance of these trials?

This breakthrough gives great hope that we have a proven, highly effective prevention tool to protect people from HIV.

There were 1.3 million new HIV infections globally in the past year. Although that's fewer than the 2 million infections seen in 2010, it is clear that at this rate we are not going to meet the HIV new infection target that UNAIDS set for 2025 (fewer than 500,000 globally) or potentially even the goal to end AIDS by 2030.

PrEP is not the only prevention tool.

PrEP should be provided alongside HIV self-testing, access to condoms, screening and treatment for sexually transmitted infections and access to contraception for women of childbearing potential.

In addition, young men should be offered medical male circumcision for health reasons.

But despite these options, we haven't quite got to the point where we have been able to stop new infections, particularly among young people.

For young people, the daily decision to take a pill or use a condom or take a pill at the time of sexual intercourse can be very challenging.

HIV scientists and activists hope that young people may find that having to make this "prevention decision" only twice a year may reduce unpredictability and barriers.

For a young woman who struggles to get to an appointment at a clinic in a town or who can't keep pills without facing stigma or violence, an injection just twice a year is the option that could keep her free of HIV.

What happens now?

The plan is that the Purpose 1 trial will go on but now in an "open label" phase. This means that study participants will be "unblinded": they will be told whether they have been in the "injectable" or oral TDF or oral TAF groups.

They will be offered the choice of PrEP they would prefer as the trial continues.

A sister trial is also under way: Purpose 2 is being conducted in a number of regions including some sites in Africa among cisgender men, and transgender and nonbinary people who have sex with men.

It's important to conduct trials among different groups because we have seen differences in effectiveness. Whether the sex is anal or vaginal is important and may have an impact on effectiveness.

How long until the drug is rolled out?

We have read in a Gilead Sciences press statement that within the next couple of months the company will submit the dossier with all the results to a number of country regulators, particularly the Ugandan and South African regulators.

The World Health Organization will also review the data and may issue recommendations.

We hope then that this new drug will be adopted into WHO and country guidelines.

We also hope we may begin to see the drug being tested in more studies to understand better how to incorporate it into real world settings.

Price is a critical factor to ensure access and distribution in the public sector where it is badly needed.

Gilead Sciences has said it will offer licences to companies that make generic drugs, which is another critical way to get prices down.

In an ideal world, governments will be able to purchase this affordably and it will be offered to all who want it and need protection against HIV.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Around 2,400 people treated in Oregon hospitals may have been exposed to HIV, hepatitis or other blood-borne infections due to an anesthesiologist's improper administration of drugs.

Providence, a health care system that operates in several states, notified the public of the exposure risk in a statement Thursday (July 11). 

"We recently learned that Providence's comprehensive infection control practices may not have been followed by a physician during some procedures at Portland-area hospitals," the statement reads. These hospitals include Providence Willamette Falls Medical Center and Providence Portland Medical Center. Providence is notifying "approximately 2,200 patients" seen at the former facility and two seen at the latter medical center of this potential risk.

In addition, the same physician practiced at a Legacy Health hospital called Legacy Mount Hood Medical Center. "We are in the process of sending letters notifying 221 patients who may have been impacted," a Legacy spokesperson shared in a statement emailed to Live Science.

Related: Nearly 450 hospital patients in Massachusetts may have been exposed to hepatitis and HIV

The physician was an anesthesiologist employed by Oregon Anesthesiology Group (OAG), which partners with hospitals and ambulatory surgery centers in western Oregon. 

"When we learned that the physician had violated infection control practices, we suspended him, informed our partners Legacy Health and Providence, and then began an investigation that resulted in the physician's termination," an OAG spokesperson told Live Science in an email. "Even though the risk of infection was low, new protocols and procedures have been put in place to prevent similar incidents in the future."

The physician's name has not been disclosed, the Associated Press (AP) reported.

The actions of this anesthesiologist put patients "at low risk" of being exposed to various blood-borne diseases, including HIV and hepatitis B and C, Providence representatives said. According to the AP report, the provider worked with Providence between 2017 and 2023. 

"Out of an abundance of caution, we are encouraging these patients to get a blood test to screen for the aforementioned infections, at no cost," Providence said. Any patients that test positive will be notified and then informed of possible next steps. 

Legacy Health emphasized that "this was an isolated situation involving a single provider." The anesthesiologist was contracted to work at the Legacy facility for about six months, starting in December 2023. 

The health care systems' statements don't note exactly how their safety protocols were violated. However, the Oregon Health Authority told the AP that the investigation centered around an anesthesiologist who delivered intravenous anesthesia and practiced "unacceptable" infection control while doing so. 

Generally speaking, health care facilities have strict standards for how to sanitize needles, syringes and other equipment before they're used on a given patient, and a single needle and syringe should never be used for multiple people.

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An HIV vaccine is one step closer to reality following a human trial that produced rare and elusive antibodies, a new study reports. 

Many hurdles stand in the way of an effective HIV vaccine. The virus is a master of evasion, dodging the immune system by coating itself in sugars that resemble those made by the body, said Dr. Barton Haynes, a leader of the recent trial and director of the Duke Human Vaccine Institute. The virus also mutates rapidly, changing its form so that the immune system struggles to make antibodies that can grab hold of it.

A major goal in HIV vaccine development is triggering the production of broadly neutralizing antibodies, which latch onto parts of the virus's outer coating, or envelope, that are very similar between different HIV strains. This makes the antibodies protective against a wide variety of strains, regardless of how they mutate.

The challenge is that "these antibodies, naturally during infection, are very rare to find," said Thomas Hope, a professor of cell and developmental biology who studies HIV at Northwestern University Feinberg School of Medicine. "It takes a couple years of real infection to make these antibodies," said Hope, who was not involved in the new study but has collaborated with some of its authors in the past.

Related: We could end the AIDS epidemic in less than a decade. Here's how.

Vaccines typically work by eliciting a similar immune reaction to what's seen during a real infection. But in the case of HIV, vaccine developers have to dramatically expedite the process, calling forth antibodies in weeks that would usually take years to show up. 

Now, in a study published Friday (May 17) in the journal Cell, scientists have demonstrated that this feat is possible in humans.

"We're gathering proof of concept that a vaccine could be made — can be made," Haynes told Live Science. "We're having to coax the immune system, to guide the immune system in a way we've never had to do."

In the trial, the researchers targeted a protein embedded in HIV's envelope — specifically, part of the protein called the membrane proximal external region (MPER). The coveted antibodies that target MPER bind to both the backbone of this protein and to the fatty membrane it's embedded within. 

"These are very unusual because they bind two things at once," Haynes said, and this makes the antibodies oddly shaped. To make antibodies of the right shape, immune cells must pick up genetic mutations over time, following exposure to a pathogen. But for reasons not fully understood, the mutations required to make antibodies against MPER and similar targets happen only very rarely. 

The idea behind the new vaccine is to make these mutations more probable by exposing the immune system to a series of reaction-triggering substances. These substances, or immunogens, contain short snippets of protein and bubbles of fat. "What we're learning to do is design immunogens that can select for these rare mutations very efficiently," Haynes said. 

This strategy has been demonstrated in various animal models and early human studies that aimed for targets other than MPER. These previous studies successfully coaxed immune cells to make precursors to the final, desired antibodies — but the new trial represents the first time that the end-goal antibodies have been achieved in people.

"This supports the whole concept," Hope told Live Science. "Many worry if this is possible," so the new study lends credence to this iterative HIV vaccination strategy. 

The trial included 20 HIV-negative volunteers. Fifteen received two vaccine doses, spaced two months apart, while the remaining five got a third dose four months after their second. Tests showed that two doses of vaccine triggered a robust response from immune cells and kicked off the production of broadly neutralizing antibodies. The team further confirmed the presence of these antibodies in the three-dose group by closely analyzing their immune cells.

The original goal of the trial was for everyone to get four doses, but it was paused after one participant given three doses had a serious allergic reaction to a vaccine ingredient called polyethylene glycol (PEG). PEG helps to stabilize certain types of vaccines in the body, but rarely, patients can have a reaction to it. The researchers have now reformulated the vaccine without PEG and will soon test the new version.

This is just one step toward making an effective HIV vaccine, Haynes emphasized. The ideal vaccine would induce four different types of broadly neutralizing antibodies — that is, anti-MPER antibodies plus three more kinds. This would help prevent HIV from escaping the vaccine's protection. In addition, the antibodies need to be made in high quantities and hang around in the body for a long time.

"It's a decent starting point and it can be built upon and combined with other people's work," Hope said of the recent trial. He added that he hopes this vaccine strategy pans out, given the potential it has shown so far. Hope has been studying HIV since the late 1980s. 

"I would really like to see the end of this virus," he said. "It'll lose eventually, but I'd like to see it losing."

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A new treatment for human immunodeficiency virus (HIV) can drive the virus out of its hiding spots in the body, an early clinical trial finds. That, in turn, raises hopes these reservoirs of HIV could then be wiped out.

The treatment isn't enough to cure HIV on its own. But the new results, published in the Journal of Infectious Diseases on Feb. 13, hint that it could be possible to use this strategy as a step toward curing a person of HIV.

"This is not a home run," said study leader Dr. David Margolis, a professor of medicine, microbiology and immunology, and epidemiology at the University of North Carolina (UNC) Chapel Hill School of Medicine.

"Clearly we need better tools, better drugs, better approaches," he said, "but it does suggest that this strategy itself is deserving of more work."

Related: We could end the AIDS epidemic in less than a decade. Here's how.

HIV in hiding

With modern antiretroviral drugs, doctors can prevent HIV from spreading from cell-to-cell inside the body, allowing people with the infection to live normal lives. Many achieve undetectable viral loads, meaning they cannot transmit HIV to others via sex.

But HIV is a retrovirus, meaning it incorporates its genetic code into cells' DNA and hides out indefinitely, creating a viral reservoir that can retrigger a full-blown infection at any time. To stop an HIV infection from progressing to acquired immunodeficiency syndrome (AIDS), people with HIV must stay on antiretroviral drugs for life.

To truly cure the infection, the latent HIV reservoir must be driven out and destroyed. That's challenging, though, said Edward Browne, a professor of medicine at UNC's School of Medicine who has previously collaborated with Margolis but was not involved in the recent trial.

HIV hides lots of different types of cells in hard-to-treat places, such as the gut and nervous system. And driving the virus out isn't enough to destroy it.

"We have to hit two home runs at the same time," Browne told Live Science. "We have to reactivate enough viral proteins that the immune system can see it, and we have to get immune effector mechanisms in the right place at the right time to kill them off."

Margolis and his team attempted this with vorinostat, a drug shown to "wake up" HIV from latency in many previous studies. To attack the activated virus, they took patients' own immune cells, identified those programmed to attack HIV, and then grew these cells and reinfused them into the patients.

Six patients in the first phase of the trial got a standard dose of specialized immune cells. Vorinostat did, in fact, reactivate their latent HIV, but the HIV reservoir shrunk in only one patient of the six, by one measurement.

Related: How are people cured of HIV? Here's everything you need to know

In a separate group of three patients, the researchers upped the dose of anti-HIV cells by five times and saw a small decline in the HIV reservoir of all three people. The decline wasn't dramatic enough to take the patients off their HIV-suppressing medications, but it was promising that the results seemed to be dependent on the dose of the immune cells, Margolis said.

"It's a little more convincing that it happened three out of three times with the higher dose and maybe one out of six times at the lower dose," he said.

Reversing latency

Margolis and his team are now working on a strategy using vorinostat and an lab-made antibody against HIV that might do a better job of marking the reactivated virus for destruction. They're also studying another method of reversing HIV latency that seems to work better than vorinostat, which they first described in a 2020 Nature paper.

Several other groups are trying to drive out and kill latent HIV. Some are using medications, others are using immune proteins, while still others are attempting to slice HIV from cells with the gene-editing system CRISPR. Meanwhile, researchers are still unraveling the basic science of HIV latency. Some are exploring the notion of pushing the virus deeper into latency, ensuring that it will never reactivate.

When HIV first emerged, doctors could do little to prevent patients from developing AIDS and dying of related complications, Margolis said. The advent of the first antiretroviral drug changed that. If researchers uncover a working strategy, the landscape of HIV could similarly shift overnight.

"We don't know if we're 20 years away from something that really works or maybe we're just a couple years away from something that works," Margolis said. "There's no way to know."

This article is for informational purposes only and is not meant to offer medical advice.

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Teens and young adults often don't use HIV-prevention medications known as PrEP, even when they could benefit from these drugs. But a few simple strategies, including telehealth coaching appointments and automated text messages, can dramatically boost usage in this group, a new study finds.

The nearly 900 young people in the trial were split into four groups, with one group getting only text messages, two receiving texts and one additional intervention each, and a final group getting a trio of interventions. This last group — who received text messages, coaching and access to an online support group of peers — doubled their use of PrEP, from 10% to 20%. If mirrored nationally, this rate would bring young people's PrEP coverage more in line with that of U.S. adults indicated for the medications.

The three interventions all provided information about PrEP and connected participants with services to help pay for the medications. But beyond that, they aimed to help the young people handle stressors in other aspects of their lives.    

"We've known for decades now that HIV prevention is not a high priority for many people struggling with daily survival needs, other mental or physical health priorities, or other priorities in their lives," said Dallas Swendeman, lead author of the report and a behavioral scientist at UCLA's Center for HIV Identification, Prevention, and Treatment Services.

The researchers wanted to support participants through all these other challenges in their lives so that they'd be able to better prioritize HIV prevention, Swendeman told Live Science in an email.

Related: We could end the AIDS epidemic in less than a decade. Here's how.

The trial's results, published Wednesday (Feb. 21) in the journal The Lancet Digital Health, are now guiding Swendeman and his colleagues' efforts to roll out these treatments on a larger scale.

How to get more young people to use PrEP

PrEP is available as daily pills and as long-acting injections, and both treatment options are about 99% effective at preventing the spread of HIV via sex when used as prescribed, according to the Centers for Disease Control and Prevention (CDC). However, while PrEP is extremely effective, only about 30% of the estimated 1.2 million people at heightened risk of HIV were prescribed them in 2021, CDC data suggest.

To find ways of boosting PrEP use among young people, Swendeman and colleagues recruited hundreds of teens and young adults ages 12 to 24 in Los Angeles and New Orleans. The trial focused on gay and bisexual men and other men who have sex with men, as well as on transgender and gender-diverse people, as more than 80% of young people with HIV in the U.S. belong to these categories.

The participants were recruited through adolescent health clinics and community organizations for vulnerable youth, such as those in the LGBT community, those with housing insecurity and those who were previously incarcerated. They also recruited through social venues, like clubs; and via apps, like Grindr. Black and African American people made up about 40% of the study participants, followed by Latinx and Hispanic people (29%), white people (21%), and Asian and Pacific Islander people (6%).

The texts relayed information or motivational messages on physical health, substance use, mental health and wellness. The researchers also sent text medication reminders, if applicable. For example, one text might have read, "Friends can be good medicine. If you need to talk, give a friend a call" and another, "Going out of town? Don’t forget to pack your meds." Others provided links to explore health insurance options or to learn about people's personal experiences with PrEP.

The peer-support groups enabled young people to chat about topics ranging from current events and pop culture to mental health and jobs. They were also safe spaces for participants to ask questions about PrEP, share experiences and raise concerns.

Normalizing the use of PrEP can encourage young people to try the medications, Swendeman noted.

Finally, participants received coaching from people whose backgrounds closely matched their own. Coaches started by interviewing the participants to identify strengths and challenges in their daily lives. From there, they directed the participants to relevant services and helped them set and troubleshoot personal goals, with at least one centered on HIV prevention.

The group that received all three interventions roughly doubled their PrEP use within eight months of the trial's start. That rate stayed fairly steady for the following 16 months of the two-year study. In comparison, the other three groups saw smaller bumps in PrEP use — up to about 15% — that then wavered and fell again over time.

The strategies are designed to be flexible — either used in tandem or customized to a given person's needs.

As follow-up work, the team is looking into using chatbots to scale up the effort. For instance, bots could make the automated texts more personalized and interactive, as well as help automate aspects of monitoring the support group, Swendeman said. And with the release of technologies like ChatGPT, such automations could now be within reach, he said.

"It's a very exciting time," but there's still work to do to ensure chatbots deliver accurate information and are used as a tool to improve a person's care, rather than being used as a total replacement for a human clinician or coach, he said.

This article is for informational purposes only and is not meant to offer medical advice.

Among people with HIV, young children are the likeliest to die while receiving treatment.

This is likely because many children under 5 already have severely weakened immune systems by the time they're diagnosed with HIV, if they are ever diagnosed, according to a Centers for Disease Control and Prevention Morbidity and Mortality Weekly Report (MMWR) published Friday (Dec. 1).

Once on medication, young kids are also more likely than older groups to have interruptions in their treatment. HIV drugs, called antiretroviral therapy (ART), work by driving down the amount of virus in a person's blood until it's undetectable — but if treatment is stopped, viral levels rebound and the infection progresses towards AIDS.

Moreover, young children in low-resource settings, including regions in sub-Saharan Africa, suffer high death rates from other conditions, such as pneumonia and malnutrition, which compound their risk of death with HIV, according to the report.

And these death and treatment-interruption rates "are likely underreported," as children are lost to follow-up and there are inconsistencies in how the data is tracked between locations, the MMWR authors added. Children's HIV services must be prioritized in order to get more kids on consistent ART treatment and avoid preventable deaths, the report concluded.

Related: We could end the AIDS epidemic in less than a decade. Here's how.

It was already known that children under 5 are less likely to receive an HIV diagnosis and be started on ART than older age groups. But less was known about the disparities between young children and older people that are both on ART.

The new report focused on people receiving ART through the United States President's Emergency Plan for AIDS Relief (PEPFAR), a program launched in 2003 to help extinguish the HIV epidemic across the world. PEPFAR currently works in 55 countries in which 78% of people with HIV live, according to the 2023 report from the Joint United Nations Programme on HIV/AIDS (UNAIDS).

The rate of new HIV infections in kids has been falling in these countries, from 287,000 in 2010 to 109,000 in 2022, UNAIDS reported. However, when children do contract HIV, they often don't receive the treatment they need. Globally in 2022, only 57% of the 1.5 million children with HIV received treatment, and an estimated 84,000 died of AIDS-related illnesses. Only 46% of all children with HIV were "virally suppressed," meaning the virus in their blood was undetectable, compared with about 71% of all HIV-positive adults.

The new report looked at people who received ART through PEPFAR between October 2020 and September 2022. That included nearly 18 million people each quarter, including nearly 12,000 infants and 105,000 children ages 1 to 4.

Each year, nearly 5% of the treated infants died, as did 2.5% of the other children under 5. These death rates are many times higher than those in people of older ages, according to the MMWR. Children under 5 were also more likely to have pauses in treatment and less likely to be virally suppressed.

To improve matters, kids must be diagnosed as early as possible and be started on ART immediately after an HIV diagnosis. On this front, there are ongoing global efforts to ensure more children with HIV get tested and onboarded into consistent HIV care that suits their families' needs. Children must simultaneously be protected from other diseases, through vaccinations, for example, and from malnutrition, the MMWR authors noted.

One major challenge is that there are few child-friendly HIV drug formulas, but some recent advancements have helped to overcome that obstacle and make kids' ART easier to maintain.

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An HIV diagnosis hasn't been a death sentence for years, thanks to powerful medications.

Despite incredible progress, however, HIV (human immunodeficiency virus) remains a global public health threat, with 1.3 million new infections and around half that many deaths in 2022 alone.

While new HIV infections have dropped steadily since their peak in 1995, as people live longer with the disease, the pool of people who are HIV-positive has only grown. People with HIV must consistently take medications to prevent the virus from becoming transmissible again or progressing to AIDS (acquired immunodeficiency syndrome). As a result, new infections could actually rebound fast if the world doesn't dramatically ramp up the number of people being regularly treated, tested and protected from new HIV infections.

But we could head off that rebound risk by the end of the decade, experts say.

Countries around the world have signed onto an ambitious United Nations program with a goal to "reduce the rate of new HIV infections and AIDS-related deaths to below the reproductive rate of 1," country by country, Quarraisha Abdool Karim, associate scientific director of the Centre for the AIDS Programme of Research in South Africa and a joint United Nations Programme on HIV/AIDS (UNAIDS) special ambassador, told Live Science. That would mean each person living with HIV would infect fewer than one additional person in their lifetime.

If the program is successful, we'd see 200,000 new HIV infections and 130,000 AIDS-related deaths worldwide in 2030 — 90% fewer than in 2010. While eradicating the virus would require a vaccine and cure, we could eventually drive HIV infections and death rates to near zero without those tools, Abdool Karim said.

"We do have the tools to end AIDS as a public health threat. We do have the biomedical interventions," she said. "The challenge is, how do we all get to that point?"

Related: Could CRISPR cure HIV someday?

From the first treatment to ending AIDS 

The first, imperfect HIV treatment, AZT (azidothymidine), was approved in 1987. Nearly four decades and more than 40 million AIDS-related deaths later, we're still hunting for a vaccine and a cure for HIV, but our treatments have dramatically improved.

"We've had really powerful treatments, really, since 1996, but they just get better all the time," Dr. Monica Gandhi, director of the University of California, San Francisco Center for AIDS Research and medical director of the HIV Clinic at San Francisco General Hospital, told Live Science.

Today's standard treatment, combination antiretroviral therapy (ART), uses several drugs to disrupt HIV's ability to replicate and invade immune cells. Given as daily pills or monthly or bimonthly injections, ART slashes the amount of HIV in a person's blood until it's undetectable. If maintained, "viral suppression" extends a person's life span to about that of HIV-negative people and eliminates their chance of spreading HIV via sex.

"People living with HIV, on treatment and undetectable, are not infectious — full stop, end of statement — to their sexual partners," Dr. Raphael Landovitz, co-director of UCLA's Center for HIV Identification, Prevention, and Treatment Services, told Live Science. Viral suppression also nearly eliminates HIV spread to babies during pregnancy or childbirth, greatly reduces spread via breastfeeding and likely lowers spread from sharing syringes.

We also have powerful medicines that prevent HIV-negative people from contracting the virus if exposed. Known as pre-exposure prophylaxis (PrEP), these drugs are available as daily pills. There's also an injectable drug called cabotegravir (brand name Apretude) that's given bimonthly. Some African countries have also licensed a vaginal ring for HIV prevention; it's less effective than PrEP pills but works for a full month. And condom use and voluntary male circumcision also cut transmission.

By 2014, there was strong consensus that the drugs we had could end the AIDS epidemic. But those drugs weren't being rolled out fast enough to head off rebounds in infection, UNAIDS cautioned. At that time, models predicted that if treatment and prevention services didn't reach more people over time, the number of people with HIV would balloon to 41.5 million by 2030. To prevent this, UNAIDS set forth ambitious targets to scale up the global HIV response. Hitting these targets would prevent 28 million new HIV infections and at least 21 million AIDS-related deaths between 2015 and 2030, they projected.

One major goal, the "95-95-95" target, is set for 2025. Achieving it would mean 95% of people with HIV know their status, 95% of those diagnosed take HIV drugs, and 95% of those treated are "virally suppressed," meaning the drugs keep them from spreading the infection via sex. This translates to around 86% of people with HIV being virally suppressed.

Other 2025 targets aim to ensure that 95% of people at risk of HIV have access to prevention and that PrEP be made available to at least 10 million at-risk people.

So far, we're not on target: In 2022, only 76% of the total 39 million people with HIV worldwide were taking ART, and 71% were virally suppressed, according to the latest UNAIDS report.

So what can we do to reach 95% across the board?

Related: How are people cured of HIV? Here's everything you need to know

Vulnerable populations 

A big hurdle to ending the AIDS epidemic is getting treatments to vulnerable populations, including children. In 2022, only 57% of the 1.5 million children under 15 with HIV received treatment, 46% were virally suppressed and an estimated 84,000 died of AIDS-related illnesses.

That's partly because kids aren't typically included in initial clinical trials for treatments, so there are relatively few child-friendly formulas, Abdool Karim said. The preferred treatment for children, a tablet that dissolves in water, was just approved in 2021 and has been adopted only recently in many countries. However, most other HIV drugs for kids taste bad, are difficult to swallow or must be taken several times a day, UNAIDS notes, so improving these formulations could make their HIV regimens easier to maintain.

Long-acting ART options — meaning those that don't require daily pills — are nonexistent for children under 12, Gandhi said. To help make long-acting ART suitable for young children, the National Institutes of Health is supporting research into how to best adapt drugs approved for adults, she noted. But that grant opens in 2024, so it's unclear if it could make a dent before 2030.

And even if better drugs are widely available, "children are not going to be able to access antiretroviral therapy in a vacuum," said Dr. Anjali Sharma, a professor of medicine who now studies complications of HIV at the Albert Einstein College of Medicine in New York and has studied ART adherence in different settings.

"The pediatric care really has to be integrated with other services, potentially the mom's treatment or things that are going to work with the family as a unit," she said.

Related: Kids under 5 with HIV are dying at high rates. Here's why.

Hitting the 95-95-95 target will also require better reaching teen girls and young women, especially with prevention and testing. Nearly 1 in 6 new HIV cases in 2022 were in girls and women ages 15 to 24, many of whom are in sub-Saharan Africa.

Once diagnosed and started on ART, women's viral suppression rates are "high and so are survival benefits," Abdool Karim said. Among all diagnosed women over 15, 82% had access to ART and 76% were virally suppressed in 2022. But starting ART first requires being tested for HIV, and testing rates remain low in hard-hit regions, particularly among teens.

Many of the hardest-hit regions lack prevention programs for young women, and the few existing programs often miss girls who are not in school. Girls facing a lack of education, poverty and food insecurity have an especially high risk of HIV, as do girls with older male partners. Intimate-partner violence and sexual coercion often mean they cannot control when they are exposed to HIV. Plus, in some countries, HIV services require parental consent, which can also reduce girls' access to prevention and treatment.

Improving girls' access to discreet prevention services as well as sex education — both in and out of school — will be key to reducing their HIV rates. Cabotegravir, which is "stunningly effective against vaginal acquisition of HIV," could be a powerful tool for HIV prevention in women, Landovitz said.

Other populations that are far from the targets include transgender people with HIV, an estimated 44% of whom are on ART, and HIV-positive men who have sex with men, who have 78% ART coverage. In addition, just 65% of HIV-positive sex workers and 69% of HIV-positive people who inject drugs take ART. Compared with the general adult population, these groups have far higher HIV prevalence, ranging from fourfold greater among sex workers to 14-fold greater among transgender people.

And those numbers could be an undercount, as many countries don't track these populations. Punitive laws, police harassment, harsh stigma and social taboos keep many people out of HIV care, while high rates of incarceration and sexual violence also raise their risk of acquiring HIV. Lifting discriminatory policies and weaving HIV care into trusted, community-based programs will be key to reaching these demographics.

Related: Patient's immune system 'naturally' cures HIV in the second case of its kind

Cost barriers 

The tools to end the epidemic by 2030 will work, but only if they get to the people who need them. "The science is a first step, but access is what will translate its true potential and value," Abdool Karim told Live Science.

For instance, the number of people taking PrEP pills rose more than tenfold from 2019 to 2022. But cabotegravir, a potential game changer, is not yet widely used due to its high cost — $3,700 per dose in the U.S. The drug's nonprofit price will be around $30 a dose, the drug's maker recently told the South African news outlet Bhekisisa, and generic versions will be manufactured in coming years. But the current high price means HIV programs have yet to fold cabotegravir into their budgets, Landovitz said.

"There's still not a drop of cabotegravir to be had anywhere in Africa," where some of the highest rates of new HIV infections occur, Abdool Karim said.

And regardless of the type of ART they take, a patient should have their viral load checked regularly. In 2022, 21 million people underwent routine viral-load testing, up from 6 million in 2015. Viral-load tests are expensive, though, so proxy measures — such as a urine test Gandhi and colleagues designed to track ART levels — could help fulfill the same purpose cheaply.

In addition, an estimated 25% of people stop ART treatment, sometimes for six months or more, often because they face stigma, can't get to the clinic or can't afford treatment. These individuals, many of whom come from vulnerable populations, represent a growing proportion of the AIDS cases seen in hospitals.

"That is preventable and avoidable and really represents a failure on many levels," Sharma told Live Science. "But the failure isn't really the drug itself." It's a failure of the support system that could keep people on ART, she said.

Related: HIV may hide out in brain cells, ready to infect other organs

Success stories and further work 

Despite the hurdles, some countries are well on their way to meeting UNAIDS' goals. Botswana, Eswatini, Rwanda, the United Republic of Tanzania and Zimbabwe have already hit the 95-95-95 target set for 2025, and an additional 16 countries are close to reaching these milestones.

The U.S. trails behind. In 2021, 75% of the people diagnosed in the country received "some HIV care," and 66% were virally suppressed. Men who have sex with men made up the highest proportion of new infections in the U.S., with Black, Hispanic and Latino populations predominantly affected.

Countries that have hit the 95-95-95 targets offer universal, free ART access, Landovitz noted, while the U.S. government only has programs to help cover uninsured people's HIV treatment. Racism, homophobia and transphobia often keep people from getting care, he said. And especially in urban centers, people dealing with housing insecurity, substance use and mental health issues struggle to access ART consistently, Gandhi said.

Eastern Europe and Central Asia also lag far behind, with just 51% of people with HIV getting ART and less than half being virally suppressed.

Related: Oldest 'nearly complete' HIV genome found in forgotten tissue sample from 1966

Beyond 2030

We face many obstacles on the road to ending the AIDS epidemic — but we do hold all of the tools to get there, Abdool Karim, Sharma, Gandhi and Landovitz agreed. By using those tools effectively, we could begin to meaningfully drive the number of new HIV infections toward zero. At that point, HIV would become a manageable, chronic disease of the elderly.

Already, about a quarter of people with HIV worldwide, and about half of adults with HIV in Western and Central Europe and North America, are at least 50 years old. "They're growing older with HIV; they're not dying from HIV or AIDS," said Sharma, whose research focuses on aging populations with HIV.

But that doesn't mean the quest for an HIV vaccine or cure is any less important, even if neither is likely to materialize in the next seven years, Abdool Karim said.

"We need to continue our investments to find a vaccine, to find a cure," she told Live Science. "Because that will then say, 'That's it.'"

In an ongoing clinical trial, researchers are testing whether just one dose of a new gene therapy that might effectively cure human immunodeficiency virus (HIV) infections is safe in humans. 

The therapy, named EBT-101, involves using CRISPR-Cas9 gene editing to treat HIV. This potential treatment strategy has been studied in animal models since the development of CRISPR-Cas9 in 2012. However, this is the first time such a gene-editing treatment for HIV has been tried in humans. The latest data from the trial suggest that EBT-101 is safe at the doses tested, but we don't yet know if it cures HIV.

According to the United Nations Programme on HIV/AIDS (UNAIDS), approximately 39 million people globally were living with HIV in 2022, and there were about 630,000 AIDS-related deaths that year, making HIV a continued public health burden. There is no vaccine or easily accessible cure for HIV, although a handful of people have been effectively cured through intensive stem-cell transplants. 

The EBT-101 trial "is an important step forward in the development of this technology to treat human disease and infection, including HIV," Thomas Hope, a professor of cell and developmental biology at Northwestern University who was not involved in the work, told Live Science in an email. 

But how likely is it, really, that we could use CRISPR to cure HIV someday?

Related: We could end the AIDS epidemic in less than a decade. Here's how.

How CRISPR could (theoretically) cure HIV

HIV infects immune cells that are normally used to fight infection in the virus's host. The virus uses an immune cell's machinery to insert its own DNA into the host's genome, allowing the virus to replicate. If an HIV infection is not treated, it can lead to acquired immunodeficiency syndrome (AIDS), which results in a severely weakened immune system and leaves the infected person highly vulnerable to other infections, cancers and early death.

Combination antiretroviral therapies (cARTs) are the mainstay in HIV treatment and limit the virus' replication, thus extending people's lives to near-normal lengths and cutting their chance of spreading HIV. However, these therapies must be taken for a lifetime and fall short of being a cure.

"The existing challenge in HIV treatment lies in the virus creating resilient genetic reservoirs within human cells," Elena Herrera-Carrillo, an associate professor of infectious disease at Amsterdam University Medical Centers, told Live Science. Herrera-Carrillo's lab focuses on using CRISPR to edit cells that harbor HIV reservoirs, despite ongoing cART therapy. This phenomenon is known as "latent HIV" and occurs when the virus infects a type of immune cell called CD4+ memory T cells, which can persist for decades.

cART therapies can suppress viral replication, but if the treatment is interrupted, "the dormant proviruses can reactivate, making a cure elusive," Herrera-Carrillo told Live Science.

CRISPR works by targeting and cleaving specific sequences of DNA from the genome; a "guide" leads CRISPR's famous "molecular scissors" to the targeted gene. This either deactivates the gene or allows it to be removed and swapped for different DNA. Research groups believe this strategy could be effective in removing latent HIV infections, because it can target the viral DNA embedded in the genome, rather than only stopping replication.

Using CRISPR for HIV gene therapy has shown promise in several test-tube studies, a 2020 review in The Journal of Clinical Investigation notes. Various groups have been working to bring the therapies from test tubes to human patients — and that brings us to EBT-101.

Related: The world's 1st CRISPR therapy has just been approved. Here's everything you need to know

All about EBT-101

According to a recent presentation at the annual meeting of the European Society for Gene and Cell Therapy in Brussels, EBT-101 uses multiple guides to target multiple sites in the genome and snip out large sections of latently integrated HIV DNA. This stops HIV from replicating.

Kamel Kahlili, a professor of neurovirology and gene editing at Temple University and co-founder of Excision BioTherapeutics, has been working with the company to develop EBT-101 for a decade. In 2020 and 2023, Khalili and his team published reports that showed that EBT-100, a precursor to EBT-101, safely targeted and removed HIV DNA in infected primates.

Now, they're testing their EBT-101 targeting strategy in humans in an early-stage clinical trial that primarily focuses on the safety of the treatment. Initial results from three treated patients showed no toxic effects or serious adverse events. All of the patients' HIV is currently suppressed with cART.

"The initial safety results are promising because no adverse outcomes have been observed to date," said Hope, whose lab studies the mechanisms behind HIV infections. "But more time is needed to be sure because of the way genetic off-target mutations can take years to manifest into complications," he added.

Off-target effects of CRISPR refer to when the CRISPR molecule alters DNA at sites other than those targeted. These unintended snips have long been a worry for researchers designing CRISPR treatments, so they'll be something to watch for with EBT-101, especially since the treatment targets multiple sites in the genome.

Additionally, experts told Live Science that even though the ongoing trial hints that the therapy has a positive safety profile, we still don't know whether one dose can effectively target latent HIV cells and whether it can control HIV in humans.

"It is crucial to approach this with caution," Herrera-Carrillo said. "While optimism about being on the right track is justified, it's important to recognize the substantial work that still needs to be done."

The clinical trial will next test additional doses of EBT-101 for safety and then determine whether the virus stays suppressed when patients are taken off cART. cART therapies pump the brakes on HIV replication, so the only way to determine whether the latent cell reservoirs have been disabled is to temporarily lift those brakes.

Interruptions to HIV treatment are necessary to determine whether a patient is in remission — as has occurred in the few people cured of HIV — but in general, purposeful treatment interruptions have been debated due to their inherent risks.

Following these tests, EBT-101 trial participants will be enrolled in a long-term follow-up study for 15 years following their initial dose to check for long-term adverse effects. So the data is on its way, but will take years to arrive.

Ever wonder why some people build muscle more easily than others or why freckles come out in the sun? Send us your questions about how the human body works to community@livescience.com with the subject line "Health Desk Q," and you may see your question answered on the website!

Nearly 450 patients treated at Salem Hospital in Massachusetts could have been exposed to hepatitis and HIV due to improperly administered IV drugs.

"Earlier this year, Salem Hospital was made aware of an isolated practice involving a small portion of endoscopy patients who were potentially exposed to infection due to the administration of their intravenous medication in a manner not consistent with our best practice," according to a statement from Mass General Brigham (MGB), the health care system Salem Hospital belongs to. (Endoscopies involve a doctor inserting a tubelike instrument into a patient's body to capture images of specific tissues.)

"Once identified, the practice was immediately corrected, and the hospital's quality and infection control teams were notified," according to the statement, which was shared with Live Science via email. The practice involved a single contracted individual who no longer works at Salem Hospital, MGB spokesperson Adam Bagni added in an email.

Once notified, the hospital reviewed the situation and consulted with the Massachusetts Department of Public Health. Together with the public health officials, the hospital staff determined that "the infection risk to patients from this event is extremely small." So far, there has been no evidence of any infections caused by the incident.

Related: Nobel Prize in medicine goes to discoverers of hepatitis C

Salem Hospital has contacted all patients who were potentially affected and is offering free screening for two types of viral hepatitis — hepatitis B and hepatitis C — and HIV, "which are standard tests for a potential exposure of this kind," Bagni said. The hospital has also established a clinician-staffed hotline to answer patients' questions.

The potential exposures took place between June 14, 2021, and April 19, 2023, local news outlet The Salem News reported. That's according to a message sent to patients by Dr. Mitchell Rein, former chief medical officer at Salem Hospital.

To avoid potentially exposing patients to blood-borne diseases such as hepatitis B, hepatitis C and HIV, health care workers should ensure they never use the same needle and syringe on more than one patient, Dr. Shira Doron, chief infection control officer for the Tufts Medicine health system, told NBC News. They should also avoid placing a cap on a used syringe with a needle in it, so other workers don't mistakenly believe it's safe to use. Health care facilities also have strict standards for how to sanitize needles, syringes and other equipment before they're used, she added.

In its statement, MGB did not specify the exact nature of the improper practice that put the endoscopy patients at risk of exposure.

However, Geoff Millar, a patient who reported being contacted by the hospital about a potential exposure, told The Salem News that he'd called the hospital's hotline and was told a piece of equipment intended for single use had been reused for his procedure. It was not the IV needle or endoscopy tube that was reused but a different piece of equipment needed to administer anesthesia.

A class-action lawsuit is now reportedly being filed against Salem Hospital over the incident, NBC News' Boston affiliate reported.

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A sixth person is in long-term remission from HIV following a stem cell transplant, scientists reported this week at a major HIV research conference — but the patient's case differs dramatically from earlier ones, and it cannot yet be explained.

"What has happened to me is wonderful and magical," the anonymous patient said in a statement. "We can now focus on the future."

The man, referred to as the "Geneva patient," had both cancer and HIV at the time of his transplant procedure. He'd been living with HIV since the early 1990s, when he began taking anti-HIV medication, known as antiretroviral therapy (ART), to suppress the virus and prevent any progression toward AIDS. He later developed an aggressive form of leukemia, a blood cell cancer, and underwent a stem cell transplant in 2018 to treat the condition.

This part of the Geneva patient's story echoes those of the five people who previously entered remission from HIV after similar transplants. All five of those previous patients had ART-controlled HIV and cancer at the time of their transplants. The transplants primarily served as cancer treatments, but at least in the first five patients' cases, doctors also used the transplants as an opportunity to treat HIV.

Related: How are people cured of HIV? Here's everything you need to know 

They did this by identifying stem cell donors with a rare HIV-resistant genetic mutation. That mutation, called CCR5-delta 32, disables a protein on the surface of human cells that most HIV strains use to break inside and jump-start infection. Once inside a patient's body, the HIV-resistant transplant essentially replaces the patient's HIV-vulnerable cells with ones that the virus can't invade. This makes it so the virus can no longer multiply, and patients can stop ART.    

In the Geneva patient's case, "there was indeed an attempt to find a CCR5-delta 32 compatible donor," Asier Sáez-Cirión, head of the Viral Reservoirs and Immune Control Unit at the Institut Pasteur in Paris, told Live Science in an email. Sáez-Cirión presented the patient's case Monday (July 24) at the 12th International AIDS Society Conference on HIV Science (IAS 2023) in Brisbane, Australia.

Despite their search, the team did not find a stem cell donor with the HIV-resistant mutation, but they did find a donor with a "wild-type," or nonmutant, version of the CCR5 gene, Sáez-Cirión said. "The decision was to proceed with the transplant from this donor as the priority was to treat the hematological disease."  

A month after the transplant, the patient's blood cells had been replaced by the donor's cells. At the same time, the number of HIV-infected cells in his body plummeted and no antibodies against the virus could be detected, Sáez-Cirión said. In observing this, the patient and his treating physician decided to simplify his ART regimen, progressively cutting down from three drugs to two and then one. 

The patient stopped ART completely in November 2021. He's now been off treatment for about 20 months with no viral rebound, meaning no viral particles have been detected in his body and there's been no sign of anti-HIV immune activity.

At least in test-tube experiments, the patient's cells are still fully susceptible to HIV infection, Sáez-Cirión said. So what has kept the virus at bay?

The patient has experienced graft-versus-host disease — a complication of stem cell transplants in which the donor cells attack the recipient's body — and it's possible that this reaction actually helped clear any lingering HIV-infected cells from the patient, Sáez-Cirión theorized. The patient also took immune-suppressing drugs to treat the graft-versus-host disease, which might have hindered HIV's ability to replicate in his immune cells.

"There may be other factors not yet identified that could explain the absence of viral rebound," Sáez-Cirión added.

While scientists don't yet fully understand the Geneva patient's case, it does suggest that HIV remission can be achieved after transplant, even without the help of the CCR5-delta 32 mutation. As his case continues to be studied, the patient will be closely monitored for any signs of viral rebound.

"Through this unique situation, we are exploring new avenues in the hope that HIV remission or even cure will one day no longer be a one-off occurrence," Dr. Alexandra Calmy, the HIV/AIDS Unit director at the Geneva University Hospitals, said in the statement.

People with HIV who take medication to suppress the virus can't transmit it through sex once its levels become undetectable in their blood, a new review of studies has confirmed. 

The researchers also revealed something that had never been definitively shown: Even those with low, but still detectable levels of HIV have "almost zero" chance of spreading the virus via sex.  

"These findings are important as they indicate that it is extremely rare for people who maintain low levels of HIV to transmit it to their sexual partners," lead author Dr. Laura Broyles, an infectious-disease specialist at Grady Memorial Hospital in Atlanta and chief of programs for the Global Health Impact Group, said in a statement. 

Crucially, this finding suggests that, in places with limited access to supersensitive blood tests for HIV, simpler testing methods could feasibly be used to help people track their status, she said. The results were published Saturday (July 22) in the journal The Lancet and will also be presented virtually and in Brisbane, Australia as part of the 12th International AIDS Society Conference on HIV Science (IAS 2023), which begins July 23.

Related: How are people cured of HIV? Here's everything you need to know

HIV is treated with antiretroviral therapy (ART), which typically involves taking daily pills. (More recently, however, an injectable anti-HIV medication was approved that needs to be administered only six times a year.)

Over the past 15 years, mounting evidence has shown that, once ART lowers the amount of HIV in a person's blood below a certain threshold, they can no longer spread the virus via sex. Below that level, they also have a reduced chance of spreading the virus by sharing injection equipment, and a lower chance of transmitting it to their kids during pregnancy or childbirth. 

That threshold is 200 copies of the virus per milliliter (mL) of blood, and anything lower than that is considered undetectable. On the back of this evidence, health officials spread the word that "undetectable equals untransmittable" — a public health message often shortened to "U = U."

Sometimes, people are put on ART but still maintain more than 1,000 virus copies/mL of blood, which presents a risk of transmission. That may be because they've either developed resistance to ART or haven't adhered to the treatment regimen. However, for people with low but still detectable virus — between 200 and 1,000 copies/mL — the risk of spreading the virus was unclear.

The new review pulled data from studies published between January 2010 and November 2022 that tracked HIV transmission in couples where one partner didn't have HIV and the other partner did. The reviewers assessed eight studies, including three clinical trials that had control groups, that together included more than 7,700 couples in 25 countries.

Related: 1st long-acting injection to prevent HIV has been approved by the FDA

Across all of the studies, there were 323 instances in which HIV spread from one partner to the other, and at least 80% involved people whose virus levels exceeded 10,000 copies/mL. Only two of the transmission events occurred in people with fewer than 1,000 copies/mL, and no transmission occurred in those with fewer than 200 copies/mL. 

The findings highlight the importance of viral load testing for people taking ART, but they also raise the idea that less-sensitive tests could still be useful and expand testing access in low- and middle-income countries, experts not involved in the review wrote in a commentary. "And most importantly, this study provides strong support for the global undetectable equals untransmittable (U=U) campaign," they noted.

Still, there might be reasons to aim for undetectable levels of virus. The study does not address the personal health risks that might come with maintaining low-but-detectable levels of HIV, the commentary authors noted. And the review doesn't address other routes of transmission, such as from parent-to-child during pregnancy or via intravenous drug use, although again, past studies suggest ART generally reduces transmission risk in these cases. 

"These new findings are also significant as they indicate that the risk of sexual transmission of HIV at low viral loads is almost zero," review co-author Dr. Lara Vojnov, the diagnostics adviser in the World Health Organization's HIV and Hepatitis Department, said in a statement. "This provides a powerful opportunity to help destigmatise HIV, promote the benefits of adhering to antiretroviral therapy, and support people living with HIV." 

People in the U.S. can now get a free at-home HIV test, thanks to a nationwide program that will distribute a million tests over the next five years. The program, called Together TakeMeHome, has partnered with the popular dating app Grindr to help spread the word to populations most affected by the viral infection.

The Grindr app now has a side menu button that reads "Free HIV Home Test," which will direct users to the Together TakeMeHome website. Grindr will collect no data in the process, the app's developers said in a statement.

Together TakeMeHome distributes tests by mail to residents of all 50 states and Puerto Rico who are at least 17 years old. The tests themselves are OraQuick devices, made by OraSure Technologies and approved by the Food and Drug Administration (FDA). These tests involve the use of mouth swabs and deliver results in 20 minutes, according to Emory University, one of the project's leaders. People who enroll in the program can order up to two test kits every 90 days. 

Clinical studies suggest the tests are highly accurate, according to the FDA — if HIV is present, the tests are expected to accurately detect the virus 92% of the time, and if HIV is not present, the tests give a negative result 99.98% of the time.

Related: 1st woman given stem cell transplant to cure HIV is still virus-free 5 years later 

The program website provides information about how to use the self-test kits, what to do based on the test result, and how to access other HIV prevention and sexual health services. Trained staff will be available through the program website to provide referrals to HIV prevention and care services, including ways to access pre-exposure prophylaxis (PrEP) — highly effective drugs used to prevent HIV. 

(The program's PrEP navigation team can be reached at the phone number 628-899-4662 or at support@together.takemehome.org.)

"By giving people an easy option to know their HIV status, Together TakeMeHome can help people, particularly those disproportionately affected by HIV, take this first important step in preventing and treating HIV," Dr. Travis Sanchez, a professor at Emory University’s Rollins School of Public Health and the program's executive director, said in the statement. 

Editor's note: This article was last updated on July 27, 2023.  

In the past 20 years, a handful of people have been cured of human immunodeficiency virus (HIV), the virus that causes AIDS, through intensive medical procedures. 

Several more people have received the treatment and also appear to be HIV-free, but it's too soon to definitively declare these patients cured. For now, they're described as being in long-term remission, and their cases are considered "possible" cures. All these patients received stem cell transplants, with cells collected either from adult bone marrow or from umbilical cord blood.

Scientists reported the first definitive HIV cure in 2008, and since then, two more definitive cures and two possible cures have been reported. The most recent reports of such cases — one definitive cure and one possible cure — came out in early 2023. 

Experts say these treatments may become more common in upcoming years as scientists better understand them. However, for now, these treatments are risky and largely inaccessible to the tens of millions of people living with HIV worldwide. Thankfully, drugs for HIV, called antiretroviral therapies (ART), can greatly extend HIV-positive people's lifespans and cut their risk of spreading the virus, but the medications must be taken daily and for life, can interact with other drugs and carry a small risk of serious side effects.  

So scientists hope these exceptional cure cases will pave the way to new, more-accessible treatment strategies that will rid more people of the virus.

Here's what we know about curing HIV.

What treatments can cure HIV? 

All of the people cured and potentially cured of HIV have been treated with stem cell transplants. In addition to being HIV-positive, all the patients had some form of cancer, typically acute myeloid leukemia or Hodgkin's lymphoma. These cancers affect white blood cells, a key component of the immune system, and can be treated with stem cell transplants.

In general, to simultaneously treat these patients' cancers and HIV, their doctors sought out stem cells from people with two copies of a rare genetic mutation: CCR5 delta 32. This mutation disables a protein on the cell surface called CCR5, which many HIV strains use to break into cells. The virus does this by first latching onto a different cell surface protein and changing shape; then, it grabs hold of CCR5 to invade the cell. Without CCR5, it's essentially locked out.

(Some less-common HIV strains use a different surface protein, called CXCR4, instead of CCR5, and some strains can use both, according to a 2021 review in the journal Frontiers in Immunology. Therefore, prior to their transplants, patients were screened to ensure that most or all of the virus in their body used CCR5.) 

A donor with the CCR5 delta 32 mutation was found for all but one of the patients who entered long-term remission from HIV following a stem cell transplant. His mysterious case is still being investigated.

To prepare for the transplant, the patients underwent aggressive radiation or chemotherapy to wipe out the cancerous and HIV-vulnerable T cells — a type of immune cell — in their bodies. This weakened patients' immune systems until the transplanted stem cells could produce new, HIV-resistant immune cells. For some time post-transplant, patients also took immune-suppressing drugs to avoid graft-versus-host disease (GVHD), where the donor-derived immune cells attack the body.

Most patients received stem cells taken from the bone marrow of adult donors. These cells must be carefully "matched," meaning both the donor and recipient must carry specific proteins, called HLAs, in their body tissues. An HLA mismatch can result in a catastrophic immune reaction.    

One patient — the first woman to undergo a stem cell transplant for HIV and enter long-term remission — received stem cells from umbilical cord blood that had been donated at the time of a baby's delivery. These immature cells adapt more easily to a recipient's body, so the patient had to be only "partially matched." She also received stem cells from an adult relative, to help bolster her immune system as the umbilical cells took over.

Because umbilical cord stem cells don't need to be a perfect match and they're easier to source than bone marrow, such transplants could potentially be offered to more patients in the future. 

However, HIV-positive patients shouldn't undergo the risky procedure unless they have another disease that requires a stem cell transplant, Dr. Yvonne Bryson, director of the Los Angeles-Brazil AIDS Consortium at the University of California, Los Angeles and one of the cured patient's doctors, said at a March 2023 news conference. 

Who was the first person cured of HIV? 

The first person cured of HIV was initially called the "Berlin patient," because he'd been treated in Berlin, Germany. In 2010, he revealed his identity. 

American Timothy Ray Brown was diagnosed with HIV in 1995 while attending a university in Berlin and started ART to reduce the amount of HIV in his body. In 2006, Brown was diagnosed with acute myeloid leukemia, and in 2007, he received radiation therapy and a bone marrow transplant to treat the disease. Brown's doctor saw this as an opportunity to treat his patient's leukemia and HIV at the same time.

Brown was HIV-free after the radiation and transplant, but his cancer later returned and he required a second transplant in 2008. That year, researchers announced that the "Berlin patient" was the first person cured of HIV. 

Brown remained free of HIV through the end of his life. He died of cancer in 2020 at age 54, after his leukemia returned and spread to his spine and brain.  

How many people have been cured of HIV? 

As of March 2023, three people had been cured of HIV and two more were in long-term remission. In July 2023, researchers announced that an additional person was in long-term remission following a stem cell transplant, bringing that number to three.  

In addition to Timothy Ray Brown, the cured individuals include the London patient, later revealed to be Adam Castillejo; and the anonymous Düsseldorf patient. 

The three possible HIV cures include a man known as the City of Hope patient; the New York patient, the first woman to receive the treatment; and a man known as the Geneva patient, whose case is unusual and being closely monitored. (The City of Hope patient revealed his name — Paul Edmonds — on April 3, 2023, having received his transplant in February 2019 and stopped ART in March 2021.)   

At present, there's no official distinction between being cured and being in long-term remission from HIV, Dr. Deborah Persaud, who helped oversee the New York case and is the interim director of pediatric infectious diseases at Johns Hopkins, said at a March 2023 news conference.

"[The Düsseldorf patient] was likely the second person to be cured, but the team was really conservative, and stopped antiretroviral therapy after several years, and waited a long time to conclude that he was cured," Dr. Steven Deeks, an HIV expert and professor of medicine at the University of California, San Francisco, who was not involved in the patient's case, told Live Science in an email.

The Düsseldorf patient was treated in 2013, continued ART for nearly six years and has now been off the medication for more than four. Meanwhile, Castillejo received his transplant in 2016, stopped ART a little over a year later and was confirmed cured in 2020, before the Düsseldorf patient. 

What can we learn from HIV cures? 

These cases provide information about how the body changes after a curative transplant as well insight into future strategies to cure HIV.

Scientists have found that, even post-transplant, supersensitive tests pick up "sporadic traces" of HIV DNA and RNA (a molecular cousin of DNA needed to build proteins). However, these viral remnants cannot replicate, said Dr. Björn-Erik Ole Jensen, a senior physician at the University Hospital of Düsseldorf who ran exhaustive tests on such remnants from the Düsseldorf patient. 

That means none of these viral traces could make copies of themselves, he told Live Science. Doctors involved in the other cure cases ran similar tests, and got the same result.

Changes in the immune system might be a better measure of how well a transplant has worked, Jenson told Live Science. For about two years post-transplant, the Düsseldorf patient carried immune cells that reacted to HIV-related proteins, meaning they'd encountered and stored a "memory" of the virus. 

"But over time, these responses faded away," Jenson said, as the reservoir of functional HIV dwindled to nothing. This change in immune activity was a convincing sign that the Düsseldorf patient could stop ART, he added.

Are scientists researching other ways to cure HIV? 

Scientists are working on alternative treatments that can trigger these same changes in the body without relying on donor stem cells, Jenson said. By avoiding stem cell transplants, future treatments might eliminate the need for harsh chemotherapy, radiation and immunosuppressants, and the risk of GVHD.   

Some research groups are developing an HIV cure based on a modified cancer therapy, in which they take some of a patient's immune cells, delete the CCR5 receptor and make the cells reactive to HIV proteins before returning them to the body.

Another potential cure strategy involves gene therapies that edit the DNA of cells within the body, to delete the gene for CCR5 or to prompt cells to make proteins that block or disable CCR5. Some researchers are developing ways to target CXCR4.

"With the revolution of gene editing now occurring in other areas of medicine, we may someday be able to do this with a single shot," Deeks said. These approaches are still being tested in lab dishes and animals, so scientists don't yet know how they'd work in humans, Jenson noted.

Nevertheless,"I think there is hope."

A woman known as the "New York patient" received a stem cell transplant to cure her HIV, and now, she's been virus-free and off her HIV medication for about 30 months, researchers report.

"We're calling this a possible cure rather than a definitive cure — basically waiting on a longer period of follow up," Dr. Yvonne Bryson, director of the Los Angeles-Brazil AIDS Consortium at the University of California, Los Angeles and one of the doctors who oversaw the case, said during a news conference held Wednesday (March 15). 

Only a handful of people have been cured of HIV, so at this point, there's no official distinction between being cured and being in long-term remission, said Dr. Deborah Persaud, the interim director of pediatric infectious diseases at Johns Hopkins University School of Medicine, who also oversaw the case. Although the New York patient's prognosis is very good, "I think we're reluctant to say at this point whether she's cured," Persaud said at the news conference.

Bryson and her colleagues released early data on the New York patient in February 2022 and published more details of the case on Thursday (March 16) in the journal Cell. The new report covers the majority of the patient's case, up to the point when she had stopped taking antiretroviral therapy (ART) — the standard treatment for HIV — for about 18 months.

Related: UK man becomes second person cured of HIV after 30 months virus-free 

The patient received a stem cell transplant in August 2017 and stopped taking ART a little over three years later. Now, she's been off the medication for roughly 2.5 years, and "right now, she's still doing very well, enjoying her life," Dr. Jingmei Hsu, director of the Cellular Therapy Laboratory at NYU Langone Health and one of the transplant team leaders, said at the news conference.

Earlier HIV cure cases — including definitive cures in men treated in London, Berlin and Düsseldorf, and one case of long-term remission in a man treated in Los Angeles — had received stem cell transplants taken from bone marrow as a dual treatment for both cancer and HIV. (The first patient cured of HIV, a man from Berlin, died in 2020 after a cancer relapse.) 

All these transplants used bone marrow stem cells from adult donors who carried two copies of a rare genetic mutation: CCR5 delta 32. This mutation alters the doorway that HIV typically uses to enter white blood cells and thus blocks the virus from entering. After transplantation, the donor stem cells essentially take over the patient's immune system, replacing their old, HIV-vulnerable cells with new, HIV-resistant ones. To clear the way for the new immune cells, doctors wipe out the original immune cell population using chemotherapy or radiation therapy.

Like previous cases, the New York patient had both cancer and HIV and underwent chemotherapy prior to her transplant. However, she received stem cells taken from umbilical cord blood that contained the HIV-resistance genes. The umbilical cord blood was donated by an unrelated baby's parents at the time of delivery and later screened for the CCR5 delta 32 mutation.

To supplement those umbilical cord stem cells, as they were relatively few in number, the patient also received stem cells that had been donated by a relative, which helped bridge the gap as her HIV-resistant cells began to come in.

Because umbilical cord blood is easier to access than adult bone marrow, and more easily "matched" between donors and recipients, such procedures could become more common in the future. However, stem cell transplants wouldn't be appropriate for patients who are HIV-positive but don't have a second serious disease, like cancer, because it involves wiping out the immune system, Bryson said.

Rates of sexually transmitted infections (STIs), such as syphilis, have been rising over the past few years in the U.S. But why are STI rates surging now, and what can be done to reverse that trend?

Reduced public health focus on sexual health has been a big factor in rising STI rates, experts told Live Science. 

"Increasing opioid use, COVID-19, and the mpox outbreak have exacerbated a lack of funding and resources in sexual healthcare, creating a perfect storm that's driving up cases in recent years," Casey Pinto, an associate professor of public health sciences at the PennState Cancer Institute, told Live Science.  

Changes in sexual behavior, such as a decrease in condom usage and an increase in risky sexual behavior due to opioid use, are likely also playing a role, experts told Live Science.

Related: New 'concerning' strain of drug-resistant gonorrhea found in U.S. for 1st time

Why are STI rates increasing? 

The U.S. Centers for Disease Control and Prevention (CDC) tracks the national rate of gonorrhea, chlamydia and syphilis infections. Rates of these bacterial STIs were already rising in the six years preceding the pandemic. Over this period, gonorrhea rates increased by an average of roughly 10% each year, chlamydia rates increased by an average 3.6% annually and syphilis rates increased by an average 14% annually. 

In 2021, during the pandemic, gonorrhea and chlamydia rates continued to increase, rising by around 2.5% compared to 2020, according to the latest CDC data. Both diseases can make sex painful and lead to infertility, while gonorrhea can also lead to yellow-green discharge from the genitals. 

Syphilis case rates surged more sharply in the same time period, to their highest rate in three decades — a 27% uptick compared to 2020. Syphilis can cause genital ulcers and rashes across the hands and feet. 

Soaring syphilis infections are particularly concerning as they are tied to rising rates of congenital syphilis, where the bacteria pass through the placenta during pregnancy, potentially causing bone deformities, nerve problems and, in some cases, miscarriage, stillbirth or death of the newborn. Congenital syphilis infection rates roughly tripled from 2017 to 2021, according to the CDC data.

"In the early 2000s, we were near eradicating syphilis here in the U.S., so it's a bit terrifying to see how much syphilis has come back, ripping and roaring through our communities," Dr. Joseph Cherabie, an assistant professor of medicine and medical director at the St. Louis County Sexual Health clinic, told Live Science.

The true picture may be even worse as "cases were underreported," especially amid pandemic-related disruptions that caused widespread closures of sexual health clinics and diverted staff from tracking STIs to monitoring COVID-19, Cherabie said. These disruptions, along with those caused by last year's mpox outbreak, probably increased STI rates because more people were having sex while unknowingly being infected, Cherabie said.

One factor many scientists think is behind the rise in STI rates is the growing opioid epidemic. Use of opioids, including prescribed painkillers and illicit drugs such as heroin and fentanyl, reached new heights amid the pandemic and has been linked to risky sexual behavior that raise the risk of STI spread, such as not using a condom and having many sexual partners, Cherabie said.

In addition, the high levels of opioid use seen in American Indian and Alaska Native (AI/AN) communities may help explain their rising rates of HIV seen in recent years, Cherabie said. 

After decreasing for some time, rates of new HIV diagnoses among AI/AN people began rising again between 2018 and 2021, CDC data suggest. This could theoretically be linked to opioid use, since needle sharing can increase people's risk of contracting HIV, which also spreads through sexual contact, Cherabie said. What's more, medications that dramatically reduce the chance of getting HIV, called pre-exposure prophylaxis (PrEP), are less readily available in these communities, compared to groups whose HIV rates are declining, he said. 

Another driver of surging STI rates is the declining use of condoms, Dr. Jodie Dionne, an assistant professor of infectious diseases at the University of Alabama at Birmingham told Live Science. 

"Several studies are showing a pretty consistent decrease in condom use," which acts as a physical barrier against the transfer of STIs, Dionne said. One study that surveyed condom use among over 29,000 female U.S. residents ages 15 to 44 found that 3% fewer people reported using a condom during their last instance of vaginal sex between 2017 and 2019, compared to rates reported a decade earlier.

Condoms are particularly falling out of favor among those taking PrEP, Cherabie added. A recent study found that, between 2012 and 2017, rates of condomless sex have increased among men who have sex with men, and other research suggests this shift in behavior may be partially tied to the increased use of PrEP, which guards against HIV but not other STIs.

"We need to make sure these people are aware they can get other STIs apart from HIV, and they need to get tested every three to six months if they are having new sexual partners," Cherabie said. 

How can STI rates be reduced?

So what measures can reverse this trend?

One strategy is to increase STI testing. Strengthening efforts to screen for STIs, as well as congenital syphilis, through increased funding could help to reverse rises in infection rates, Cherabie said. Sexual healthcare has been underfunded for decades, he said.

A "terrific opportunity" to boost testing is via at-home test kits, Dionne said. "One useful thing we learned during the COVID-19 pandemic is how readily people can perform self-swabbing at home when high quality test kits are made available. We can and should expand this self-testing capacity to include chlamydia and gonorrhea self-testing outside of the clinic," Dionne said. Self-testing for syphilis may be trickier as it requires a blood test, she noted.

Ongoing trials are exploring the feasibility of government-funded test kits for chlamydia, gonorrhea and HIV, which can each cost from around $80 to $300. "In trials in Jefferson County, Alabama, we've seen that many people ordering free STI self-testing kits have rarely or never been screened for STIs in the past," Dionne said. At-home tests could be a worthwhile investment if they reach historically stigmatized groups who face a disproportionate risk of STIs, she said. 

Using less stigmatizing language to inform vulnerable groups about STIs could also encourage people to get tested, which could drive down infection rates, Cherabie said. Whether that will actually impact outcomes, however, is unclear — researchers have a "very limited understanding" as to whether changing levels of stigmatization contributed to the recent rise in STI rates, Dionne said.

Scientists initially wondered whether STIs rates are increasing due to emerging antibiotic resistance among pathogens. But so far, that doesn't seem to be the case, Dionne said. Nevertheless, antimicrobial-resistant strains are "something we want to keep an eye on, because with increasing antimicrobial resistance, we are less likely to get rid of the infection," Cherabie said.

As the burden of STIs grows larger, the CDC announced funding for a new STI research consortium aimed at reversing current trends on Feb. 27, 2023. This could be a first step in slowing or reversing the rise in STI rates.

Humans have been fighting viruses since the species has existed. For some viral diseases, vaccines and antiviral drugs have prevented widespread infection or helped people recover. And we've even been able to eradicate one disease — smallpox. 

Some viruses pose a bigger threat than others. The viral strain that drove the 2014-2016 Ebola outbreak in West Africa kills up to 90% of the people it infects, making it the most lethal member of the Ebola family.

Related: 20 of the worst epidemics and pandemics in history

But there are other viruses that are are even deadlier. Some viruses, including the novel coronavirus currently driving outbreaks around the globe, have lower fatality rates, but still pose a serious threat to public health because they infect so many people. 

Here are the 12 worst killers, based on the likelihood that a person will die if they are infected with one of them, the sheer numbers of people they have killed and whether they represent a growing threat.

Marburg virus

According to the World Health Organization (WHO), the Marburg virus was first identified by scientists in 1967, when small outbreaks occurred among lab workers in Germany who were exposed to infected monkeys imported from Uganda. Marburg virus symptoms are similar to Ebola in that both viruses can cause hemorrhagic fever, meaning that infected people develop high fevers, and bleeding throughout the body that can lead to shock, organ failure and death, according to Mayo Clinic.

The case fatality rate in the first outbreak (1967) was 24%, but it was 83% in the 1998-2000 outbreak in the Democratic Republic of Congo, and 100% in the 2017 outbreak in Uganda, according to the WHO. 

The first known Marburg virus outbreak in West Africa was confirmed in August 2021. The case was a male from south-western Guinea, who developed a fever, headache, fatigue, abdominal pain and gingival hemorrhage before ultimately dying of the disease. This outbreak lasted for six weeks and, while there were 170 high-risk contacts, only one case was confirmed, according to Reuters.

Ebola virus

In 1976, the first known Ebola outbreaks in humans struck simultaneously in the Republic of the Sudan and the Democratic Republic of Congo. Ebola is spread through contact with blood or other body fluids, or tissue from infected people or animals. The known strains vary dramatically in their deadliness, Dr. Elke Muhlberger, an Ebola virus expert and associate professor of microbiology at Boston University, told Live Science.

One strain, Ebola Reston, doesn't even make people sick, though it is deadly to other primates, according to Essential Human Virology (2016). But for the Bundibugyo strain, the human fatality rate is up to 25%, and it is up to 90% for the Zaire strain.

The largest Ebola outbreak on record  emerged in West Africa in early 2014 and took two years to resolve. During that time, it infected 28,652 people and claimed 11,325 lives, according to the Centers for Disease Control and Transmission (CDC).

In December 2020, the Ervebo vaccine was approved by the U.S. Food and Drug Administration. This vaccine helps to defend against the Zaire ebola virus and a global stockpile became available from January 2021. 

Rabies

Although rabies vaccines for pets, which were introduced in the 1920s, helped to make the disease extremely rare in the developed world, this condition remains a serious problem in India and parts of Africa. About 59,000 people die every year from the virus, according to a 2019 study in the CDC's Morbidity and Mortality Weekly Report.

Infection from this virus develops after a bite or scratch from an infected mammal. Once a person is bitten, they must immediately get rabies vaccines or antibody treatments to prevent the disease from progressing. If they don't, the virus will damage the brain and nerves. Once symptoms begin to show, death almost always follows; the virus has a 99% fatality rate, according to the CDC.

"It destroys the brain, it's a really, really bad disease," Muhlberger said. "We have a vaccine against rabies, and we have antibodies that work against rabies, so if someone gets bitten by a rabid animal we can treat this person," she said.

However, she said, "if you don't get treatment, there's a 100% possibility you will die."

HIV

In the modern world, the deadliest virus of all may be HIV. 

"It is still the one that is the biggest killer," Dr. Amesh Adalja, an infectious disease physician and spokesman for the Infectious Disease Society of America told Live Science.

An estimated 32 million people have died from HIV since the disease was first recognized in the early 1980s. "The infectious disease that takes the biggest toll on mankind right now is HIV," Adalja said.

Powerful antiviral drugs have made it possible for people to live for years with HIV. And in rare cases, stem cell transplants have cured the disease. But the disease continues to devastate many low- and middle-income countries, where 95% of new HIV infections occur. 

Nearly 1 in every 25 adults within the World Health Organization Africa region  is HIV-positive, meaning that there are over two-thirds of the people living with HIV worldwide, according to the WHO. In 2021, there were 650,000 HIV-related deaths worldwide.  

Smallpox

In 1980, the World Health Assembly declared the world free of smallpox. But before that, humans had battled smallpox for thousands of years, and the more severe version of the disease, Variola major, killed about 30% of those it infected, according to the WHO. It left survivors with deep, permanent scars and, often, blindness.

In populations outside of Europe, where people had little contact with the virus before visitors brought it to their regions, mortality rates were much higher. For example, historians estimate that smallpox, which was introduced by European explorers, killed 90% of the native population of the Americas. In the 20th century alone, smallpox killed 300 million people, according to National Geographic.

"It was something that had a huge burden on the planet, not just death but also blindness, and that's what spurred the campaign to eradicate from the Earth," Adalja said.

Hantavirus

Hantavirus pulmonary syndrome (HPS) is a deadly disease for those who contract it, but it has killed relatively few people. It first gained wide attention in the U.S. in 1993, according to the CDC). A healthy, young Navajo man and his fiancée living in the Four Corners area of the United States died within days of developing shortness of breath. A few months later, health authorities isolated hantavirus from a deer mouse living in the home of one of the infected people. More than 833 people in the U.S. have contracted HPS as of the end of 2020, the last year that data was reported for, and 35% have died from the disease, according to the CDC.

The virus is not transmitted from one person to another, rather, people contract the disease from exposure to the droppings of infected mice.

Previously, a different hantavirus, called Korean hemorrhagic fever, caused an outbreak in the early 1950s, during the Korean War, according to a 2010 paper in the journal Clinical Microbiology Reviews. More than 3,000 United Nations troops became infected, and about 12% of them died.

While the virus was new to Western medicine when it was discovered in the U.S., researchers realized later that Navajo medical traditions describe a similar illness, and linked the disease to mice.

Influenza

Influenza kills a small proportion of the people it infects, at about 1.8 in 100,000 people every year, according to the CDC. But because it infects so many people,  it's one of the leading killers worldwide. During a typical flu season, up to 650,000 people worldwide will die from the illness, according to WHO. 

And occasionally,  a new flu strain emerges, and a pandemic spreads across the globe. Often, these new strains have higher mortality rates than endemic flu.

The most deadly flu pandemic, sometimes called the Spanish flu, began in 1918 and sickened up to 40% of the world's population, killing an estimated 50 million people, according to CDC.

"I think that it is possible that something like the 1918 flu outbreak could occur again," Muhlberger said. "If a new influenza strain found its way in the human population, and could be transmitted easily between humans, and caused severe illness, we would have a big problem."

Dengue

Dengue hemorrhagic fever, caused by the dengue virus, is a mosquito-borne disease that first appeared in the 1950s in the Philippines and Thailand. It has since spread throughout the tropical and subtropical regions of the globe, according to a 2009 study in the journal  Clinical Microbiology Reviews. Up to 40% of the world's population now lives in areas where dengue is endemic and the disease will spread farther as climate change enables the mosquitoes that carry it to spread to other regions, according to the journal Nature .

According to WHO, dengue infects 100 to 400 million people a year. Although dengue fever has a lower mortality rate than some other viruses, at around 1%, the virus can cause an Ebola-like disease called dengue hemorrhagic fever, which has a mortality rate of 20% if left untreated. "We really need to think more about dengue virus because it is a real threat to us," Muhlberger said. 

A vaccine for dengue, called Dengvaxia was approved in 2019 by the U.S. Food and Drug Administration for use in children ages 9 to 16 years old living in areas where dengue is common and with a confirmed history of virus infection, according to the CDC. In some countries, an approved vaccine is available for those who are 9 to 45 years old, but again, recipients must have contracted a confirmed case of dengue in the past. Those who have not caught the virus before could be put at risk of developing severe dengue if given the vaccine.   

Rotavirus

Rotavirus is a diarrheal disease that kills about 200,000 children annually, mostly in Nigeria and India, according to PreventRotavirus, a council dedicated to widespread use of rotavirus vaccines. 

The virus can spread rapidly, through what researchers call the fecal-oral route (meaning that small particles of feces end up being consumed).

Thanks to vaccines, children in the developed world rarely die from the infection. But the disease is a killer in the developing world, where rehydration treatments are not widely available.

The WHO estimates that worldwide, there are more than 25 million outpatient visits and two million hospitalizations each year due to rotavirus infections. Countries that have introduced the vaccine have reported sharp declines in rotavirus hospitalizations and deaths. 

Two vaccines are now available to protect children from rotavirus, the leading cause of severe diarrheal illness among babies and young children.

SARS-CoV

The virus that causes severe acute respiratory syndrome, or SARS, was first identified in 2003 during an outbreak in China, according to the WHO. The virus likely emerged in bats initially, then hopped into nocturnal mammals called civets before finally infecting humans, according to the Journal of Virology. After triggering an outbreak in China, SARS spread to 26 countries around the world, infecting  8,096 people and killing more than 774 over the course of several months, according to the CDC.

The disease causes fever, chills and body aches, and often progresses to pneumonia, a severe condition in which the lungs become inflamed and fill with pus. SARS has an estimated mortality rate of 9.6%, however, no new cases of SARS have been reported since the early 2000s, according to the CDC.  

SARS-CoV-2

SARS-CoV-2 may not kill a huge fraction of the people it infects, but the disease caused by the virus, called COVID-19, has become the leading viral cause of death in since it exploded onto the scene in 2020. As of October 2022, the virus has caused more than 6.57 million deaths worldwide and counting, and has infected at least 626 million people, according to OurWorldInData.

SARS-CoV-2 belongs to the same large family of viruses as SARS-CoV, known as coronaviruses, and was first identified in December 2019 in the Chinese city of Wuhan. The virus may have originated in bats and passed through an intermediate animal before infecting people, according to a 2021 study in the journal Nature. 

The initial outbreak prompted an extensive quarantine of Wuhan and nearby cities, restrictions on travel to and from affected countries and a worldwide effort to develop diagnostics, treatments and vaccines. 

Estimating an infection fatality rate, or the fraction of people who die after being infected, is difficult, because many mild cases are never diagnosed. But age is clearly a huge factor in the virus' lethality: One study in the journal The Lancet estimated that the virus killed about 0.0023% of children under age 7 that it infected and about 20% of those infected over age 90.

The virus also poses a higher risk to people who have underlying health conditions such as diabetes, high blood pressure or obesity, according to WHO. Common symptoms include fever, cough, loss of taste or smell and shortness of breath and more serious symptoms include breathing difficulties, chest pain and loss of mobility. 

Several COVID-19 vaccines, as well as booster doses for those vaccines, are currently approved for use in both children and adults. These vaccines dramatically reduce the odds of severe disease and death, according to the CDC.

MERS-CoV

The virus that causes Middle East respiratory syndrome, or MERS, sparked an outbreak in Saudi Arabia in 2012 and another in South Korea in 2015. It has a high case fatality rate, killing about 35% of people diagnosed with it. But the virus has killed only 858 people as of 2021, because it does not spread easily between people.

 The MERS virus belongs to the same family of viruses as SARS-CoV and SARS-CoV-2. According to WHO, the disease infected camels before passing into humans and can trigger a fever, coughing and shortness of breath in infected people. 

MERS is deadly because, like its less lethal cousins SARS and SARS-CoV-2, it often progresses to severe pneumonia. There is no vaccine available to prevent this disease. The best way to reduce the chances of infection is to wash hands regularly, avoid contact with camels and not consume products containing raw animal milk.  

How has Magic Johnson survived with HIV? When the former professional basketball player was diagnosed with human immunodeficiency virus in 1991, a lack of understanding and stigmatization surrounding the virus led to questions being raised over his future life prospects. However, thanks to advancements in antiretroviral drugs and management of the condition, the 63-year-old continues to thrive in his roles as a sports analyst, businessman and HIV activist more than 30 years later.

On Nov. 8, 1991, the day after the Los Angeles Lakers star announced he had been diagnosed with the virus, Mark Heisler of the Los Angeles Times wrote: "Many people [diagnosed] with HIV live many years with few serious effects on their health. The average period between infection with the human immunodeficiency virus and diagnosis of […] AIDS is now ten years, according to experts.”

At the time, HIV/AIDS was widely associated with death at a young age, so for many people this outcome might have seemed impossible. But today, thanks to advancements in antiretroviral drugs, the life expectancy of a young person diagnosed with HIV is not dissimilar from that of a similarly aged person without HIV, according to Healthline. It is precisely these kinds of drugs that have helped Magic Johnson manage the disease and have made HIV a chronic health condition rather than a fatal disease.

"There is nothing unique about Magic," Spencer Lieb, senior epidemiologist and HIV/AIDS research coordinator for the Florida Consortium for HIV/AIDS Research told Live Science. "There are still people alive and kicking and doing very well 20 and 30 years after infection." 

Lieb said that in the state of Florida alone, hundreds of patients have lived full lives since being diagnosed with HIV in the early 1980s, when the first confirmed AIDS cases were confirmed in the United States. But while Johnson and many others are able to manage their condition, many others are not as fortunate. According to research and estimates by the Centers for Disease Control and Prevention, as of 2019 about 1.18 million Americans have HIV, and 13 percent of them are undiagnosed. Approximately 36,000 people are diagnosed with HIV each year, and more than 15,000 die annually, although these deaths can be from any cause, not necessarily from an AIDS-related illness.

Managing HIV

Despite new advances in medical science HIV remains incurable thanks to "the presence of a latent viral reservoir. During the life cycle of the virus, HIV integrates into the host DNA. A subset of integrated HIV provirus remains transcriptionally silent, producing neither viral proteins nor viral progeny, until reactivation by various physiologic stimuli. This latency of HIV allows some infected cells to escape immune detection and elimination, and these latently infected cells constitute the viral reservoir," wrote Nathan W. Cummins, MD and Andrew D. Badley, MD for Mayo Clinic Proceedings in 2015.

The key with Johnson and others has been preventing their incurable disease from progressing into AIDS.

Upon infection with HIV, a person's immune system kills off nearly all of the virus and infected cells. But some small number remain, and over time, those HIV cells replicate, attacking the immune system in seven stages, according to the National Institute of Health's HIV info page. This is a gradual process known as the HIV life cycle and it is by blocking the virus at each stage of this process that it can be prevented from advancing to AIDS.

Researchers have developed a number of powerful drugs to help people like Johnson block and contain the virus. The key weapon in the beginning was a regimen of three or four antiretroviral drugs, collectively known as antiretroviral therapy, or ART.

"They told me that the three-drug combination was going to save my life, and they were right," Johnson told The Guardian in 2021. "As we talk today, right now, I'm thinking, 'Wow' – it’s been 30 years and I'm still here, healthy. Everything has gone right. There was one drug then, now we have 30-something drugs."

One of Johnson's doctors who helped pioneer the treatment placed him on the then-experimental drug cocktail in 1994, about a year and a half before it came into widespread use in 1996, according to the Daily Beast.

"Magic got a jumpstart on experimental drugs before they were released to the general public," Lieb told Life's Little Mysteries, "but there were many people in clinical trials benefitting at the same time."

HIV medicines

HIV spreads by hijacking a subset of white blood cells called CD4 cells or T cells, which are the body's first line of defense against foreign invaders, and using the cells' DNA to make copies of itself or replicate; in this process, these T cells get destroyed, according to Healthline. The most common drugs in the ART regimen target two of the enzymes that HIV uses to replicate itself.

The first enzyme, called reverse transcriptase, turns the virus' genetic instructions encoded in a single RNA strand into double-stranded DNA. In scientific terms, this mode of replication classifies HIV as a retrovirus, hence "antiretroviral" drugs.

The second enzyme, known as protease, creates new, functional HIV particles by cutting up the proteins produced by our hijacked cellular machinery.

Medication can disrupt these processes, and to that end, Johnson is currently taking reverse transcriptase inhibitor and protease inhibitor drugs, which are contained in the pharmaceuticals Trizivir and Kaletra, respectively, according to the Daily Beast.

These and other HIV-fighting drugs are "hideously expensive," said Lieb. "High ART costs are among many structural barriers that lead to poor treatment access and adherence, contributing to suboptimal HIV outcomes in the United States," according to a report published by JAMA Internal Medicine in 2020.

Public and private medical insurance, as well as various assistance programs, make the medicines more affordable and available to the vast majority of patients in the United States and other parts of the world. It is a "myth," said Lieb, that Johnson, who is wealthy, is buying himself special treatments.

Living with HIV

By taking the right regimen every day, most people living with HIV can see the number of virus particles in a sample of their blood, or viral load, become undetectably low.

Not only does a low viral count stave off symptoms of HIV and AIDS, but it also slashes the odds of a randomly mutated copy of the virus emerging that can prove resistant to the therapy. Furthermore, a low viral load severely reduces the risk of transmitting the virus to others.

Yet even without modern drugs, in rare instances a person living with HIV can manage on their own to keep AIDS at bay. These "long-term nonprogressors" or "elite controllers," estimated at as few as one in 500, have lived for decades with HIV, despite not being on antiretroviral therapy.

It is not known if Johnson is among this "scarce breed," as Lieb called them, but more than likely "without medications, he'd be progressing."

Researchers continue to study long-term nonprogressors to get insights on HIV resistance that could help the 37.7 million people battling the virus, the current estimate of UNAIDS according to HIV.gov.

Public perception of HIV

One of the most important contributions Johnson has made to people with HIV is making people more aware and understanding of the virus. Johnson announced his retirement from the NBA and made his diagnosis public very quickly and then opened up about his experience.

"My ignorance could cost me my life, but I wanted to try and ensure that no one else would become infected with HIV for the same reason" Johnson wrote in Sports Illustrated on November 18, 1991.

"I said that because I had tested HIV-positive, I was retiring from the NBA. I also said that I was going to become a spokesperson in the fight against the human immunodeficiency virus and an advocate for practicing safe sex by using condoms. I also said I was going to beat the disease. And I will," Johnson wrote.

He lived up to that promise by making regular appearances, giving interviews and being an activist for HIV and AIDS organisations. "Johnson went on to attack the HIV stigma with the same passion he displayed on the court, launching the Magic Johnson Foundation to raise awareness about the virus, then pushing Congress and the White House to spend money to fight the disease," wrote Nelson Oliveira for CBS News.

His approach acted as a "public-health catalyst," wrote Alexander Cardazzi, Joshua C. Martin, and Zachary Rodriguez in their 2021 paper "Information Avoidance and Celebrity Exposure: The Effect of "Magic" Johnson on AIDS Diagnoses and Mortality in the U.S." for West Virginia University, as they attempted to quantify the impact his announcement in 1991 had on heterosexual men getting tested for HIV.

Originally published on Live Science on 04 March 2022 and updated on 24 August 2022. 

Additional resources and reading

HIV and AIDS are not the only conditions we're still looking to cure. You can also learn about some of the cancers we're still battling and why they're so challenging.

Mental health continues to be a field that we hope to understand and appreciate more. Find out why exercise can be important to mental health too.

Bibliography

• "Magic Johnson’s Career Ended by HIV-Positive Test" by Mark Heisler Los Angeles Times
• "Facts About HIV: Life Expectancy and Long-Term Outlook" Healthline
• "New HIV Diagnoses and People with Diagnosed HIV in the US and Dependent Areas by Area of Residence, 2019" Centers for Disease Control and Prevention
• "Can HIV Be Cured and Should We Try?" Mayo Clinic Proceedings
• "The HIV Life Cycle" National Institute of Health
• "Magic Johnson: the NBA superstar who smashed HIV stigma – then built a huge fortune" by Oliver Laughland The Guardian
• "HIV: Guide to Protease Inhibitors" Healthline
• "HIV Antiretroviral Therapy Costs in the United States, 2012-2018" JAMA Internal Medicine
• "The Global HIV/AIDS Epidemic" HIV.gov
• "I'll Deal With It: HIV Has Forced Me To Retire, But I'll Still Enjoy Life As I Speak Out About Safe Sex," by Magic Johnson, Sports Illustrated
• "Magic Johnson opens up about his health, career 30 years after HIV diagnosis: 'You just sit there and say, what does this mean? Am I gonna die?'" CBS News
• "Information Avoidance and Celebrity Exposure: The Effect of "Magic" Johnson on AIDS Diagnoses and Mortality in the U.S." by Alexander Cardazzi, Joshua C. Martin, and Zachary Rodriguez (West Virginia University, 2021)
• "Why Language Matters: Facing HIV Stigma in Our Own Words" The Well Project

It has been more than 40 years since the first reported cases of HIV, and tremendous progress has been made toward ending the epidemic, including advances in HIV treatment that allow for longer and healthier lives. Nevertheless, HIV persists as a serious public health challenge. In the United States, the South accounts for eight of the top ten states and nine of the top ten metropolitan areas with the highest rates of new infections. Globally, it’s estimated that more than 36 million people are living with HIV and 4000 individuals are newly infected each day, with the burden disproportionately faced by Sub-Saharan Africa and many low- and middle-income countries. Scaling up proven prevention interventions and strategies is essential to reduce the individual and societal burden of the virus. The HIV epidemic is not over.

The work needed to overcome the epidemic includes an unequivocal commitment to continued scientific innovation to provide solutions for the unmet and evolving needs of people around the world. Scientific breakthroughs and medical innovations have brought radical change for people and communities most affected by HIV. The advent of antiretroviral therapy and once-daily single tablet regimens represent some of the most significant milestones that have helped bring radical change in the outlook for people affected by HIV. The scientific advancements have been transformative but significant gaps in care remain. 

Since the company was founded 35 years ago, Gilead has been a leading innovator in the field of HIV, driving advances in treatment, prevention, and cure research. Gilead researchers have developed 11 HIV medications, including the first single-tablet regimen to treat HIV and the first antiretroviral for pre-exposure prophylaxis (PrEP) to reduce the risk of acquiring HIV infection. These scientific advancements have helped to transform HIV into a preventable disease and a chronic condition for the millions of people who are living with HIV. 

Last week many from the global HIV community convened in Montreal for the 24th International AIDS Conference (AIDS 2022). There, the latest advancements and discoveries in HIV science were discussed by many of the most respected researchers from around the globe. Gilead’s decades of expertise and leadership in HIV uniquely position the company to develop innovative therapeutic options that address unmet needs in HIV treatment and prevention while actively pursuing research that could, one day, lead to a cure. 

Gilead’s first guiding principle for advancing the next wave of transformational innovation in HIV is putting people at the center of the research and development process.  A person-centered approach to innovation is of particular importance to Jared Baeten, MD, Ph.D., Gilead’s Vice President of HIV Clinical Development. Under his leadership, the efforts of the HIV development team are driven by a strong sense of justice, equity, and dedication to ending the global epidemic.

“A person-centered approach to research results in the creation of clinical evidence that is meaningful and beneficial to people and communities confronting the day-to-day realities of this virus. Collaboration with researchers and community stakeholders, particularly those living with HIV or those who could benefit from PrEP, is integral in all aspects of our research development process. And, that kind of collaboration is essential if we are going to have the impact we all want, which is ending this epidemic,” notes Baeten. “Repeated and engaged opportunities to interact directly with the community, such as we were fortunate to do each day at AIDS 2022, are invaluable for helping further our HIV research efforts.”

Against this backdrop, Gilead concentrates its research and development efforts on key areas:

HIV Treatment and Prevention Research

As part of global efforts to help end the HIV epidemic, Gilead understands the critical need for continuous innovation to bring forward novel solutions to meet the challenges of the epidemic today, striving for ground-breaking advancements. As the epidemic has evolved over four decades, new challenges continue to emerge.

Although antiretroviral medications have transformed HIV into a treatable disease, Baeten believes the next wave of innovation in HIV is long-acting options that can help address the differentiated needs and preferences of the diverse range of individuals and communities affected by the epidemic. “Those diverse, unmet needs propel our research teams at Gilead, and it is paramount this work is supported by the most rigorous clinical science.” 

In addition, people with HIV have evolving needs as they age, and they require antiretroviral therapies that accommodate those needs. Those aging with HIV have several age-related chronic conditions and additional burden from the treatments they take for those other conditions. Chronic immune activation from the viral infection compounds these challenges. To confront the synergistic effects of aging with HIV, Gilead’s treatment research program focuses on advancing long-term health and quality of life. 

Advancing the science behind PrEP is a fundamental part of Gilead’s efforts aimed at ending the epidemic, and Gilead remains committed to developing novel patient-centered PrEP medication options. Understanding the needs and preferences of those who would benefit from PrEP and giving people choices that best fit their schedules – including long-acting dosing intervals – will be a key to accelerating the decline in new HIV infections worldwide. Every day, Gilead strives to incorporate the expertise of community members from around the world directly into the company’s prevention clinical development work.

HIV Cure Research :

Curing HIV is the ultimate aspiration of Gilead’s HIV research and development efforts. Through the company’s innovative cure research program, Gilead is furthering the collective scientific knowledge on potential pathways to achieve a ‘functional cure’ (defined as long-term viral suppression in the absence of antiretroviral therapy, without transmission or disease progression). 

Currently, Gilead is exploring a range of options to activate and eliminate the persistent viral reservoir that makes HIV a lifelong infection. The company’s strategy is grounded in the hypothesis that a multi-pronged approach is needed to achieve the goal of curing HIV. The discovery and development of latency-reversing agents, immune modulators, and genetically engineered effector antibodies are core areas of focus in the company’s research. Gilead has created a three-prong strategy for its research focus: pull HIV out of reservoirs, direct the immune system to clear it, and inoculate the body against any remaining virus, aiming at long-term remission. 

Illuminating the pathways to an HIV cure is an incredibly complex scientific challenge and partnerships and collaboration are key to catalysing the research.  That’s why Gilead works closely with industry, academic, and community partners on clinical studies to achieve a functional cure for HIV. “Our close connections with the field, built over decades of collaborative research and development, enable us to advance multiple preclinical and clinical programs aimed at functional cure for HIV,” said Baeten. As part of Gilead’s cure grants program, more than $36 million in grants have been awarded to academic institutions, non-profit organizations, and community groups engaged in HIV cure initiatives.

Gilead’s work to develop a cure for HIV is one part of the company’s larger role in the global efforts to help end the HIV epidemic and part of Gilead’s focus on person-centric innovation.

“Continued scientific innovation and inclusive approaches are essential in the discovery and development of person-centered options that address the evolving needs of a broad range of individuals and communities affected by HIV,” underscored Baeten. “Our scientific advancements are grounded in collaboration with community and research partners around the world. AIDS 2022 brought us back in-person with those partners, after two years of being unable to gather together. The time we spent highlighted how strong the need for continued innovation is, and further strengthened our belief that we will dedicate the time and resources to develop innovative new medicines that will draw us closer to helping end the HIV epidemic for everyone, everywhere.” 

Read stories from community collaborators that help make Gilead’s work in HIV possible on GileadHIVTogether.com and follow Gilead on LinkedIn, Twitter, Instagram, and YouTube. 

After receiving a stem cell transplant, a 66-year-old man may be the fifth person to be cured of HIV, the virus that causes AIDS, researchers reported Wednesday (July 27). The patient, who wishes to remain anonymous, is the oldest person yet to undergo the procedure and enter long-term remission from the disease. 

The man — known as the "City of Hope patient" in reference to the medical center in Los Angeles where he was treated — was first diagnosed with HIV, the human immunodeficiency virus, in 1988, according to a statement shared by City of Hope. "When I was diagnosed with HIV in 1988, like many others, I thought it was a death sentence," the patient said.  

Just the year before, in March 1987, the U.S. Food and Drug Administration approved the first antiretroviral therapy, or medication for HIV, called azidothymidine (AZT), according to the National Institute of Allergy and Infectious Diseases. It wasn't until the mid-1990s that combination therapies for HIV would come into use; these therapies combined two to three HIV drugs to boost the efficacy of the treatment and help prevent patients from developing resistance to the drugs. Such combination therapies are now the standard of care for the treatment of HIV. 

The City of Hope patient took antiretroviral drugs for more than 31 years to control his HIV. At one point, the man's condition had progressed to AIDS (acquired immunodeficiency syndrome), meaning his white blood cell count had fallen to critically low levels, NBC News reported. He took AZT and some of the other early HIV medications, which were prescribed individually, before switching to a highly effective combination antiretroviral treatment in the 1990s.   

Related: UK man becomes second person cured of HIV after 30 months virus-free 

Several decades later, in 2018, the patient developed acute myelogenous leukemia (also called acute myeloid leukemia, or AML), a cancer of the blood and bone marrow. As a treatment for both the cancer and HIV, doctors performed a blood stem cell transplant with cells from a donor who carried a rare genetic mutation. This mutation, called homozygous CCR5 delta 32, renders its carrier resistant to HIV by altering the entryway that the virus usually exploits to invade the body's white blood cells. 

Following the man's transplant, these mutant, HIV-resistant cells steadily took over his immune system. In March 2021, under the careful supervision of his medical team, the patient stopped taking antiretroviral medications, and to date, there have been no signs of HIV replication in his body. 

The team describe the patient as being in long-term remission, as there's been no trace of viable virus in his system for 17 months; they will continue to monitor his condition and may declare him officially "cured" at a later date, if his status remains unchanged, NBC News reported.   

The City of Hope patient's case is very similar to that of the so-called Berlin patient, the first person cured of HIV. 

The Berlin patient, who later revealed his name to be Timothy Ray Brown, also developed AML and received a bone marrow transplant from a donor with an HIV-resistant genetic mutation. (Bone marrow contains blood stem cells.) Two others — the Düsseldorf and London patients — were cured using the same procedure, according to NBC News, and recently, one woman was cured after receiving a stem cell transplant that used cells from umbilical cord blood, Live Science previously reported. 

"[The City of Hope patient's case] is yet another case that resembles Timothy Brown from years ago," David D. Ho, one of the world's leading AIDS researchers and director of the Aaron Diamond AIDS Research Center at Columbia University, told The Washington Post. However, given the risks of the transplant procedure and the rarity of the HIV-resistant mutation, such treatments aren't accessible to the majority of HIV patients, Ho said.

"While a transplant is not an option for most people with HIV, these cases are still interesting, still inspiring and illuminate the search for a cure," Dr. Sharon Lewin, an infectious-disease specialist at the Peter Doherty Institute for Infection and Immunity at the University of Melbourne in Australia, said at a news conference, according to NBC News. Some research groups are working to develop gene editing techniques that could introduce the HIV-resistant mutation into patients, The Washington Post reported.

Dr. Jana K. Dickter, a City of Hope associate clinical professor in the Division of Infectious Diseases, spoke about the City of Hope patient's case Wednesday at the 2022 International AIDS Conference in Montreal.

Originally published on Live Science.

A large outbreak of meningococcal disease — a potentially deadly infection — has been reported among gay and bisexual men in Florida, according to health officials, who are urging people in these populations to get vaccinated against the disease.

Officials with the Florida Department of Health said on April 7 that the number of cases of meningococcal disease reported in the state this year had surpassed the state's five-year average. The outbreak is primarily affecting gay and bisexual men in Florida, including people with HIV, according to the Centers for Disease Control and Prevention (CDC). Some cases have also been reported in people who traveled to Florida. 

In response to the outbreak, the CDC is encouraging men who have sex with men and live in Florida to get the meningococcal conjugate vaccine, which is called the MenACWY vaccine. People in this population who are traveling to Florida should talk with their healthcare provider about getting the vaccine, according to the CDC..

In addition, the Florida health department recommends the meningococcal conjugate vaccine to the following groups during this outbreak: College and university students, people with weakened immune systems (immunocompromised) and people with HIV.

Multiple cases of meningococcal disease have also been reported among Florida college students over the last few months, but at this time, there is no evidence that the cases among college students are related to the larger outbreak among men who have sex with men, CDC officials said. 

Related: 28 devastating infectious diseases 

Meningococcal disease is a rare but serious illness caused by the bacterium Neisseria meningitidis. The most common types of meningococcal disease include meningitis, an infection of the membranes that line the brain and spinal cord, and bloodstream infections, according to the CDC. 

The disease is spread through respiratory secretions, meaning  saliva, according to the CDC. It generally takes close or prolonged contact with an infected person to spread the disease. For example, kissing or being close to someone who is coughing can spread the disease, according to the CDC.

Symptoms of meningitis include fever, headache, stiff neck, nausea, vomiting, light sensitivity and confusion. Symptoms of bloodstream infections with N. meningitidis include fever, chills, fatigue, vomiting, cold hands and feet, severe muscle aches, rapid breathing, diarrhea and, in late stages of the disease, a dark purple rash, according to the CDC.

The disease can be treated with antibiotics, and treatment should begin as soon as possible. The condition is extremely serious — even with antibiotics, 10 to 15 people out of every 100 people with meningococcal disease die from it, according to the CDC. 

In the general population, people at risk for meningococcal disease include babies, teens and young adults, and people with certain medical conditions, including HIV, which weakens the immune system. 

In the current outbreak among men who have sex with men in Florida, "unfortunately, it seems that was the population that was struck first, and this virus spreads through close prolonged contact," Jill Roberts, an assistant professor at the University of South Florida who specializes in molecular epidemiology, told local news outlet WTSP. "There is nothing special about Neisseria that it particularly wants to spread in that population." 

Originally published on Live Science.

A woman became the third person ever to be cured of HIV, the virus that causes AIDS, after she received a stem-cell transplant that used cells from umbilical cord blood, scientists reported Tuesday (Feb. 15).

The two other people cured of HIV, Timothy Brown and Adam Castillejo, both received bone marrow transplants from donors who carried a genetic mutation that blocks HIV infection, Live Science previously reported. These transplants contained adult hematopoietic stem cells, which are stem cells that develop into all types of blood cells, including white blood cells, a key component of the immune system.

This genetic mutation is rare and has been identified in only about 20,000 bone marrow donors to date, The New York Times reported. The bone marrow transplant procedure itself takes a heavy toll on the body, both during the highly invasive procedure and for some time afterward. In both Brown and Castillejo, immune cells from the donors' bone marrow launched an attack against cells in the patients' bodies; this condition is known as "graft versus host disease." Following this initial reaction, though, both men were cured of HIV. 

However, the woman recently cured of HIV had a very different experience from the two men cured before her. 

Related: The deadliest viruses in history 

She left the hospital just 17 days after her procedure, without any signs of graft versus host disease, Dr. JingMei Hsu, the patient’s physician at Weill Cornell Medicine in New York, told the Times. Her case dispels an existing theory that triggering graft versus host disease might be a necessary step in curing someone of HIV, Dr. Sharon Lewin, president-elect of the International AIDS Society, who was not involved in the work, told the Times. 

In addition to being HIV-positive, the woman had acute myeloid leukemia, a cancer that affects blood-forming cells in the bone marrow, Reuters reported. She had received the umbilical cord blood as both a treatment for the cancer and for her HIV, as her doctors identified a donor with the HIV-blocking genetic mutation. Cord blood contains a high quantity of hematopoietic stem cells; the blood is collected at the time of a baby's birth and then donated by the parents, according to the Memorial Sloan Kettering (MSK) Cancer Center. 

Cord blood offers an advantage over bone marrow because donors don't need to be closely "matched" to their transplant recipient, according to MSK. For bone marrow transplants, doctors check the donor's and recipient's human leukocyte antigen (HLA) tissue type, which refers to whether the individuals carry specific proteins, called HLAs, in the tissues of their bodies. HLAs come in different flavors, and these flavors must be closely matched between a bone marrow donor and a recipient to avoid a catastrophic immune reaction. 

But because a baby's immune system is still quite immature at the time of birth, the HLAs of the baby and cord blood recipient don't have to match as closely as the HLAs of a bone marrow donor and recipient, MSK notes. The baby's immature cells adapt to the recipient's body more easily than adult cells. In the woman's case, her donor was "partially matched," and she also received stem cells from a close relative to help bolster her immune system after the transplant procedure, the Times reported.

"The transplant from the relative is like a bridge that got her through to the point of the cord blood being able to take over," Dr. Marshall Glesby, an infectious-diseases expert at Weill Cornell Medicine and part of the research team, told the Times.

The woman's procedure took place in August 2017, according to The Guardian. She elected to stop taking antiretroviral drugs, the standard treatment for HIV, 37 months after her transplant, the Times reported. More than 14 months have passed since then, and still, no trace of the virus or antibodies against the virus can be found in her blood, the Times reported.

The woman's case is part of a larger U.S.-based study that will follow a total of 25 people with HIV, Reuters reported. These individuals will undergo an umbilical cord stem-cell transplant for the treatment of cancer, and the trial organizers will then monitor them to see whether their HIV status changes following the procedure. In general, umbilical cord blood is more widely available and more easily matched to recipients than bone marrow. So some scientists think the procedure may be more accessible than bone marrow transplants to HIV patients.

"We estimate that there are approximately 50 patients per year in the U.S. who could benefit from this procedure," Dr. Koen van Besien, director of the stem cell transplant program at Weill Cornell Medicine and one of the doctors involved in the treatment, told The Guardian. Worldwide, nearly 38 million people are living with HIV, according to the Times.

"The ability to use partially matched umbilical cord blood grafts greatly increases the likelihood of finding suitable donors for such patients," van Besien said.

Originally published on Live Science. 

A newfound variant of HIV, the virus that causes AIDS, has been uncovered in the Netherlands and appears to cause faster disease progression compared with other versions of the virus.

The human immunodeficiency virus (HIV) infects and destroys immune cells called CD4 cells in the body, causing the number of these cells to plummet. If left untreated, the infection then progresses to AIDS. In people infected with the newfound HIV variant, called the VB variant, the CD4 counts fall at about twice the rate as those of people infected with closely related HIV strains, meaning those of the same genetic subtype (B).   

Without treatment, infections with the VB variant would likely progress to AIDS, on average, within two to three years of a person's initial HIV diagnosis, researchers reported Thursday (Feb. 3) in the journal Science. With other versions of the virus, a similar degree of decline occurs about six to seven years after diagnosis, on average.

Related: Do other viruses have as many variants as SARS-CoV-2? 

"We found that on average, individuals with this variant would be expected to progress from diagnosis to 'advanced HIV' in nine months, if they do not start treatment and if diagnosed in their thirties," first author Chris Wymant, a senior researcher in statistical genetics and pathogen dynamics at the University of Oxford, told Live Science in an email. The disease's progression would be even faster in an older person, he said. 

Thankfully, in their study, the team found that antiretroviral drugs, the standard treatment for HIV, work just as well against the VB variant as they do against other versions of the virus. "For an individual on successful treatment, the deterioration of the immune system towards AIDS is stopped, and transmission of their virus to other individuals is stopped," Wymant said.

"The authors use the case study to underpin the importance of universal access to treatment," said Katie Atkins, chancellor's fellow at Edinburgh Medical School and an associate professor at the London School of Hygiene and Tropical Medicine who was not involved in the study. "Both because we want to directly reduce the number of people dying unnecessarily of AIDS, but also as a means to reduce the amount of circulating virus and therefore reduce the chance of new, more deadly variants emerging," she told Live Science in an email.

How the variant was spotted 

Wymant and infectious-disease epidemiologist Christophe Fraser, the study's senior author, are both key members of the BEEHIVE project, an effort to better understand HIV biology, evolution and epidemiology. "The BEEHIVE project, begun in 2014, was created to understand how changes in the virus, encoded in its genetics, cause differences in disease," Wymant said. "The project brings together data from seven national HIV cohorts in Europe plus one in Uganda."

While analyzing data from the ongoing study, the team identified 17 individuals infected with a "distinct" HIV variant, all of whom carried strikingly high concentrations of the virus in their blood early in infection — between six months and two years post-diagnosis. Fifteen of the infected individuals were from the Netherlands, one was from Switzerland and one was from Belgium.

The newfound variant belongs to the genetic subtype B, a group of related HIV viruses most commonly found in Europe and the U.S., the team found. To see if they could find more examples of the variant in the Netherlands, the researchers screened data from the ATHENA national observational HIV cohort, a large group of HIV-positive individuals in the Netherlands who were diagnosed between 1981 and 2015. 

Viral genetic sequence data was available for more than 8,000 of these individuals, and of these, about 6,700 were infected with subtype B viruses. Within this group, the researchers identified 92 individuals with the distinctive VB variant, which brought their total to 109.

Based on the available clinical data, these 109 individuals carried 3.5-fold to 5.5-fold higher viral loads than people infected with other subtype B strains. And at their time of diagnosis, the individuals infected with the VB variant already had lower CD4 counts than those infected with other strains. So compared with other people newly diagnosed with HIV, their CD4 counts both started lower and fell faster. 

Related: 11 surprising facts about the immune system

To explain how this sharp uptick in virulence arose, the researchers went back to the VB variant genome, searching for clues. They found that the variant carries many mutations, scattered throughout its genome, so for now, they couldn't pinpoint a single, isolated genetic cause for the virus's increased virulence, they reported.

"It is unlikely that one mutation, or even one gene, is responsible for this change," said Joel Wertheim, an associate professor of medicine at the University of California, San Diego, who was not involved in the study. "Working out this mechanism is of great interest," he told Live Science in an email.

The team was able to construct a diagram called a phylogenetic tree based on the available genetic data, "very similar to normal family trees for humans" that show how closely different individuals are related to each other, Wymant said. Based on this tree, they estimated that the VB variant likely first appeared during the late 1980s or 1990s in the Netherlands. Around that time, the first antiretroviral treatment for HIV had just been approved by the U.S. Food and Drug Administration, and treatments using combinations of antiretrovirals were not yet available, according to a 2019 review in the journal Health Affairs.  

"During this decade, there would have been a high prevalence of untreated HIV infected individuals who were not virally suppressed in Western Europe," Atkins said. "This high number of people who were not virally suppressed would have provided a large virus population in which a new variant could have emerged."

The tree suggested that individuals who caught the VB variant carried "viruses that were unusually closely related to each other," Wymant said. This finding suggests that little viral evolution occurred between the time that someone acquired the virus and the point when they passed it on to someone else. 

In other words, on top of being highly virulent, the VB variant may also be more transmissible than other versions of HIV. However, this finding is less conclusive than the evidence of increased virulence, since the tree provides only indirect evidence of the virus's transmissibility, Wymant said.   

After the VB variant emerged in the 1980s or 1990s, the number of people infected with the variant steadily increased until about 2010. At the same time, the proportion of new VB cases among all new subtype B cases began to increase. This increase peaked around 2008 and then steadily declined, the team found. 

"This is most likely a by-product of the strong efforts in the Netherlands to decrease transmission of any HIV, regardless what variant it is," Wymant said. Absolute numbers of both VB and non-VB diagnoses were declining at this time, and there is some uncertainty in the data as to the exact ratio of VB to non-VB infections, the authors noted.

The discovery of a highly virulent HIV variant isn't necessarily surprising, Wertheim said. "This finding is in line with both evolutionary theory and the trends towards increased virulence we've seen in the United States over the decades," he told Live Science. "I am most surprised by how stark and distinct this newly described cluster is." 

Looking forward, Wertheim said he expects many groups around the world to begin screening their data to see if the VB variant has spread beyond the Netherlands. "Also, I am curious as to whether similar variants have emerged elsewhere in the world," Wertheim said.

Other than the cases detected in people from Switzerland and Belgium, the team found no initial evidence of the variant beyond the Netherlands.  They searched publicly available viral genetic sequences and found no trace elsewhere, but there may be at least a few others infected with the variant that have yet to be identified, Wymant said. "By making the genetic sequence of the VB variant openly available, we are allowing other investigators in different countries to check their own private data," he said.

Future studies of the VB variant could reveal how it builds up in the blood and decimates CD4 cells so quickly, and also provide more details as to how the variant first evolved. The team found evidence that the variant steadily picked up its mutations, one by one, over time, but they couldn't tell if this evolution occurred in multiple individuals or just one, Wymant said.

In the meantime, should the general public be concerned about the newfound VB variant? 

"The public needn't be worried," Wymant said. "Finding this variant emphasises the importance of guidance that was already in place: that individuals at risk of acquiring HIV have access to regular testing to allow early diagnosis, followed by immediate treatment … These principles apply equally to the VB variant." 

Originally published on Live Science.

For a second year, the COVID-19 pandemic has dominated health news headlines, and for good reason. But amid all the talk of viral variants and vaccine boosters, you may have missed some of this year's most amazing medical cases and breakthroughs. In 2021, scientists made great strides in the world of organ transplants, cancer treatment trials and gut microbiome research, and doctors shared some amazing treatment success stories.  

Here are 10 cool medical stories you may have missed this year. 

Baby born at 21 weeks survives, against all odds 

Curtis Means and his twin, C'Asya, were born only 21 weeks and 1 day into their gestation, meaning they were about 19 weeks premature. C'Asya did not respond to treatment and died shortly after birth, but Curtis' vitals steadily began to improve. Even so, doctors estimated that he had only a 1% chance of survival. Over the following months, he received constant care to maintain his breathing and body temperature, and to take in adequate nutrition. He was able to come off his ventilator at 3 months old, and he was discharged from the hospital at 9 months. After six months at home, Curtis and his family received a Guinness World Record certificate acknowledging Curtis as the most premature baby in the world to survive. 

Read more: Baby born at 21 weeks survives, breaks world record 

Working pig kidney is successfully hooked up to a human

With human organs in short supply for transplant surgeries, scientists have long been working to make animal-to-human transplants safe, feasible and widely available. This year, in a watershed experiment, doctors connected a pig kidney to a human and watched as it effectively filtered waste from the body and produced urine. The experiment was conducted in a brain-dead patient who was a registered organ donor and whose family granted permission for the procedure. The team used a kidney from a genetically modified pig that lacked the gene for alpha-gal, a type of sugar that can trigger an intense immune reaction in humans. The successful experiment could signal a big step forward for animal-to-human transplants, but many questions remain. 

Read more: Pig kidney successfully hooked up to human patient in watershed experiment

Poop transplants boosted skin cancer patients' treatment 

Immunotherapies theoretically rally the immune system against cancer cells, but they don't work for all cancer patients. Only about 40% of patients with advanced melanoma, for instance, reap long-term benefits from immunotherapy drugs. But a small study published in February in the journal Science hints that tweaking cancer patients' gut bacteria can help boost the drugs' effectiveness. 

In the study, scientists collected stool from melanoma patients who responded well to immunotherapy and then transplanted the patients' feces — which was chock-full of microbes — into the guts of 15 patients who had never responded to the drugs. After the transplant, six of the 15 patients responded to immunotherapy for the first time, showing either tumor reduction or disease stabilization that lasted more than a year. Looking forward, the scientists plan to investigate exactly why the poop transplant helped these six patients and why the other nine patients didn't seem to benefit.

Read more: Cancer patients weren't responding to therapy. Then they got a poop transplant.

Discovery reveals potential weapon against bacterial superbugs 

A study conducted in lab dishes and mice hints at a new way to take down drug-resistant bacteria. This new weapon could make existing antibiotics more effective, thus reducing the need to formulate brand-new antibiotic medications. In the study, published in June in the journal Science, scientists ran experiments with Staphylococcus aureus and Pseudomonas aeruginosa, two bacteria that show pervasive resistance to multiple drugs and rank among the leading causes of hospital-acquired infections. These so-called superbugs use a specific enzyme to shield themselves from harm by antibiotics, so the team searched for molecules that could block the enzyme and leave the bugs defenseless. The molecules the scientists identified made antibiotics two- to 15-fold more potent against the microbes, depending on the antibiotic being used and the bacterial strain being targeted. Now, they'll have to see if the same strategy can work in humans.

Read more: New discovery could help take down drug-resistant bacteria

A second person is "naturally" cured of HIV 

A woman now known as the Esperanza Patient was diagnosed with HIV, the virus that can cause AIDS, in 2013. But as of this year, doctors can find no trace of the virus in her body. The woman received neither a bone marrow transplant nor any drug intervention; her immune system has apparently eliminated HIV from her system on its own. This had happened once before, in a California woman named Loreen Willenberg. And although the two women are anomalies, their cases give scientists hope of finding a cure for HIV/AIDS. 

Read more: Patient's immune system 'naturally' cures HIV in the second case of its kind 

Cancer vaccine shows promise in small trial

An experimental "cancer vaccine" works by training immune cells to better recognize and attack cancer cells in the body, without harming healthy cells. In a small trial of eight patients with advanced melanoma, the vaccine helped prevent the patients' tumors from growing for years after vaccination. By the end of the four-year follow-up period, all eight patients were alive and six out of eight showed no signs of active disease. Two had experienced cancer recurrence and received additional treatments called "checkpoint blockades," which essentially rip the brakes off of immune cells known as T cells. In combination with the T cell-targeting cancer vaccine, these checkpoint blockades were highly effective. This hints that such vaccines could serve as a very important therapy, to be used in tandem with other cancer treatments, but more and larger trials are still needed to know for sure.

Read more: Cancer vaccine helped keep melanoma under control for years in small study

Dietary supplement restores gut bugs, helps malnourished kids grow 

A new dietary supplement helped malnourished children put on weight and gain height at a faster rate than children who were given a standard "ready-to-use supplementary food." What made the difference? The new supplement helped to restore the kids' gut bacteria so they more closely resembled the gut bacteria of healthy children. 

Malnourishment leaves kids' gut microbes "stunted," as the microbes don't have adequate fuel to grow and multiply. Through exhaustive animal studies and a small pilot trial with human children, a team of scientists came up with a formula to both deliver kids the calories they need and help restore their gut bacteria. In a larger trial, published in April in The New England Journal of Medicine, they found that the supplement not only helped kids grow faster but also increased the concentrations of key proteins in their blood, including those involved in bone growth and nerve and brain development.

Read more: Tweaking the gut bacteria of malnourished kids could help them grow 

Experimental HIV vaccine successfully stimulates rare immune cells 

The first in-human trials of a new HIV vaccine stirred up excitement about the experimental shot, as it showed 97% success at stimulating a rare set of immune cells that play a key role in fighting the virus. 

The human immunodeficiency virus poses a huge challenge for vaccine developers because it mutates so quickly, but in this case, the researchers targeted the pathogen using a unique approach: They designed their vaccine to target a specific subset of B cells, a kind of immune cell that produces "broadly neutralizing antibodies," proteins that can latch onto a key protein on HIV and stop the virus from infecting cells. In a trial of 48 people, the vaccine was safe and induced neutralizing antibody production in 97% of the participants. Although this hints that the vaccine may work well, the trial didn't directly test whether the vaccine prevented HIV infection; that will be the next step in development.

Read more: HIV vaccine stimulates 'rare immune cells' in early human trials 

Centenarians' gut bacteria may hint at how they survive to 100 

People who live to age 100 and beyond may partially have their gut bacteria to thank, according to a study published in July in the journal Nature. In the study, researchers examined the communities of gut microbes, or microbiota, living in 160 centenarians, who were, on average, 107 years old. The researchers compared the centenarians' gut microbiota to those of 112 people ages 85 to 89, and 47 people ages 21 to 55. The centenarians showed a distinct gut microbe "signature," meaning specific microbes appeared in higher or lower abundance than in the younger groups. In addition, they had significantly higher levels of so-called secondary bile acids, a fluid produced by the liver and released into the intestine. In particular, they produced high concentrations of the secondary bile acid isoalloLCA, which the researchers found to have potent antimicrobial properties that may inhibit the growth of harmful bacteria in the gut. 

More research is needed to know if and how the centenarians' gut bugs help them survive to such advanced ages and whether this knowledge could be used to boost other people's longevity.

Read more: People who live to 100 have unique gut bacteria signatures

HPV vaccine cuts cervical cancer rates more than 85% in UK women 

A recent study found that the human papillomavirus (HPV) vaccine has reduced the number of cervical cancer cases by 87% among women in the U.K. Using cancer registry data gathered between 2006 and 2019, researchers compared the cervical cancer rates among women who were vaccinated with the HPV vaccine Cervarix when they were young, between the ages of 12 and 13, with the cervical cancer rates of women who received the vaccine slightly later and with the rates of those who did not receive the vaccine at all.

The researchers found that the vaccine was most effective when given to the youngest cohort; women who had been vaccinated with Cervarix between the ages of 12 and 13 had 87% fewer cases of cervical cancer compared with those who weren't vaccinated. There was a 62% reduction in cases among women who had been vaccinated between the ages of 14 and 16, and a 34% reduction in cases in women vaccinated between 16 and 18, compared to the unvaccinated population.

Read more: HPV vaccine slashes cervical cancer rates by 87% among women in the UK 

Originally published on Live Science. 

The world's first injectable medication to reduce the risk of acquiring HIV has been approved by the Food and Drug Administration (FDA), the agency announced Monday (Dec. 20).

The injectable drug — called Apretude or its generic name, "cabotegravir extended-release injectable suspension" — provides an alternative to daily pills for HIV prevention, such as Truvada and Descovy. These pills are up to 99% effective at preventing the sexual transmission of HIV, but must be taken every day to be that effective, according to the Centers for Disease Control and Prevention (CDC). 

By contrast, to start Apretude, people initially receive two shots, spaced one month apart, and then they receive an injection every two months thereafter, according to the FDA statement.

Related: 12 amazing images in medicine 

"This injection, given every two months, will be critical to addressing the HIV epidemic in the U.S., including helping high-risk individuals and certain groups where adherence to daily medication has been a major challenge or not a realistic option," Dr. Debra Birnkrant, director of the Division of Antivirals in the FDA’s Center for Drug Evaluation and Research, said in the statement. 

The FDA hopes that the availability of a long-acting injectable drug for HIV prevention will increase the uptake of such medications in high-risk groups, the statement reads. Pre-exposure prophylaxis (PrEP), meaning medications taken to prevent HIV, are recommended for about 1.2 million people in the U.S., and in 2020, about 25% of those individuals received a prescription for PrEP pills. That's up from only 3% in 2015, but "there remains significant room for improvement," the statement says.

Two clinical trials suggest that Apretude reduces the risk of HIV infection more effectively than the daily pill Truvada. The trials met the gold standard for these types of studies, because they were randomized and double-blind, meaning those who received the actual medication were randomly chosen and neither the doctors nor the patients knew who was receiving the real medication over the placebo. 

The first trial included nearly 4,600 cisgender men and transgender women who have sex with men, Live Science previously reported. Those who took Apretude had 69% lower risk of getting infected with HIV than the participants who took Truvada. The second trial, which included about 3,200 cisgender women at risk of acquiring HIV, found that those who took Apretude had 90% lower risk of getting infected with HIV, compared with participants who took Truvada, according to the FDA statement. 

The trial participants who took Apretude did experience more side effects than those who took Truvada, including headaches, fever, fatigue, back pain, myalgia, rash and reactions at the injection site, according to the statement. 

As of Dec. 20, Apretude has been approved for use in at-risk adults and adolescents weighing at least 77 pounds (35 kilograms), according to the FDA statement. Patients have the option to take an oral formulation of cabotegravir, called Vocabria, daily for four weeks prior to starting the injections, to see how well they tolerate the drug. Patients should be tested for HIV and confirmed negative before starting Apretude and should be confirmed negative before each injection, to avoid the risk of developing drug-resistant HIV.

"Drug-resistant HIV-1 variants have been identified with use of Apretude for HIV-1 PrEP by individuals with undiagnosed HIV-1 infection," according to a statement from the drug's manufacturer, ViiV Healthcare. "Individuals who become infected with HIV-1 while receiving Apretude for PrEP must transition to a complete HIV-1 treatment regimen." 

Earlier this month, the CDC updated its guidance regarding how doctors should inform patients about PrEP, The Hill reported. The agency now recommends that health care providers inform all sexually active adults and adolescents about PrEP and offer the medications to all who ask for them, regardless of whether they report specific behaviors that would put them at high risk of HIV exposure. Apretude now joins the list of possible options that can be presented to these patients.

Apretude has a list price of $3,700 per dose (or $22,200 per year, for six doses) and is expected to ship to wholesalers and specialty distributors in the U.S. early next year, NBC News reported. In July, the federal government mandated that most U.S. insurance companies must cover Truvada and Descovy, as well as the lab tests and clinic visits needed to maintain the prescriptions, with no cost sharing; but as of yet, insurers are not required to cover all the costs of taking Apretude.

Originally published on Live Science.

In 2013, doctors delivered a life-altering diagnosis to a woman in Esperanza, Argentina: She had acquired HIV, the virus that causes AIDS. Eight years later, the virus has all but disappeared from her system. 

In fact, stunned researchers were unable to find evidence of any HIV viral particles in her body, "despite analysis of massive numbers of cells from blood and tissues, suggesting that this patient may have naturally achieved a sterilizing cure," they wrote on Nov. 16 in the journal Annals of Internal Medicine. However, they cautioned that science cannot definitively prove that no trace of the human immunodeficiency virus remains.

Related: The 12 deadliest viruses in history

This represents the second known case of a person's immune system eliminating HIV without a bone marrow transplant or drug intervention, according to STAT. The first such case was a California woman named Loreen Willenberg, who in 2020 found out that the virus was absent from her body for the first time in 27 years, The New York Times reported. Just two other people — pseudonymously known as the London Patient and the Berlin Patient — have ever been cured of HIV, but only after having their immune cells completely replaced via stem cell therapy, according to research published in 2020 in The Lancet. 

The Argentine woman was dubbed the "Esperanza Patient" by her doctors in order to protect her anonymity in a country where people are still stigmatized for HIV-positive status. Medical professionals say that she belongs to a rare group of HIV patients called "elite controllers." Although the virus is present in these folks' systems, they are able to maintain a low enough viral load that they don't develop symptoms, even without treatment. 

Elite controllers represent just 1% of the global HIV-positive population, according to research published in 2019 in the Journal of Virus Eradication. Scientists aren't exactly sure how their immune systems eliminate the virus — at least, not yet.

"I'm very keen to learn more about this seemingly new phenomenon of extraordinary elite control," Rowena Johnston, director of research at amfAR, The Foundation for AIDS Research, told NBC News. 

For now, Willenberg and the Esperanza Patient are special cases, even among elite controllers. But their very existence offers a glimmer of hope in the ongoing search for an HIV/AIDS cure, doctors say. 

"This makes us hopeful that a natural cure of HIV is actually possible," Xu You, a viral immunologist at the Ragon Institute in Boston and one of the lead investigators of the study, told Medscape. "That's the beauty of the name, right?" In addition to being the name of the patient's hometown, "Esperanza" means "hope" in Spanish.

Meanwhile, the patient is expecting her second child and she is reportedly enjoying her HIV-free life. But she wants to make sure others living with HIV have a second chance as well. "Just thinking that my condition might help achieve a cure for this virus makes me feel a great responsibility and commitment to make this a reality," she told STAT in an email. 

Originally published on Live Science.

Charles Kuen Kao: Bringing broadband to the masses 

1933-2018

Known as the father of fiber-optic communication, Charles Kuen Kao revolutionized the way we communicate. 

In the mid-1960s, Kao proposed a way to deliver information, in the form of light, through fiber-optic cables. The cables consisted of long, glass pipes along which light beams would be fired. To prevent light from leaking out the sides, Kao used purified glass in which the walls of the pipe acted as a mirror for the photons, or light particles, forcing them to bounce within the pipe and continue traveling down the pipe — a phenomenon called total internal reflection, according to the journal Mayo Clinic Proceedings. 

Thanks to this innovation, light information can be transmitted across large distances, which is perfect for telecommunications. In 2009, Kao won the Nobel Prize in Physics for the groundbreaking achievement.

Patricia Bath: Zapping cataracts with lasers

1942-2019

As we grow older, our ability to see can become compromised. One common age-related ailment is the development of cataracts. At the front of each eye, a glass-like lens focuses images of the outside world onto light-sensing cells at the back of the eye. As we age, the proteins that make up that lens can slowly break down and turn a once-crystal-clear lens cloudy, according to the U.K.'s National Eye Institute (NEI). In extreme cases, images can be shrouded in darkness. 

As Live Science previously reported, more than 90% of Americans have at least one cataract by the age of 65. Half of people between the ages of 75 and 85 have lost some vision because of the condition, according to the University of Michigan Kellogg Eye Center.

Various treatments for cataracts have been around since the fifth century B.C., according to a 2016 article in the journal Missouri Medicine. One of these treatments, called "couching," used a needle to dislodge the cataract away from the visual axis of the eye, enabling the patient to regain their sight, albeit only temporarily. 

However, over the centuries, the methods of removing, replacing and obliterating the cloudy buildup have evolved, and a major medical breakthrough occurred in 1986, when Patricia Bath invented the Laserphaco Probe, according to MIT. 

Before Bath's pioneering technique was introduced, ophthalmologists would insert a needle into the eye to reach the lens and then use an ultrasound probe to break apart the cloudy cataract. Bath's method replaced ultrasound with lasers, giving doctors the ability to conduct the surgery with greater accuracy and better results.

Two years after inventing the Laserphaco Probe, Bath received a patent for her creation, becoming the first African American female doctor to receive a medical patent, according to The Washington Post. 

Flossie Wong-Staal: Cracking HIV's genetic code 

1946-2020

Flossie Wong-Staal, a virologist who left Hong Kong for the U.S. in 1964, played a pivotal role in AIDS research. Wong-Staal was working at the National Cancer Institute (NCI) in Bethesda, Maryland, when the AIDS epidemic exploded in the U.S. She was part of the team that first identified the human immunodeficiency virus (HIV) as the cause of AIDS, according to an obituary in The Lancet. Additionally, Wong-Staal and her colleague Robert Gallo cloned HIV and figured out how it hides from the immune system, according to The Lancet. While at NCI, Wong-Staal also devised a blood test to detect HIV.

Christine Darden: Revealing the secret of sonic booms 

1942-present

In 1955, at the dawn of the space race between the U.S. and the Soviet Union, NASA employed a team of "human computers" to calculate flight trajectories, propulsion and rocket dynamics. One of these human computers was Christine Darden, who joined NASA's ranks in 1967. Eight years later, Darden started a position at Langley Research Center as one of a handful of female engineers, according to NASA. 

Darden's first assignment was to design computer programs to calculate the effects of sonic booms, the incredibly loud noises produced when planes travel faster than the speed of sound. This phenomenon occurs because a hypersonic plane shoves air molecules together, creating a cone of pressurized air that then radiates back and down to the ground in waves, according to NASA. 

While working on the project full time, Darden earned a doctorate in 1983 from The George Washington University in Washington, D.C. For her dissertation, she used her work at NASA to explore the environmental impacts of supersonic transport. An object, such as a plane, that travels faster than the speed of sound creates a shock wave of pressurized air, which can be heard as a sonic boom. The thunderous noise of a sonic boom is caused by the sudden change in air pressure around the plane, according to NASA. 

Teams of NASA scientists replicated the booms using wind tunnels and model planes, while Darden used computer models to calculate the effects of the booms. Darden's simulation results matched the wind tunnel outcomes, although Darden's method proved cheaper and more efficient than building a scale model, according to "Distinguished African American Scientists of the 20th Century" (Oryx Press, 1996). 

Charles Drew: Invention of the blood bank

1904-1950

Charles Drew is often referred to as the father of modern-day blood banks. Drew was born in 1904 and graduated from the McGill University Faculty of Medicine in Montreal in 1933. In 1935, he became chief surgical resident at Freedmen's Hospital (now Howard University Hospital) in Washington, D.C., before studying at Columbia University, where he won a fellowship to train at the Presbyterian Hospital in New York City. 

Afterward, Drew was assigned to work under John Scudder, who had been granted funds to work on the first-ever blood bank. Having studied blood chemistry, fluid replacement, transfusion and storage, Drew became a leading expert on all things to do with blood. 

As the casualties mounted in Europe during World War II, so did the need for blood transfusions. In 1940, the U.S. formed the Blood for Britain project, with the aim of shipping blood overseas, according to the U.S. National Library of Medicine. Drew was appointed head of the project, and he and Scudder devised a way to separate plasma from blood. 

Untreated blood needs to be refrigerated to remain viable, but the electrolyte-carrying plasma within the blood does not. If plasma were extracted from the blood and mixed in a saline solution, it could be shipped abroad to Allied troops without refrigeration and remain viable for transfusions. Plasma could also be used regardless of the blood type of the patient receiving it. 

By the time the project concluded in 1941, itt had collected 14,556 blood donations and shipped more than 1,300 gallons (5,000 liters) of plasma to the U.K., according to the U.S National Library of Medicine.

The techniques pioneered by Drew were adopted elsewhere, such as by the American Red Cross, and helped to shape modern blood bank drives. 

Drew's method of separation

George Carruthers: World's first lunar telescope 

1939-2020

In 1972, scientist George Carruthers opened humanity's eyes to the universe through the lens of his Lunar Surface Ultraviolet Camera (also called the Far Ultraviolet Camera/Spectrograph), according to the Smithsonian National Air and Space Museum. The camera was designed to observe Earth's atmosphere from a perch on the moon and to detect the radiation from stars and nebulas. The camera was shipped aboard Apollo 16 and placed on the lunar surface. While there, it took more than 550 ultraviolet images of stars, nebulas and galaxies across the cosmos. Carruthers' creation also collected data on Earth's atmosphere, including the concentration of pollutants, helping to expand our knowledge of our planet.

Alice Ball: Treating leprosy

1892-1916

Long before Alice Ball was born, leprosy caused nerve damage and skin lesions in millions of people around the world. In 1873, Norwegian physician Dr. Gerhard Henrik Armauer Hansen discovered that a bacterium called Mycobacterium leprae was the culprit, according to the Journal of Skin and Sexually Transmitted Diseases.

The first modestly successful treatment for the condition used oil from a chaulmoogra nut, which was applied topically, ingested or even injected. Although patients who underwent this treatment sometimes improved, it caused abscesses and nausea, according to the journal Pharmacy History. 

In 1915, Ball developed a new method to extract the beneficial compounds from the chaulmoogra nut. At the time, Ball was working toward a master's degree in chemistry, focused on the chemical makeup of the herb kava (Piper methysticum), Live Science previously reported. This work brought her to the attention of Dr. Harry Hollmann, an assistant surgeon at Kalihi Hospital, which was then a treatment center for leprosy patients. While working with Hollmann, Ball developed a new way to isolate the active ingredient in chaulmoogra nut oil. Ball then engineered a water-soluble injection of this extract as an alternative treatment.  

By 1918, 78 people who received treatment using Ball's method, were free of lesions and discharged from hospital care, according to New Scientist. This injection became the standard leprosy treatment for decades. 

Ball died in 1916, at only 24 years old, before her work could be published. Credit for her revolutionary method was attributed to her colleague and college president Arthur L. Dean, who neglected to mention Ball's involvement in the "Dean Method." Finally, in 1922, Ball received recognition posthumously for her exemplary work when Hollmann dubbed the scientific advancement the Ball Method, according to JSTOR Daily.

A new vaccine for HIV is raising excitement after its first in-human trials showed 97% success at stimulating a rare set of immune cells that play a key role in fighting the virus. 

The vaccine approach is a new attempt to head off the fast-mutating human immunodeficiency virus, which has eluded vaccines in the past because it attacks part of the immune system directly and is good at evading other immune defenses. Developed by scientists at Scripps Research in San Diego and the nonprofit International AIDS Vaccine Initiative (IAVI), the vaccine is in Phase I clinical trials and has been tested in only 48 people so far. 

However, the results of the trial generated excitement, especially because Scripps and IAVI will now partner with Moderna to make an mRNA version of the vaccine — a step that could lead to faster vaccine availability, according to Scripps Research. 

Related: The 12 deadliest viruses on Earth

"With our many collaborators on the study team, we showed that vaccines can be designed to stimulate rare immune cells with specific properties, and this targeted stimulation can be very efficient in humans," William Schief, an immunologist at Scripps whose laboratory led the vaccine development, said in a statement. "We believe this approach will be key in making an HIV vaccine and possibly important for making vaccines against other pathogens."

A challenging vaccine

HIV vaccine research started in the 1980s, not long after the discovery of the virus that causes AIDS. However, progress has been slow, with only one two-vaccine combination — tested in the Thai RV144 trial — shown to have an effect. The results of that trial, released in 2009, showed a 31% reduction in infection due to the vaccine combination. That is too low to submit for regulatory approval, but the vaccine developers continue to study what does and does not work about the combination. Follow-up research suggested that this limited protection faded after about a year. 

The virus is a difficult target for vaccination because it's expert at evading the body's antibody response. Antibodies are proteins that are primed to recognize a foreign invader, or antigen, and bind to that invader right away, neutralizing it or tagging it for destruction by other immune cells. Vaccines work by presenting a dead or harmless antigen to the immune system, allowing antibodies to develop without the threat of disease. But because HIV mutates quickly to avoid antibodies, a highly effective vaccine has yet to be developed.

The new approach focuses on a rare set of antibodies known as broadly neutralizing antibodies. These antibodies can bind to the spike proteins on HIV, a part of the virus that doesn't vary much among different strains. The spike protein is the key the virus uses to enter cells, so it can't mutate much without locking the virus out. 

The problem is that broadly neutralizing antibodies are secreted by only a handful — about 1 in every 1 million — of the immune system's B cells, Schief said. B cells are the cells that produce antibodies.

"To get the right antibody response, we first need to prime the right B cells," he said. 

New technologies for new vaccines

The new approach targets this specific set of B cells with a vaccine compound called eOD-GT8 60mer. In the early safety trial, 48 healthy adult volunteers were given either the vaccine candidate or a placebo shot. The trials didn't directly test whether the vaccine prevented HIV infection but instead looked at whether the vaccine was safe and whether the participants who received the shot produced more broadly neutralizing antibodies than the comparison group who received a placebo. 

The results, presented Feb. 3 at the International AIDS Society HIV Research for Prevention virtual conference, showed that the desired antibodies were found in 97% of the participants who received the vaccine.

There is a long road ahead for a potential new HIV vaccine, including follow-up trials to test the effectiveness and safety in large groups of people. The researchers hope that partnering with Moderna to use mRNA technology will help them piggyback on the safety and efficacy success seen in the company's COVID-19 vaccines, thereby speeding the process. 

Originally published on Live Science.

An Australian COVID-19 vaccine that had shown promising results in early trials is being abandoned after researchers found that the shot caused false-positive results on HIV tests.

On Friday (Dec. 11), Australian officials said they had canceled an order for some 51 million doses of the vaccine, which was being developed by The University of Queensland and CSL Ltd., a local biotech company, according to The New York Times.

In an early trial with 216 participants, the vaccine appeared to be safe and to produce a robust immune response against COVID-19, according to a statement from CSL. But some volunteers falsely tested positive for HIV, which officials feared would undermine trust in the vaccine, the Times reported. 

"[The vaccine] was likely to work. But we knew that we didn't want to have any issues with confidence, and this false-positive test may have caused some confusion and lack of confidence," Brendan Murphy, secretary of Australia's Department of Health, told the BBC.

The vaccine contained small fragments of an HIV protein, which helped stabilize the vaccine. Some of the participants developed antibodies against these fragments, and these antibodies triggered false positive results on some HIV tests.

It's important to note that there is no way for the vaccine to cause an HIV infection, because it contains harmless fragments of the virus.

Trial participants had been informed that they might generate some antibodies to this portion of the vaccine, "but it was unexpected that the levels [of antibodies] induced would interfere with certain HIV tests," the CSL statement said.

The Australian government plans to increase orders of other COVID-19 vaccines, including vaccines made by AstraZeneca and Novavax, the Times reported.

Originally published on Live Science.  

Scientists have finally recreated the initial steps of HIV infection in a test tube, offering an incredibly zoomed-in view of the virus in action.

The amazing images show a cone-shaped shell of geometric tiles, called the capsid, that sits at the virus's center and contains its genetic material, known as RNA. Before infiltrating a cell, the capsid is surrounded by an envelope of fatty molecules; this envelope fuses to the host cell to let the capsid inside, where it then carries the RNA to the cell's nucleus. On the way, the RNA replicates, and once inside the nucleus, it invades the host's DNA. 

By granting a closer look at this replication process, the new study highlights that the capsid itself plays a critical role in infection and that specific criteria must be met for the virus to interweave its genome with the host cell's.

Knowing how to recreate the initial steps of HIV infection "means we have many more tools for dissecting the process of replication," said study author Wesley Sundquist, a distinguished professor of biochemistry at University of Utah Health. In particular, the study, published Oct. 8 in the journal Science, describes a cell-free system that can be used to study how HIV invades the host genome — such a system could "revolutionize HIV experiments in many labs," Leo James, a group leader at the MRC Laboratory of Molecular Biology, who was not involved in the study, told Live Science in an email.

"To have accomplished all this is a real tour de force," James said. Beyond basic research, the system could also help explain how experimental drugs that target the capsid work to limit HIV replication, Sundquist said in a statement. 

Related: 12 amazing images in medicine 

Test tube trials 

Although the test tube experiments capture aspects of HIV infection in superb detail, they cannot recreate every step in the process, Sundquist noted. Infection typically starts when the outer membrane of the virus fuses with the membrane of a host cell, allowing the capsid and its innards to sneak inside. But with a cell-free system, the authors had to bypass this initial step.

They instead used a compound found in bee venom, called melittin, to "permeabilize" the viral membrane and release the capsid held within. 

The HIV capsid has tiny pores in it, and normally, as a virus particle floats through a human cell's cytoplasm, it picks up the cellular building blocks of DNA, called deoxynucleotide triphosphates, that are already there, according to a 2017 report in the journal Nature. As it travels to the nucleus, the virus particle uses those building blocks to make copies of full strands of DNA, thanks to a special enzyme housed inside the capsid. This is how the virus copies its genetic material to later insert into the host genome. How the virus "knows" when to start this so-called reverse transcription is still somewhat mysterious, but studies hint that biochemical properties of the host cell act as cues for the reaction to begin.

But a test tube doesn't automatically have DNA building blocks in solution, so to jumpstart reverse transcription, the authors added them. "This method has been around for a while, but it's tricky to get the reaction to go until completion," James noted. But the study authors managed to get reverse transcription running smoothly; to do so, they learned that the capsid must stay mostly intact throughout the process.

Related: Going viral: 6 new findings about viruses

"The capsid has to be largely intact, and it has to be of the proper stability or flexibility, to support reverse transcription," meaning the capsid must be bound tightly enough to not fall apart during reverse transcription, but able to open up when the capsid enters the nucleus, in order to unleash its copied DNA, Sundquist said. Fortunately, scientists recently discovered a way to keep the capsid just stable enough.

Study author Owen Pornillos, an associate professor of molecular physiology and biological physics at the University of Virginia, and his colleagues found that a compound called IP6 binds to the capsid's tiled surface, they reported in 2018 in the journal Nature. IP6 carries a negative charge, while each tile carries a positive charge on the side that points in toward the center of the capsid; since opposites attract, when IP6 binds to the capsid, it helps pull the tiles into a tighter, more stable arrangement.

"Before the discovery of IP6, someone would remove the [viral] envelope in vitro and everything would fall apart and they could not see anything," said João Mamede, an assistant professor in the Department of Microbial Pathogens and Immunity at Rush University, who was not involved in the study.

IP6 is "quite abundant" in cells, so in their test tube experiments, the authors added similar concentrations of the compound as would be found in cells, Sundquist said. "That was really the trick," he added. "Until we knew it, we were working with capsids that were far too unstable."

Seeing is believing

Using computer models of molecules and an electron microscope, the authors could literally see that the 240 tiles making up the capsid held their lattice-like structure stable throughout reverse transcription. As the DNA strands grew larger, their ends sometimes poked through tiny gaps in the lattice weave, the authors noted, and sometimes singular tiles could be seen dislodging while the rest of the capsid stayed intact.

The capsid may need to stay stable to keep the RNA and transcribing enzyme close to each other, said Christopher Aiken, a professor of pathology, microbiology and immunology at Vanderbilt University, who was not involved in the study. The enzyme tends to fall off the RNA during transcription, so "by keeping the enzyme contained, it can rebind the template and continue DNA synthesis," Aiken told Live Science in an email.

With reverse transcription complete, the authors then moved on to the next step in infection: integration, where the viral DNA infiltrates the host genome. They introduced DNA strands known as plasmids into their test tubes, to serve as proxies for the DNA in a human nucleus, but integration would not begin without an additional ingredient. Only "whole cell extracts," a mix of proteins and molecules drawn from cells, would allow the viral DNA to pervade the plasmids.

In the future, the team hopes to pinpoint precisely which ingredients in the cell extracts trigger integration, Sundquist said. "It's likely to be more than one thing," he noted. One challenge is that, in test tube experiments, "it's always difficult to know if you're missing something," he said. 

Related: The 12 deadliest viruses on Earth 

One limitation of the study is that it can't perfectly recreate cellular conditions, James said. 

"Any in vitro system, however powerful, can only be used to test the components we know about and can add into the reaction," James said. For instance, in actual cells, the capsid must travel to the cell nucleus, where the DNA is held, and then slip through portals known as the nuclear pores. There may be unknown factors that alter the capsid during this journey, Sundquist noted. 

That said, the new cell-free system could help reveal the identity of those unknown factors, Mamede added. Scientists can now make observations in a cell-free environment and then check to see if the same behavior appears in actual cells, he said. 

In addition, the system could be useful in drug development. "You can test [new drugs] more readily with one of these simplified systems than with a cell," Mamede told Live Science. "This way, you can see mechanistically what it's really doing to the virus." 

The pharmaceutical company Gilead Sciences currently has a new drug in human trials that targets the HIV capsid specifically, according to ClinicalTrials.gov. Based on early data, the drug appears to alter the capsid at various points of infection, including during reverse transcription. Sundquist said that the cell-free study underscores that the capsid is a "critical component" of HIV infection, and that corrupting the capsid can limit the virus's ability to multiply. 

Originally published on Live Science.

Timothy Ray Brown, famous for being the first person to be cured of HIV, has died from cancer at age 54.

Known as the "Berlin patient," Brown was diagnosed with both HIV and acute myeloid leukemia, a cancer of the white blood cells, while living in Berlin more than a decade ago, according to Reuters. After his cancer diagnosis in 2006, Brown received radiation therapy and a bone marrow transplant in 2007; the goal of the treatment was to kill the existing cancer in his body and jumpstart production of healthy white blood cells, which are generated in the bone marrow. 

But the physician who led the procedure, Dr. Gero Huetter, aimed to treat both Brown's leukemia and his HIV using the same operation, according to The Associated Press. 

Related: 7 revolutionary Nobel Prizes in medicine

Huetter sought out a bone marrow donor with a rare genetic mutation that provides natural resistance against HIV infection. The virus normally targets white blood cells called CD4-T cells, which it infiltrates through a specific receptor on the cells' surfaces; people with the genetic mutation have an altered version of this receptor, so the virus can't slip inside, Live Science previously reported.

After his initial bone marrow transplant in 2007, Brown was cleared of HIV and remained free of the virus until his death, The Associated Press reported. He required a second transplant in 2008 to eliminate his leukemia, but after years in remission, the cancer returned last year and spread to his spine and brain, Reuters reported.

"I'm heartbroken that my hero is now gone. Tim was truly the sweetest person in the world," Brown's partner Tim Hoeffgen wrote in a Facebook post, according to Reuters.

"We owe Timothy and his doctor, Gero Huetter, a great deal of gratitude for opening the door for scientists to explore the concept that a cure for HIV is possible," Adeeba Kamarulzaman, president of the International AIDS Society, told Reuters.

Originally published on Live Science. 

Some people with HIV have a seemingly miraculous ability to control the disease without life-long antiviral medications or risky bone marrow transplants, and now, a new study hints at how this "elite" group bridles the infection.

In less than 0.5% of people with HIV, the virus stops replicating without the need for drugs, even though some latent virus continues to persist in the body, according to the study, published Aug. 26 in the journal Nature. HIV hides out inside human genes, but the new research suggests that sometimes these genes tuck the pathogen away in regions of the genome where it cannot be copied, The New York Times reported, thus preventing the virus from replicating and keeping the infection under control. 

For one patient, the researchers were unable to detect any trace of the virus in blood cells, or in cells from her intestines or rectum, the Times reported. The 66-year-old patient, named Loreen Willenberg, has successfully suppressed the virus without medication for decades and has participated in studies of HIV for over 25 years. 

Although scientists have known about her case for years, data from the new study suggests she could perhaps be considered "cured" of the infection. To date, only two people in the world are considered cured of HIV, and both underwent bone-marrow transplants to make their immune systems resistant to the virus, Live Science previously reported. Willenberg would join the short list of fully-recovered HIV patients if she can be confirmed free of the virus.

Related: The 12 deadliest viruses on Earth

"She could be added to the list of what I think is a cure, through a very different path" compared with bone-marrow transplantation, Dr. Sharon Lewin, director of the Peter Doherty Institute for Infection and Immunity, who was not involved in the study, told the Times. 

On the other hand, virologist Dr. Una O’Doherty of the University of Pennsylvania, who was not involved with the study, said she needs more data before confirming that Willenberg has been functionally cured of HIV. "It’s certainly encouraging, but speculative," O’Doherty told the Times. 

The study authors speculated that some people taking antiviral drugs for HIV could potentially reach recovery as Willenberg might have, if the virus inside them gets similarly trapped in genetic prisons, unable to replicate. And in fact, about 10% of the people who control HIV with drugs can eventually stop taking antiviral medication and continue to suppress the virus without assistance, according to The New York Times; the new study hints at how that might be possible.

"It does suggest that treatment itself can cure people, which goes against all the dogma," study author Dr. Steve Deeks, an AIDS expert at the University of California, San Francisco, told the Times.

In addition to Willenberg, the study included 63 other people who suppressed the virus without antiviral drugs, the Times reported. Among the 64 patients, 11 stood out as "exceptional controllers;" these individuals only had detectable levels of the virus in densely-packed regions of the genome where cells cannot readily access it. Normally, HIV would hijack the cellular machinery used to make proteins to instead make copies of itself, but when HIV genes get sequestered by certain genes, the pathogen has no way to replicate.

Related: 11 surprising facts about the immune system  

By analyzing the immune cells of study participants, the authors came up with a theory as to how the virus gets stuck in the first place. They suspect that, in some people, immune cells known as T-cells target and kill infected cells that carry HIV in easily-accessible portions of the genome — in regions where it can be copied. HIV remained untouched in cells where it was trapped in "blocked and locked" regions of the genome, senior author Dr. Xu Yu of the Ragon Institute told the Times.

"That’s really the only explanation" the researchers have for why the virus would persist in some cells without being able to replicate, study author Dr. Bruce Walker, a researcher at the Ragon Institute, told The New York Times.

Since submitting the results of their study, the authors have found several other people like Willenberg who may be effectively cured of HIV, Yu told The New York Times. "We believe there’s definitely many of them out there," he said. The team also aims to study people with HIV who have taken antivirals for decades, to see if their immune systems have similarly trapped the virus in genetic prisons.  

Still, it's unclear if the findings could translate to most people with HIV. "The real challenge, of course, is how you can intervene to make this relevant to the 37 million people living with HIV," Lewin told the Times. In other words, could these findings pave the way to a functional cure for others with the disease? We need more data to know for sure.

Originally published on Live Science. 

A woman's migraine medication caused a rare reaction: a burning sensation in her legs and the loss of one of her toes, according to a new report of the case.

Doctors diagnosed the woman with ergotism — also known as  St. Anthony's fire — a now uncommon condition that once caused mysterious outbreaks in medieval Europe. Her medication was derived from the same natural chemical behind these historical outbreaks.

The 24-year-old woman went to the doctor after she suddenly began to experience a severe burning pain in her legs, from her midthigh down to her toes, according to the report, published Wednesday (July 22) in The New England Journal of Medicine. She also had discoloration in her feet and trouble walking, and both legs were cold to the touch, according to the authors, from Government Medical College in Thiruvananthapuram, a city in southern India. Four days earlier, she had started taking a medication called ergotamine for migraine headaches. The woman was also born with HIV and was taking several antiviral medications to treat the disease.

A CT scan revealed that the arteries in both her legs had narrowed and thus reduced blood flow to the area.

Related: 27 oddest medical cases

Based on her symptoms, her doctors suspected she had ergotism, a disease traditionally caused by ingesting poisonous compounds made by a fungus called Claviceps purpurea, which infects cereal grains such as rye. In the Middle Ages, the disease caused large outbreaks among people who ate tainted rye, according to the American Society for Microbiology (ASM). Afflicted individuals developed mystifying symptoms including burning pain and gangrene in their limbs, while others experienced convulsions and hallucinations. Some researchers hypothesize that ergotism was also behind the mysterious symptoms experienced by girls accused of "bewitchment" in the 17th-century Salem witch trials, according to a 2016 paper in the journal JAMA Dermatology.

C. purpurea produces compounds called "ergot alkaloids," which affect the cells that line blood vessel walls and lead to constriction, or narrowing, of the blood vessels, resulting in reduced blood flow, according to a 2016 paper in the International Journal of Angiology.

Public health measures to prevent ergotism — such as removal of infected grains (which appear black) from the harvest — started in the 1800s, and the disease has been rare since then, according to ASM. But the same fungal compounds that cause ergotism were later isolated and used for medical purposes, including treatment of headaches, as is the case for the drug ergotamine. Today, most cases of ergotism are due to ergot alkaloid treatments, for instance, if the doses are too high or the treatment is prolonged, ASM said.

But people can sometimes develop ergotism even when taking normal doses of ergot-based drugs. This happens when people are taking other medications that lead to a drug interaction. One such drug is the HIV medication ritonavir, which blocks the enzyme involved in breaking down ergot compounds, according to a 1999 paper in the journal BMJ. Because of this interaction, the National Institutes of Health warns that people should not take ergotamine if they also take certain  HIV medications.

The woman in this case was taking ritonavir as part of her HIV treatment. Doctors treated her ergotism with the blood-thinning drug heparin, and her symptoms soon improved — her pain subsided and her legs became warmer. However, the treatment didn't come soon enough to prevent gangrene in one of the toes on her left foot, which had to be amputated. A CT (computed tomography) scan two weeks later showed improved blood flow in both legs, the report said.

Originally published on Live Science. 

A shot to prevent HIV has outperformed the prescription pill normally taken for the same purpose in a large clinical trial, The New York Times reported.

The injectable medication, taken once every two months, could provide an "appealing new option" for HIV prevention, as compared with pills that must be taken daily, Dr. Monica Gandhi, a researcher at the University of California, San Francisco, told the Times. 

Currently, the pharmaceutical company Gilead Sciences makes the only two HIV prevention pills on the market, known as Truvada and Descovy. The pills offer what's known as pre-exposure prophylaxis (PrEP), meaning a person takes it to prevent infection should they become exposed to HIV. But PrEP pills must be taken daily to keep blood levels of the medication high enough to block the virus, according to the U.S. Centers for Disease Control and Prevention (CDC). Taking PrEP pills daily can reduce the chance of getting HIV by about 99% — but that's only if people stick to the daily regimen.

Related: 20 of the worst epidemics and pandemics in history 

Truvada and Descovy also come with a high price tag, which may limit widespread use of PrEP, especially in poor countries, according to The New York Times. Without insurance, a 30-day supply of either pill can cost between $1,600 and $2,000, although some qualify to get the drugs for free or reduced cost in the U.S., PBS NewsHour reported. 

But soon, people may be able to opt for the new injectable drug, called cabotegravir, to protect themselves from HIV. A large clinical trial suggests that the shot is about 66% more effective than Truvada at preventing HIV infection in a real-world scenario, the Times reported. The findings, presented at the AIDS 2020 virtual conference, are "revolutionary," Dr. Rochelle Walensky, a researcher at Harvard University, told The New York Times.

The trial, conducted by a scientific collaborative called the HIV Prevention Trials Network, included nearly 4,600 cisgender men and transgender women who have sex with men from seven different countries. ViiV Healthcare, the pharmaceutical company that developed cabotegravir, made sure that at least half of the participants from the U.S. were Black men who have sex with men, representing the group most severely affected by HIV/AIDS in the country, according to The New York Times.

The trial had two groups: one that received cabotegravir and another that took Truvada. The study was blinded, so that people in the Truvada group got a placebo shot, while those in the cabotegravir group took placebo pills, and neither the participants nor the trial conductors knew who was getting what, according to ClinicalTrials.gov. Whereas 13 participants who received cabotegravir contracted HIV, 39 who took Truvada became infected.

Related: UK man becomes second person cured of HIV after 30 months virus-free

In addition, in a sample of 372 people who took Truvada, blood tests demonstrated that only 75% took the pills consistently. When only compared with patients who took Truvada exactly as prescribed, cabotegravir was still more effective at preventing infection. While cabotegravir still requires patients to stick to a schedule, Gandhi suggested that health care facilities could offer short appointment slots solely for the shot, or that the shots could be given at pharmacies or from mobile vans, the Times reported.

Cabotegravir is also being tested among women in sub-Saharan Africa, but it has taken longer to enroll participants, the Times reported. The drug has not yet been tested in transgender men.  

If cabotegravir is approved by the U.S. Food and Drug Administration in the next year or two, the drug could compete with a generic formation of Truvada, which is expected to become available in 2021, Walensky noted. With this in mind, ViiV Healthcare should set their price low, as competitors' drugs will likely grow less and less expensive, she said. 

"It's exciting to have another pharma company in the PrEP mix," Walensky told the Times. "This will create competition and ideally drive costs down."

Originally published on Live Science. 

The HIV virus can take refuge in the brain even when treated with antiretroviral therapies, only to later infect other organs in the body if that treatment is stopped, a new study in mice and human tissue suggests.

Untreated HIV, the virus that causes AIDS, cripples the immune system and leaves the body vulnerable to life-threatening illness. Combination antiretroviral therapy, or cART, can significantly lower concentrations of the virus in the body, to the point that the pathogen can become undetectable, symptoms largely disappear and the treated person is no longer infectious to others. But cART must be taken daily, and if treatment pauses, the virus may reemerge from hidden sanctuaries in the body. 

The new study, published June 11 in the journal PLOS Pathogens, suggests that one of these hideouts is in brain cells called astrocytes. Astrocytes constitute roughly 60% of the total cells in the human brain, according to the report, and in an infected person, the study authors estimate that between 1% and 3% of these cells could harbor HIV. 

Related: Going viral: 6 new findings about viruses

"Even 1% could be significant as a reservoir, as a sanctuary site, for the virus," said study author Lena Al-Harthi, a professor and chair in the Department of Microbial Pathogens and Immunity at Rush University Medical Center in Chicago. "If we're going to try to find an HIV cure, you can't neglect the role of the brain as a reservoir." 

Al-Harthi and her colleagues drew their conclusions from a mouse model of HIV injected with human cells, as well as examinations of postmortem human brain tissue. While both experiments provide insight into the role of astrocytes in HIV infection, more work must be done to nail down exactly how the virus takes hold in human patients, an expert told Live Science. 

"Animal models can tell us quite a bit. They're not humans, but they can inform us quite a bit," said Dr. Lishomwa Ndhlovu, a professor of immunology in medicine at Weill Cornell Medicine, who was not involved in the study. If astrocytes can act as a reservoir for HIV in human infection, and that virus can exit the brain and trigger infection elsewhere, as the mouse study indicates, "we do need to figure out how to eliminate the virus from these compartments" to devise a successful cure, he said. 

Lying in wait 

Astrocytes, named for their star-like shape, come in a variety of subtypes and play critical roles in the central nervous system, according to BrainFacts.org, a public information initiative run in part by the Society for Neuroscience. The cells help deliver nutrients to neurons, or the brain cells that transmit electrical signals, and they can spur or subdue inflammatory reactions in the brain. Astrocytes also shape and maintain the wiring of the central nervous system and fortify the blood-brain barrier, a border of tissue separating circulating blood from brain cells. 

Scientists knew that the HIV virus infiltrates the brain during infection, as infected people can develop dementia and other cognitive deficits. 

"The role of astrocytes in HIV infection has always been controversial," Al-Harthi told Live Science. Previous studies suggested that the star-shaped cells can become infected with HIV, but much of the research used cells in petri dishes, which may not replicate  infection processes in a living animal, Al-Harthi wrote in a 2018 report published in The Journal of NeuroVirology. A few studies have utilized live animals but used "traditional" methods, such as tagging viral proteins or genetic material with fluorescent compounds, to scan for the virus that may not be sensitive enough to accurately detect the low levels of HIV present in astrocytes. No study attempted to address whether, once infected, astrocytes could somehow release HIV to organs beyond the brain. 

Al-Harthi and her team developed two new mouse models to address this crucial question. 

Related: Top 10 mysterious diseases 

First, the authors placed human fetal astrocytes, derived from extracted brain tissue, in petri dishes and infected those cells with HIV. They then injected the infected cells into the brains of lab mice, one set of newborn mice and one set of adult mice. They found that, in both sets of mice, the infected astrocytes passed on the virus to CD4 cells — a type of immune cell that helps orchestrate the body's immune response and are specifically targeted by the HIV virus. 

After picking up an infection from astrocytes, infected CD4 cells migrate out of the brain and into other tissues. When "the brain is already seeded, the virus can come out and reseed peripheral organs," Al-Harthi said. 

In particular, the authors noted that the spleen and lymph nodes become infected as a result of this process. By blocking the movement of CD4 cells, the authors could cut this chain of viral transmission.

To ensure that the virus could infect astrocytes on its own, without their assistance, the authors also ran an experiment in which they injected healthy human astrocytes into mice and infected the animals with HIV afterward. In this scenario, some human astrocytes still became infected and released HIV into the rest of the body. Notably, the virus could still escape from the brains of mice given cART treatment, "albeit at low levels" compared to untreated mice. If the treatment was stopped, the virus from the brain triggered a full-blown infection.

To confirm aspects of their mouse experiments, the authors examined the donated brains of four HIV-infected individuals, all of whom received effective cART treatment. (The report did not specify how each donor died, but noted that the virus was effectively suppressed by cART at the time of death.) The team found that a small percentage of astrocytes contained HIV genetic material in their nuclei, indicating that the cells had been infected. 

Working toward a cure 

Many questions about astrocytes and HIV remain to be answered. For instance, certain subtypes of astrocytes may serve as reservoirs of HIV, while others don't, Al-Harthi said. And while the mouse experiments demonstrated that HIV can exit the brain, the postmortem tissue analysis could not confirm that the same occurs in humans. 

"Animal models, none of them are perfect," so there may be differences in how infection unfolds in people, Al-Harthi said. 

For example, during natural HIV infection, the virus can accumulate genetic mutations each time it replicates, and the genetic material required for infection can be lost in the process, Ndhlovu said. To fully understand the role of astrocytes in HIV, researchers will need to determine how much of the virus present in human astrocytes can actually trigger infection, he said.

Al-Harthi and her team began to address this question by examining postmortem brain tissue and analyzing what segments of HIV genetic material could be found within — but further studies will need to confirm that the found virus is both able to infect cells and migrate to other organs in the body, Ndhlovu said. In addition, scientists will need to determine the exact route HIV takes out of the brain in order to infect other organs, as that information would also be crucial for developing treatments that target the brain and finding a successful cure, he added. 

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Originally published on Live Science.

The oldest known nearly complete gene sequence from the HIV strain that spread across the world has been found in a tissue sample from the Democratic Republic of the Congo (DRC), a new study finds.

The tissue sample was taken and preserved in 1966, making this HIV sequence 10 years older than the previous oldest genome, which came from a blood sample taken in 1976 in the DRC. Gene sequences like these – which come from before the virus that causes AIDS was discovered in 1983 – help pinpoint the timing of genetic mutations in the virus. Those mutations, in turn, help scientists track the spread of the virus and the timing of when transmission of HIV took hold in humans.

In that sense, the new gene sequence is "very comforting," said Sophie Gryseels, a co-author of the new study and a postdoctoral researcher in evolutionary and computational virology at the Catholic University of Leuven (KU Leuven) in Belgium. This sequence fits well with researchers' previous understanding of the timing of HIV's emergence, she told Live Science.

"This is nice to know, because it means that our evolutionary models that we are always applying to our virus sequence work well," Gryseels said. "We didn't have big surprises."

Related: 11 (sometimes) deadly diseases that hopped across species

Viral emergence

Based on genetic sequencing of samples of the virus, scientists think that HIV, or human immunodeficiency virus, first found a foothold in humans in Central Africa sometime in the early 1900s, spilling over from chimpanzees. There are multiple strains of the virus, but the ones responsible for 95% of cases worldwide are in a subgroup called HIV-1 group M. More than 32 million people have died of AIDS, the disease caused by HIV, since the pandemic began.

With at least 80 years between the start of transmission of HIV-1 in humans and the discovery of the virus, much of the disease's early dynamics remain mysterious. Mathematical models of the rate of the virus' mutation hint at when HIV first began to spread human-to-human, transmission that would eventually turn pandemic. But one big question is when and why HIV-1 group M became so successful, infecting people effectively enough to go global.

Part of the problem is that models that do a good job of calculating the rate of viral change in recent years become less reliable over longer timeframes, Gryseels said. That's partly because genetic information gets lost over time: Strains die out due to natural selection or simple luck, leaving no mark of their existence on the genomes of currently circulating viruses.

For that reason, discovering an old virus strain is a bit like discovering Archaeopteryx for paleontologists. It's a missing piece of the puzzle that helps fill in a lineage of evolutionary change.

Old HIV

Gryseel joined an ongoing project led by University of Arizona evolutionary biologist Michael Worobey, and along with other colleagues in Belgium, the United States and DRC, analyzed 1,645 biopsy specimens collected in Central Africa between 1958 and 1966 for the purposes of diagnosing medical conditions. The biopsies had been preserved in the chemical formalin and then embedded in paraffin wax. Using very sensitive PCR methods (similar methods to those used to detect the new coronavirus SARS-CoV-2 in nose-and-throat swabs), the researchers hunted for hints of HIV genomes. They found just one: A sequence in lymph node biopsies from a 38-year-old man.

There are older fragments of HIV out there, one from 1959 and one from 1960, also from DRC. But those pieces aren't as complete, and thus can't offer as much information about the virus' mutations. Those fragments were also from different subtypes of HIV, Gryseels said, which shows that the virus had been circulating for some time in humans before the 1950s.

Related: 28 devastating infectious diseases

The researchers will continue to hunt for old HIV genomes in long-ago tissue samples, Gryseels said. It would be ideal to find more samples from the 1950s or 1960s to confirm the results, she said. The next goal is to figure out when HIV-1 transitioned to an accelerating epidemic. It's possible that some change in HIV-1's genome made it more efficient, Gryseels said, but more likely that societal changes made the difference. Urbanization rose rapidly during the early 1900s in Central Africa. Between the 1910s and 1950s,  public health campaigns expanded treatments for diseases ranging from sleeping sickness to malaria and syphilis. But many of these campaigns did not properly sterilize needles, which could have spread HIV widely. Decolonization in the 1960s could also have led people to move around or behave differently, which could have helped the virus spread into new populations or transmit more rapidly.  

"If we have a better idea of the timeline of when this expansion occurred, we'll be able to weigh these different hypotheses against each other more efficiently, because they have different times in which they occurred," Gryseels said.

The researchers published their findings May 19 in the journal Proceedings of the National Academy of Sciences.

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Originally published on Live Science. 

A man in London appears to be the second person ever cured of HIV, his doctors said.

The man — whose case was first announced a year ago — has now been HIV-free for 30 months without the need for antiviral medications, according to a new report published Tuesday (March 10) in the journal The Lancet HIV.

Previously known only as the "London patient," the man revealed his identity on Monday (March 9). He is Adam Castillejo, a 40-year-old who was first diagnosed with HIV in 2003, according to The New York Times.

Last year, researchers reported that Castillejo had experienced "long-term remission" from the virus after undergoing a special bone-marrow transplant. At that time, Castillejo had been HIV-free for 18 months. Now, 12 months later, his doctors are more sure that his case does indeed represent a cure.

"We propose that these results represent the second ever case of a patient to be cured of HIV," study lead author Ravindra Kumar Gupta, a professor of clinical microbiology the University of Cambridge, said in a statement.

The first patient to be cured of HIV — Timothy Brown, also known as the "Berlin patient" — received a similar bone-marrow transplant in 2007 and has been HIV-free for more than a decade.

In the cases of both Castillejo and Brown, stem cells used for their transplants came from a donor who had a relatively rare genetic mutation that confers resistance to HIV. 

However, the researchers stressed that such a bone-marrow transplant would not work as a standard therapy for all patients with HIV. Such transplants are risky, and both Castillejo and Brown needed the transplants to treat cancer, rather than for HIV.

In the new report, doctors found no active viral infection in Castillejo's body. However, they did find "remnants" of HIV's DNA in some cells. But the authors said these traces of DNA can be thought of as "fossils," because they are unlikely to allow the virus to replicate. Such remnants were also found in Brown's case. 

Castillejo's cure "means the first one [in the Berlin patient] wasn't an anomaly or a fluke," Gupta told The Guardian.

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Originally published on Live Science. 

Over 1,000 patients at an Indiana hospital may have been exposed to HIV, hepatitis B and hepatitis C after an error in a sanitizing procedure, according to recent news reports.

Between April and September, one of the Goshen Hospital's seven surgical sterilization technicians skipped a step in a multistep cleaning process for certain surgical instruments, according to news reports and a statement from the hospital. Though those surgical instruments still went through other disinfection and sterilization procedures with a "wide margin of safety," it's not clear if the instruments were completely sterile before they were used on people, the hospital statement said.

"Even though we believe the risk to be extremely low, out of an abundance of caution, we are offering patients free testing for these viruses," hospital representatives wrote in the statement. Officials from Goshen Hospital sent out notification letters and are offering free blood draws for the 1,182 patients who underwent surgery and who might have been exposed to these infectious diseases. 

One of the patients, Linda Gierek, who underwent surgery at the hospital on June 24, filed a class-action lawsuit on Nov. 22 through attorney Walter J. Alvarez; the lawsuit lists several anonymous defendants with addresses at the hospital, according to The Goshen News. 

Related: 27 Devastating Infectious Diseases

Both hepatitis B and hepatitis C are liver infections caused by a virus that can be transmitted through blood, as can happen when people share needles. For some people, hepatitis B and C are short-term illnesses and symptoms resolve quickly, but for others, the illnesses become chronic and lead to more-serious health issues, according to the Centers for Disease Control and Prevention (CDC). Symptoms of hepatitis B can include fever, fatigue and yellowing of the eyes, while symptoms of hepatitis C — if patients have any at all — are typically mild and resemble the flu; these can include sore muscles and tiredness. 

HIV is a virus that can also be spread through blood and other bodily fluids and that slowly attacks the immune system, destroying the body's defenses such that it can't fight off disease, according to the CDC.

"As with any patient safety concern, we rigorously investigated all aspects around the incident," Dr. Daniel Nafziger, Goshen hospital chief medical officer, said in the statement. "We have put strict policies and additional safety measures in place to ensure it does not happen again."

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Originally published on Live Science.

The U.S. National Institutes of Health (NIH) wants to cure HIV and sickle cell disease with gene therapies, and will invest $100 million over the next four years towards that goal, the agency announced today (Oct. 23).

For this effort, the NIH will partner with The Bill & Melinda Gates Foundation, which will also invest $100 million.

Critically, the partnership aims to make the therapies affordable and accessible to people around the world, particularly in developing countries, where the burden of these diseases is greatest.

"This is a very bold goal, but we have decided to go big," Dr. Francis Collins, director of the NIH, said in a news conference today.

The effort aims to have the therapies ready for testing in clinical trials in the U.S. and sub-Saharan Africa within the next seven to 10 years. 

Related: 10 Amazing Things Scientists Just Did with CRISPR

The majority of the 38 million people with HIV live in developing countries, with two-thirds living in Sub-Saharan Africa. For sickle cell disease, the majority of cases also occur in Sub-Saharan Africa.

The NIH has been trying to find a cure for HIV for "decades and decades," said Dr. Anthony Fauci, director of The National Institute of Allergy and Infectious Diseases. Although current treatments with antiretroviral therapy (ART) are effective at suppressing the virus in the body, they are not a cure, and must be taken everyday. What's more, there are millions of people with HIV who don't have access to ART treatment.

Although scientists are working to develop gene-based cures for HIV, these approaches are often costly and would be difficult to implement on a large scale, Fauci said. For example, some of these therapies take cells out of a patient's body and then re-infuse them, an expensive and time-consuming intervention.

For this reason, the new collaboration will focus on developing cures that use "in vivo" approaches, meaning they happen inside the body, Fauci said. One example of this could be to remove the gene for the CCR5 receptor, which HIV uses to get inside cells. Another idea is to excise the HIV "proviral" DNA that has copied itself into the human genome and lurks in the body even after years of treatment.

Similarly, for sickle cell disease, the goal would be to develop an in vivo therapy that could repair the genetic mutation that causes the disease. This would require a gene-based delivery system that could selectively target the mutation.

"Beating these diseases will take new thinking and long-term commitment. I'm very pleased to see the innovative collaboration announced today, which has a chance to help tackle two of Africa's greatest public health challenges," Matshidiso Rebecca Moeti, the World Health Organization's Regional Director for Africa, said in a statement.

Still, much work would be needed to make sure these therapies are safe and effective.

"It is very clear we have a ways to go, which is why this is a 10 year effort to try and take that promise and turn it into a reality," Collins said.

Earlier this year, the Trump Administration announced a plan to end the HIV epidemic in the U.S. in 10 years.

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Originally published on Live Science. 

California just became the first state to allow people to buy HIV prevention drugs at pharmacies without a prescription, according to recent news reports. 

Around 1.2 million Americans currently live with AIDS, an incurable disease that develops after an individual is infected with the HIV virus. But in the last couple of decades, new treatments have increasingly allowed people with AIDS to live long and full lives; and new prevention drugs have reduced the number of people being infected with HIV in the first place. 

On Monday (Oct. 7), California Gov. Gavin Newsom signed a bill that allows people to buy these prevention drugs at pharmacies without a prescription and also prohibits insurance companies from requiring "prior authorization" before using the insurance to purchase the drugs.

Related: 27 Devastating Infectious Diseases

One of the pills, called pre-exposure prophylaxis or PrEP, is a daily pill for people who want to prevent HIV infections; the other pill, called post-exposure prophylaxis or PEP, is an emergency pill that people can take after a possible exposure to HIV in order to reduce their chances of infection.

PEP must be started within 72 hours of possible exposure to the virus, and continued for 28 days, according to the Centers for Disease Control and Prevention (CDC). That does not always allow enough time for a person to get a prescription from a doctor, Rick Zbur, the executive director of the nonprofit LGBTQ civil rights group Equality California, told the Associated Press. 

PrEP is taken by people who might be at high risk for HIV. When taken daily, it is about 99% effective at preventing infection from sexual activity and 74% effective at preventing infection from the injection of drugs, according to the CDC.

Before a person can buy either drug, they are required to be tested for HIV or prove to the pharmacist that they were tested negative for it within the last week, according to NPR. Due to concerns of long-term use without a doctor's review, the bill limits the amount of PrEP people can buy independently to 60 days; after that, they are required to visit a primary care doctor, according to the AP.

"Recent breakthroughs in the prevention and treatment of HIV can save lives," Newsom said in a statement. "All Californians deserve access to PrEP and PEP, two treatments that have transformed our fight against HIV and AIDS." About 30,000 people in California currently use PrEP and 6,000 use PEP, according to the California Health Benefits Review Program, the AP reported.

"I applaud the Legislature for taking action to expand access to these treatments and getting us closer to ending HIV and AIDS for good," Newsom added. 

Newsom also signed two other public health bills, one that lowers the cost of prescription drugs by not allowing drug manufacturers to block the making of cheaper generic drugs and another that requires health care providers caring for pregnant black women to undergo bias training.

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Originally published on Live Science.