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.

In the three decades between 1993 and 2024, measles in the U.S. was relatively rare — a few hundred cases each year, at most. But suddenly, the disease has become so entrenched in American life that it sometimes fails to make headlines when a new outbreak erupts.

As of March 2026, measles has been continuously circulating around the U.S. for more than a year, starting with an outbreak in Texas that lasted from January to August 2025. Before that outbreak was declared over, an outbreak on the Utah and Arizona border began in August and is ongoing. An outbreak in South Carolina began in September, drastically increased in January 2026, and continues.

Thirty states have had measles cases this year; 47 have seen cases since the start of 2025. Health officials across the U.S. have confirmed 1,300 infections already this year as of March 6, putting the country on track to surpass 2025’s numbers, which were the highest in 35 years.

We study outbreak preparedness and response at Brown University's Pandemic Center, and we view the return of measles in the U.S. as a grim signal of what's to come.

Low levels of vaccination across the country mean measles outbreaks will continue to occur, needlessly hospitalizing and killing the unvaccinated. But beyond these harms, the disease's resurgence serves as a serious warning about the country's capacity to manage infectious disease threats of all kinds.

An eliminated disease returns

Measles' return is no mystery: At its root is the falling vaccination rate.

Around 90% of the U.S. population has received the MMR vaccine, which protects against measles, mumps and rubella, and in some regions of the country, the rate is below 60%. Since about 2019-2020, that overall number has dropped below the 95% needed for herd immunity. It is necessary to keep that rate nationally, but maintaining herd immunity at the local level is equally important in order to prevent measles from finding pockets of unvaccinated communities.

Countries that remain free of continuous transmission for 12 months are deemed to have eliminated measles — a designation the U.S. achieved in 2000. The Pan American Health Organization was scheduled to decide in April whether the U.S. should lose that designation, but the organization postponed its meeting until November.

Current trends suggest that both the U.S. and Mexico, which has also been battling the disease, may lose this status — as Canada did in November 2025. All three countries have seen their vaccination rates fall below the 95% threshold, and their outbreaks may share epidemiological links.

A serious, long-term threat to US health

By any measure, the ongoing U.S. measles outbreaks signal that the disease has returned in a way that will have serious adverse health consequences. In 2025, three people died from measles in the U.S. That is more than in any year since the disease’s elimination 25 years ago.

Of the country's 2,283 confirmed measles cases in 2025, 11% were sick enough to be hospitalized. In South Carolina, where most measles cases have been reported in 2026, hospitals don't have to report when patients are admitted due to measles complications, so the actual number of hospitalizations due to measles could be much higher.

People who recover from measles can experience complications such as pneumonia, which can lead to death, or encephalitis, which can later lead to deafness or intellectual disabilities from the brain swelling. The virus can also affect the immune system, making people more susceptible to other infections over the long term, even ones they've had before.

In rare instances — though more likely if someone is infected as a child — measles patients can develop a progressive dementia known as subacute sclerosing panencephalitis, or SSPE, anywhere from two to 10 years after their infection. SSPE always leads to death. This past year, a school-age child in Los Angeles died of this condition years after being infected with measles as an infant, before they were old enough to be vaccinated.

Measles is an economic scourge

Recurring outbreaks of measles in the U.S. will mean high economic costs. Countries have pursued measles elimination in part because of the clear economic benefits of stopping domestic transmission of the virus.

Studies have found that the cost of containing measles outbreaks is often as much as tens of thousands of dollars per case. One outbreak in Washington state in 2018-2019, which involved 72 cases — a small outbreak compared with what states are reporting now — cost US$3.2 million for the public health response, medical expenses and productivity losses. The Common Health Coalition found that a sustained 1% drop in MMR coverage would cost the U.S. billions across health care systems and the economy.

An opening for infectious disease

As concerning as recent outbreaks of measles have been, they herald a larger systemic problem.

How a country controls measles can be viewed as a proxy for how well it would control many other diseases. That's because the steps for stopping the spread are the same: deploying vaccines to prevent infections, detecting and isolating cases when they occur, identifying exposed contacts of infected people and making sure they stay home if they're likely to be contagious, and treating sick people safely.

But besides measles, we've already seen infections that were once controlled, like whooping cough, that rose sharply in 2024 and remained high in 2025 compared with before the COVID-19 pandemic.

That's because controlling the spread of many infectious diseases depends on the public's trust in the basic components of public health. Declining MMR vaccine coverage reveals underlying challenges in public support for vaccines. Public confidence in the current Centers for Disease Control and Prevention is also eroding, according to polling from 2023 to early 2026 by the health policy organization KFF. Less than half of the people polled trust the government even "a fair amount" to provide reliable vaccine information.

These growing cracks in the country's public health armor will complicate efforts to protect Americans from future disease threats — whether an outbreak, a pandemic or a biological attack.

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

In January 2003, epidemiologists in China identified two cases of "atypical pneumonia" in patients who had visited health care workers in Guangdong province. Teams initiated contact tracing and eventually discovered that the germ responsible for the illnesses had been circulating since a patient fell ill Nov. 16, 2002.

Those early cases in November were in "food handlers" — those who either worked as chefs in restaurants or as vendors at "wet markets," where live animals, such as poultry and more-exotic animals like civet cats and raccoon dogs, were held in crowded conditions.

By the time Chinese disease investigators realized an outbreak might be unfolding, the disease had already been circulating for two months and had spread to health care workers.

The disease reached Hong Kong in February and then exploded when a nephrologist from southern China traveled to the region for a wedding on Feb. 21, 2003. He was unwell during his trip and later died of the disease.

In March, a case investigator for the World Health Organization (WHO), Dr. Carlo Urbani, came to investigate a case observed in a businessman who had traveled to Hong Kong before arriving in Hanoi, Vietnam, and being hospitalized there. Urbani ultimately acquired the disease himself and died that same month.

By March 12, the WHO had issued an alert about a severe form of pneumonia of unknown origin in people from China, Hong Kong and Vietnam. By March 15, the Centers for Disease Control and Prevention (CDC) had officially named the disease severe acute respiratory syndrome (SARS), and by March 24, they had identified a novel coronavirus as the cause.

By that time, the outbreak had neared its peak. The pandemic lasted for months, spread to 28 countries beyond China —with 29 cases in the U.S. — and affected more than 8,000 people, 774 of whom died. The disease's case-fatality rate was estimated to be around 9.6%.

In early 2004, SARS briefly flared up again, but its spread was quickly squelched through an aggressive and rapid contact-tracing-and-containment strategy.

That second flare-up enabled scientists to trace the SARS virus to palm civets and raccoon dogs sold at markets. The next year, scientists proposed that horseshoe bats were the pathogen's original animal host, but it wasn't until 2017 that researchers found the smoking gun: bats carrying a rich pool of SARS-like viruses living in remote caves in China's Yunnan province. The caves were just a mile away from villages.

"The risk of spillover into people and emergence of a disease similar to SARS is possible,” authors warned in their paper at the time.

The SARS epidemic, as scary as it was at the time, was ultimately just a dress rehearsal for the COVID-19 pandemic that swept across the globe from March 2020 to May 2023, after early cases started to emerge in November 2019. The two viruses belong to the same general family of coronaviruses and likely emerged from a similar animal host.

Scientists and public health officials successfully applied some of the lessons of SARS to the COVID pandemic. For instance, when SARS first emerged, China had a very rudimentary infectious-disease surveillance system. While they did report cases of infectious and food-borne diseases, communication was by telephone call, there was no standardized case reporting system, and they had no system in place to track contacts or collect lab results. After the SARS epidemic, China quickly implemented a thorough contact-tracing and disease-surveillance system.

That would prove crucial when SARS-CoV-2, the coronavirus that causes COVID-19, emerged in China. The country logged hundreds of thousands of cases of infections during the first wave, which ended in China by mid-February — just a few months after investigators first reported a cluster of pneumonia cases of unknown cause in Wuhan. (A draconian lockdown also likely helped contain the virus's spread within the country.)

Whereas it took months to identify the cause of the SARS pandemic, the SARS-CoV-2 virus was identified less than two weeks after the first cases were noticed. And SARS had no specific treatment, whereas by mid-March 2020, vaccines against the newly identified virus were in clinical trials, thanks to mRNA technology that had been in the works for decades.

Other lessons the world could have taken from SARS were only partially learned. In 2017, when the SARS source was identified, Dr. Kwok-Yung Yuen, a virologist at the University of Hong Kong who co-discovered the virus, told Nature News that the finding "reinforces the notion that we should not disturb wildlife habitats and never put wild animals into markets." He told Nature News that respecting nature "is the way to stay away from the harm of emerging infections." Yet the practice continued.

In some ways, the SARS epidemic also gave public health agencies a false sense of security. SARS and related coronavirus diseases, such as Middle East respiratory syndrome (MERS), were much deadlier than SARS-CoV-2 but also much easier to contain. Outbreaks were relatively easy to control using contact tracing and other public health measures, rather than requiring the distribution of vaccines.

That's because SARS had a shorter infectious window than COVID-19. It was most infectious during the second week of the illness, when people were seriously ill, whereas SARS-CoV-2 was easily transmitted from the early phases of disease, sometimes even before symptoms emerged.

Months before COVID-19 was officially declared a pandemic, public health leaders were poring over the early data coming out of China and preparing for the worst.

Dr. Seth Berkley — a renowned infectious-disease epidemiologist and former CEO of Gavi, an international organization aimed at improving children's vaccine access — was among those leaders. In January 2020, Berkley and colleagues were working to establish an infrastructure so that, if and when scientists created vaccines for this novel virus, the shots wouldn't be hoarded by high-income countries and denied to poor nations.

Now, Berkley has released a new book — "Fair Doses: An Insider's Story of the Pandemic and the Global Fight for Vaccine Equity" (University of California Press, 2025) — that recounts how that initiative unfolded and what lessons were learned through the process, while underscoring why the broader fight for vaccine equity is far from finished.

On January 23, 2020, I was high up in the Swiss Alps in Davos, attending the World Economic Forum (WEF). I was at Davos as the CEO of Gavi, the Vaccine Alliance, the largest purchaser of vaccines in the world and which worked to provide new and underutilized vaccines to children in developing countries — countries in which about half the world's children live. As usual, I was preoccupied with how we could do a better job protecting the world with vaccines for new and old diseases. And there were murmurs of a new epidemic of respiratory disease caused by a novel coronavirus in China on the horizon.

At the bar of the Hard Rock Hotel my wife, Cynthia [an academic physician and consultant], and I met with Richard Hatchett, CEO of the Coalition for Epidemic Preparedness Innovations (CEPI). Over nachos and drinks, we started to talk through what was likely to happen with the new coronavirus, which would later be named COVID-19. Discussion about the disease hadn't really reached a high political level and was not formally on the Davos agenda, but concern was growing, and many people during that week asked us our opinions.

The first question we discussed was whether this was just going to be a worrisome outbreak or the Big One that epidemiologists had long warned might come. So far, we only had official confirmation of a point outbreak, spreading from animals at the Wuhan live animal market to humans. But on the nerdy LISTSERVs about infectious disease and epidemics, there was already a lot of chatter about how the virus might be spreading from person to person, which is a huge red flag in our field. We agreed that there was potential for the new virus to spread dramatically. Regardless of whether this was or was not the Big One, we needed to prepare.

Such a scenario creates a problem for all countries, even those with access to the vaccines. But to me a far bigger concern was the unfairness of high-income countries' self-interest. People in developing nations without access to vaccines were historically already the most vulnerable to disease and the most likely to suffer complications if they got sick. They already had limited access to the most basic medical treatment.

Improving the delivery of existing vaccines and building up better delivery systems is the best way to detect outbreaks early, prepare communities for outbreaks of disease, and ensure health systems aren't overwhelmed in an emergency — as well as strengthen our epidemic stockpiles.

If vaccines against the disease could be made — and at the time, we were far from certain they could be — we knew that stocks would be quickly bought up by the richest countries. The logical conclusion was that the bulk of the world's population, and most especially those in lower income, developing countries, would be locked out of these deals, and so denied timely access to whatever vaccine supplies became available.

That was where we thought we could help. So, Richard, Cynthia, and I talked through a rough outline of what would be needed to ensure equitable access to any COVID-19 vaccines that emerged and the roles that various organizations — such as CEPI, Gavi, UNICEF, and WHO — as well as the pharmaceutical companies might play to make that happen.

Imagining ourselves in the place of government decision-makers, we envisioned that they would have an incentive to participate in a mechanism that pooled risk by making advance purchase commitments for a wide variety of candidate vaccines. Their buy-in could help us pool demand, generating enough scale to incentivize increasing production and to negotiate the best prices on everyone's behalf. We wanted to promote solidarity, to publicize and meet lower-income country needs, and to create an early, strong global movement for equitable access.

Richard went from Davos back to London and talked with the CEPI team, I went back to Geneva to talk to the Gavi team and our Alliance partners WHO and UNICEF, and we started our collaboration. That joint effort became COVAX [COVID-19 Vaccines Global Access, an initiative to ensure equitable access to COVID-19 vaccines].

Our small team working on COVAX undertook what I believe was the most ambitious public health effort of the 21st century so far. The first COVAX dose was delivered to a COVAX-supported country 39 days after the first jab in the United Kingdom. Due to the time required for WHO to prequalify the vaccine, 43 days later the first doses were administered in Africa, in Ghana and Côte d'Ivoire. Forty-two days later, COVAX vaccines had been distributed to 100 countries. There were many delays due to export bans, vaccine nationalism, and manufacturing delays. But by the end of 2021, close to 1 billion doses had been distributed; by the end of 2022, COVAX had delivered more than 1.6 billion doses to people in the world's poorest countries and was estimated to have averted 2.7 million deaths in those countries. That's the fastest rollout of vaccines to developing countries ever.

WHO estimates that some 16 million people died during the first two years of the pandemic; we are still counting, and that number will doubtlessly grow. And COVID-19 is by no means the only infectious risk: Currently, about one in seven deaths, accounting for more than 7 million people a year, is due to an infectious disease. Millions of people die from diseases for which we already have vaccines.

It's hard to put numbers on the deaths that have been prevented by vaccines, but some estimates say that vaccines have saved more than half a billion lives over the past 70 years, the time period they have been routinely available. And this only covers the 30 or so vaccines we have against the more than 300 infectious diseases known to plague humanity.

More and better vaccines need to be developed, particularly for major killers such as tuberculosis, malaria, and HIV, and, hopefully, more cancers. And in the meantime, the risks for infectious diseases are shifting.

Even those of us who had been working in the field for years were surprised at how poorly prepared the world was for an emergency of this magnitude. What's more, we faced the perils of vaccine nationalism, vaccine diplomacy, and the sometimes-selfish behaviors of manufacturers and world leaders. It was clear from the start that we wouldn't be able to do this work perfectly. But we did our best, and I've sought to set down both what we did and what I wish we could have done differently so that we can learn from our history.

As the world continues to recover from the worst of the pandemic years, we may not relish thinking about another pandemic ahead. We face complacency, fatigue, and a growing distrust of both science and institutions, fed by intentional disinformation that spreads rapidly online. But we also have an opportunity to harness what we've learned to do better next time — and there is epidemiologic certainty that a next time will come. When it does, we need to have robust public health systems in place, and ideally, vaccines.

Reprinted from Fair Doses: An Insider's Story of the Pandemic and the Global Fight for Vaccine Equity by Seth Berkley, MD, courtesy of University of California Press. Copyright 2025.

Cells use mRNA to build proteins, and after years of research, scientists learned how to harness this molecule to develop effective, safe and quick-to-make vaccines. Since the advent of this Nobel Prize-winning technology, a handful of mRNA vaccines have been approved in the United States — namely, COVID-19 and RSV shots. Vaccines still in development could someday protect against seasonal flu, bird flu, HIV and more.

But now, the U.S. federal government is slashing its investments in mRNA vaccines — a move that will immediately impact 22 projects totaling nearly $500 million, the U.S. Department of Health and Human Services (HHS) announced Tuesday (Aug. 5).

Some projects in late stages will be allowed to wrap up, but "no new mRNA-based projects will be initiated," the statement said. The department will also cease "all mRNA-based equity investments" coordinated through its partner Global Health Investment Corp., a nonprofit that supports the development of public health technologies through venture capital.

Robert F. Kennedy Jr., HHS secretary and founder of the anti-vaccine group Children's Health Defense, claimed in the statement that mRNA vaccines "fail to protect effectively against upper respiratory infections" and said that the HHS will shift to funding "safer, broader vaccine platforms." These alternatives are later defined as whole-virus vaccines and unspecified "novel" technologies.

Per the statement, this retreat from mRNA vaccines will not impact "other uses of mRNA technology." But "I can tell you that the industry doesn't trust that," said Jeff Coller, the Bloomberg distinguished professor of RNA biology and therapeutics at Johns Hopkins University, who has studied mRNA for more than 30 years. "Even though the cancellation was specific to infectious disease, it really was a shot across the bow to the entire industry."

mRNA is useful for more than combating infectious diseases. It could potentially be applied as a cancer therapy, a vehicle to deliver gene-editing treatments into the body, a way to rein in autoimmune diseases like multiple sclerosis, or a treatment for the dangerous pregnancy disorder preeclampsia, for example.

Live Science spoke with Coller about the recent funding cuts and their anticipated impacts on the mRNA field and health of Americans.

Related: What are mRNA vaccines, and how do they work?

Nicoletta Lanese: Can you talk about how the HHS stance on mRNA vaccines had been shifting prior to Tuesday's cuts?

Jeff Coller: It was clear early on, before Robert F. Kennedy was nominated for the position of secretary of HHS, that he was, first of all, a vaccine skeptic, and highly critical of mRNA-based vaccines, as well. His statements before his appointment included some things like, "The mRNA vaccines were some of the most dangerous medicines introduced into the human population."

[After his appointment], one of the first things that he did was to dissolve the committee that oversees the procedures of vaccinations within the United States called ACIP [Advisory Committee on Immunization Practices], and he appointed new individuals to that committee. One of those includes an individual who is an mRNA skeptic: Robert Malone, who has claimed on TV and Joe Rogan that mRNAs are dangerous.

In addition to that, in about March of this year, there was an internal memo sent to NIH [National Institutes of Health] employees, asking them to disclose if they were working on mRNA vaccines, as well as to disclose who their colleagues were. This was made public and was published in journals like Science and was a warning sign that they were potentially going to target individuals associated with this type of research.

So we are already starting to feel that there was a growing anti-mRNA sentiment within the HHS, and then the cancellation of Moderna's bird flu contract that happened about maybe six weeks ago was probably the first direct action of an mRNA program being canceled by the federal government. And now, what happened two days ago [was that] funding was canceled for 22 of these mRNA projects that were investigating various vaccines.

NL: Are you aware of the specifics of any of those projects?

JC: We do know of some clinical trials that were already underway [and were impacted], and this included influenza — which is, of course, the big one — as well as respiratory syncytial virus, or RSV; cytomegalovirus, which is often called CMV; Zika, Epstein-Barr virus; and hepatitis B.

NL: The HHS statement drew a line between mRNA vaccines and "other uses" of mRNA. Do you think that those other projects will be unaffected?

JC: Well, I can tell you that the industry doesn't trust that. And the reason why I know that is that I'm one of the founders of the Alliance for mRNA Medicines. This is an organization of over 75+ members, many are biotech — small biotech, large biopharma, as well as major academic medical centers, including [Johns] Hopkins and Penn [the University of Pennsylvania] and the Mayo Clinic. We did a survey very early in the [Trump] administration to ask about some of these policy changes that were coming down from HHS. The overwhelming response from our membership was that they felt that the United States was becoming an unfriendly place for mRNA-based technology.

Even though the cancellation was specific to infectious disease, it really was a shot across the bow to the entire industry. It sent a chilling effect through the industry that basically makes everyone question, should we continue to invest in these programs within the United States?

The arguments that were made [by RFK Jr.] were vague and are not based on what is accepted in the scientific community. In fact, most of his statements are false. So, given that that decision was clearly made on nonscientific beliefs, then the industry is going to be scratching their head and thinking, "Well, maybe we should probably look elsewhere to develop our products, other countries."

NL: One example I was thinking about was "cancer vaccines," which are more of an immunotherapy. Do you think HHS will carve out an exception for those?

JC: We don't know. And we've tried to move away from using the word "cancer vaccine" on purpose. We started referring to them as "cancer neoantigen therapies." To start thinking about you changing your wordage because you're worried about how the administration is going to perceive what it is you're doing is alarming.

Many of these technologies that are being developed for cancer are still very early in research and development. These are still not even in the biotech space; a lot of them are still in the academic setting. If you're an academic lab, are you really going to continue down this road if you are not going to be able to get funding? I personally know of investigators that are doing clinical trials on mRNA-based approaches for cancer who are scared — they're actually scared to talk to reporters like you. They're scared to even mention that they have mRNA-based medicines, because their patients will suffer if the funding gets cut off.

NL: Another example I was thinking of was gene editing, and specifically CRISPR-based treatments. How could those be affected?

JC: When CRISPR was discovered, gene editing had a huge promise of being able to cure rare genetic disorders. But the limitation of gene editing was that if you introduce a gene editor, you have to be able to stop it. You have to be able to go and correct the mutation, and then you have to stop that machinery from working because you don't want it to overdo its job. If it does so, it's going to continue to edit and edit and edit the genome, and then you have a problem.

What has now made gene editing possible in a human patient is mRNA. In the case of baby KJ [the first-ever recipient of a customized CRISPR treatment], the CRISPR technology was introduced as an mRNA. That is the critical feature that was necessary to get this to work. The beauty of the human body is that it makes mRNA and then it clears the mRNA; it gets it out. So by introducing the gene-editing technology as an mRNA, we could go in, get an effect for a very short period of time, and then let the body do what it normally does and get rid of it. So that was perfect to do on this little baby.

By undermining mRNA-based work, we're potentially limiting the ability to do this true personalized medicine approach of gene editing that could save millions of people's lives every year.

NL: How do you anticipate this divestment could affect pandemic preparedness in the U.S.?

JC: I actually think that these decisions were completely reckless in that regard and put America in significant harm's way, in terms of our national defense.

Through Donald Trump's leadership under Operation Warp Speed, we were able to identify a pathogen, have a sequence, make a possible vaccine, develop that in nine months, and deploy it to the American people in the next three months. That's unparalleled in human history. The reason why we're able to do that is because of the power of the mRNA platform, that it is so easy to develop and easy to produce at scale, and then easy to deploy to the greater population.

Traditional vaccines, meaning before the advent of mRNA vaccines, typically take between three to five years to develop. And you don't even know if it will be efficacious. If you have a pandemic, you do need a technology that can be rapidly deployed. Not continuing to investigate the usage of a technology that has proven itself is completely reckless and puts America and Americans in harm's way.

And the truth is that other countries recognize the power of mRNA vaccines and mRNA medicines and are doubling down on their investment — especially China. Quite frankly, if a pandemic comes out, we're going to be caught asking China for their vaccines.

NL: Do you think this could also prompt "vaccine tourism," in which Americans go abroad to get vaccinated?

JC: If there's a pandemic, like what might happen with avian flu, and we're not prepared, absolutely — if Canada has a vaccine, people are going to migrate north.

And you have to think about it even more broadly than that. The study that came from [Memorial] Sloan Kettering [Cancer Center] that showed such good efficacy on pancreatic cancer — if that research stops, and continues in Europe or in China and you're diagnosed with pancreatic cancer, you're going to go there. Right? So you can think about the different types of tourism outside of vaccine tourism, sort of medical tourism.

Related: 'Any protein you can imagine, it can deliver': AI will help discover the next breakthrough in RNA, says Nobel Prize winner Dr. Drew Weissman

NL: From an industry standpoint, what could these cuts mean for mRNA developers?

JC: First of all, you have other countries that are trying to recruit American companies to their shores through incentives. And they're trying to do the same with scientists through easy pathways to citizenship and grant and funding mechanisms. In addition to moving their brick-and-mortar operations overseas, these American companies will start developing drugs that are specific to other countries. There are viruses that are more resident in South America; the market in the United States just doesn't make sense, but we could easily sell those drugs to Brazil, for example.

That's what I think will happen in the short course. These companies will start making drugs and marketing them to other countries. But then, in the long term, they actually will move brick and mortar.

NL: Are there other impacts that you anticipate these cuts having?

JC: I think that this will certainly impact America's leadership in biomedical discovery. We're going to lose an entire generation of scientists through these types of actions.

Let's not fool ourselves: mRNA is one of the three most important molecules in the body, with the other two being DNA and protein. It's the intermediary between them. When the federal government sends a message that mRNA-based medicine and research is not wanted, you're basically saying that there's a whole branch of science that is no longer welcome within the U.S.

So if you're a young individual thinking about going to graduate school and becoming a scientist to try and use your talents to improve human health, you may not do that. You may not do that in the United States, at least. So I think the United States is going to fall dramatically behind in its leadership in biotech.

We're going to see, over the next five to 10 years, a significant brain drain, where other countries build up their infrastructure, and new scientists are not trained in the United States, and preexisting scientists flee.

NL: What's something you hope the public understands about these funding cuts and mRNA?

JC: I think that most Americans don't understand that mRNA is a natural substance, a natural part of your body. Every cell in your body has mRNA — thousands of copies of mRNA.

With mRNA-based medicines, we're not doing something that is dangerous or reckless. What we're doing as medical professionals is we're actually taking advantage of a natural system that exists within your body and using your body to help itself. It's really quite remarkable that we're able to do this. All we are doing is taking advantage of that remarkable system that preexists.

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

High-ranking federal officials have suggested that bird flu virus should be left to "rip" through poultry farms across the U.S. — but experts warn that this hands-off approach could hasten the beginning of a new pandemic

Robert F. Kennedy Jr., the secretary of Health and Human Services, and Brooke Rollins, secretary of Agriculture, have floated the notion that instead of culling birds infected with the highly pathogenic H5N1 virus, farmers should let it spread through flocks. The idea is that by doing this, farmers can "identify the birds, and preserve the birds, that are immune to it," Kennedy told Fox News on March 11.

Now, a perspective piece authored by a group of virologists, veterinarians and health security experts argues that the plan would not only be ineffective, but could also increase the risk of the virus spilling over into humans and sparking a new pandemic. The researchers published their arguments July 3 in the journal Science.

"Essentially, the longer you allow a virus that has shown to be effective in infecting multiple hosts survive in an environment, the greater the chance you give it to spread, to mutate, and to try its luck at adaptation," perspective first-author Erin Sorrell, a virologist at the Johns Hopkins Center for Health Security, told Live Science. "Worse case scenario, the virus adapts and expands its host range to become transmissible in humans … Now we have a pandemic."

Bird flu in the U.S.

H5N1 is a subtype of highly pathogenic avian influenza (HPAI), a type of bird flu that can cause severe disease and death in poultry and other birds. Since the virus began spreading widely among U.S. birds in January 2022, the Centers for Disease Control and Prevention (CDC) has reported that more than 174 million birds across all 50 states have been infected with the disease. The virus’s transmission among wild aquatic birds, commercial poultry and backyard, hobbyist flocks, has led to massive culls in farms and sent egg prices skyrocketing.

The virus typically transmits among wild birds and poultry, but it's known to have also infected more than 48 mammal species, including foxes, skunks, raccoons, seals and polar bears. It has also spread to dairy cattle, causing outbreaks in more than 1,000 herds across 17 U.S. states, according to current estimates.

Related: How to avoid bird flu

Isolated human cases have been reported amid the ongoing outbreak in animals, primarily among farm workers, according to the CDC, although the agency states that the current health risk to the general public remains low. This is because, while the disease can spread among different animals, it currently can't be passed from human to human.

Federal plans

Rollins recently issued updates about the U.S. government's plan to combat the infection's spread and lower egg prices. The five-pronged strategy denotes $500 million to improve farm biosecurity, $400 million in financial aid to farmers and $100 million for vaccine research. The government is also exploring ways to slash regulations and increase temporary import options for eggs.

Current regulations state that when infections are detected among commercial poultry, farmers must cull the affected flocks to contain the disease's spread, for which they are financially compensated by the U.S. Department of Agriculture (USDA).

Yet officials have been suggesting more radical ways to manage bird flu, leaving experts concerned. In May, Kennedy and Dr. Mehmet Oz, the administrator for the U.S. Centers for Medicare and Medicaid Services, voiced their support for the owners of a Canadian ostrich farm whose 398 birds faced a cull following confirmed cases of H5N1 bird flu in December 2024 and January this year.

"We believe significant scientific knowledge may be garnered from following the ostriches in a controlled environment," Kennedy wrote in a letter posted to the social platform X and addressed to the head of the Canadian Food Inspection Agency, which had ordered the cull. Kennedy suggested that the ostriches may have already acquired some "downstream immunity" to the virus, and Oz offered to relocate the birds to his Florida ranch for further study.

Sorrel told Live Science that these statements imply "there is still an expectation that those in the Trump administration, at least on the human health side, believe this approach has merit."

But Sorrel and her report collaborators disagree.

Allowing widespread infection of commercial flocks would kill billions of birds, drive poultry and egg prices up, as well as destabilize local economies and global trade through import restrictions imposed on U.S. products, the authors wrote. Simultaneously, it could also foster reservoirs of H5N1, increasing the virus' odds of making the leap to humans — and gaining the ability for human-to-human infection.

"Rapid culling of [H5N1] positive flocks is central to containment of the virus on a farm," Sorrel said. "Poultry infected with H5 shed a tremendous amount of virus. If effective controls designed to mitigate the quantity of viral shedding and known transmission pathways are removed, the exposure risk for other animals and humans on site and on neighboring farms will increase, and the opportunity for H5 to evolve to be a more effective poultry pathogen increases."

Kennedy's proposal is also very unlikely to work the way he's claimed it would — the birds that provide eggs and meat on farms are descendants of separate breeding populations and do not breed themselves. So even if there were a population of resilient birds that survived H5N1 infection, that doesn't mean they're passing on their genetic traits to a subsequent generation.

What's more, the mortality rate of H5N1 is extremely high among common poultry, reaching 100% in domestic chickens.

What experts propose

Instead of letting bird flu tear through farms, the scientists propose that government agencies should enhance surveillance of the virus' spread, along with improving data sharing and outbreak response measures shared between poultry producers, industry members and veterinarians. The USDA should not work alone on these measures, Sorrel said, as "interdisciplinary teams need to have the authority and means by which to activate at the state and federal levels."

Other experts agree with the team's suggestions, although they highlighted areas that need further discussion. Dr. Rocio Crespo, a poultry veterinarian at the North Carolina State University College of Veterinary Medicine, told Live Science that further details on potential vaccine strategies and biosecurity at farms should be explored.

But the USDA is now facing billions of dollars in federal funding cuts, and Crespo says that providing economic support to farmers facing outbreaks — alongside making investments to understand bird flu evolution, preventive measures and control methods — could become increasingly difficult.

"The current policies on poultry farms are effective at preventing spread to other farms," Crespo told Live Science. "However, the USDA's approach does not consider spill over and influences from other crop or animal agricultural activities."

"It appears we are continuing with the same strategies without sufficient improvement," she added. "Greater transparency and collaboration is crucial."

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

On March 20, 2025, members of the World Health Organization adopted the world's first pandemic agreement, following three years of "intensive negotiations launched by governments in response to the devastating impacts of the COVID-19 pandemic." The U.S., however, did not participate, in part because of its intention to withdraw from the WHO.

Global health experts are hailing the agreement as a historic moment.

What does the agreement mean for the world, and how can it make everyone safer and more prepared for the next pandemic?

The Conversation asked Nicole Hassoun, a professor at Binghamton University and executive director of Global Health Impact, to explain the pandemic accord, its prospects for advancing global health, and the significance of the U.S.'s absence from it.

What more should be done, and does the U.S. have a role to play?

In my view, the best way to protect public health moving forward is for countries to sign on to the agreement and devote more resources to global health initiatives. This is particularly important given declining investment and participation in the WHO and the contraction of other international health initiatives, such as USAID.

Without international coordination, it will become harder to catch and address problems early enough to prevent epidemics from becoming pandemics.

It will also be imperative for member countries to provide funding to support the agreement's goals and secure the innovation and access to new technologies. This requires building the basic health infrastructure to ensure shots can get into people's arms.

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

Disease forecasts are like weather forecasts: We cannot predict the finer details of a particular outbreak or a particular storm, but we can often identify when these threats are emerging and prepare accordingly.

The viruses that cause avian influenza are potential threats to global health. Recent animal outbreaks from a subtype called H5N1 have been especially troubling to scientists. Although human infections from H5N1 have been relatively rare, there have been a little more than 900 known cases globally since 2003 — nearly 50% of these cases have been fatal — a mortality rate about 20 times higher than that of the 1918 flu pandemic. If the worst of these rare infections ever became common among people, the results could be devastating.

Approaching potential disease threats from an anthropological perspective, my colleagues and I recently published a book called "Emerging Infections: Three Epidemiological Transitions from Prehistory to the Present" to examine the ways human behaviors have shaped the evolution of infectious diseases, beginning with their first major emergence in the Neolithic period and continuing for 10,000 years to the present day.

Related: How to avoid bird flu

Viewed from this deep time perspective, it becomes evident that H5N1 is displaying a common pattern of stepwise invasion from animal to human populations. Like many emerging viruses, H5N1 is making incremental evolutionary changes that could allow it to transmit between people. The periods between these evolutionary steps present opportunities to slow this process and possibly avert a global disaster.

Spillover and viral chatter

When a disease-causing pathogen such as a flu virus is already adapted to infect a particular animal species, it may eventually evolve the ability to infect a new species, such as humans, through a process called spillover.

Spillover is a tricky enterprise. To be successful, the pathogen must have the right set of molecular "keys" compatible with the host's molecular "locks" so it can break in and out of host cells and hijack their replication machinery. Because these locks often vary between species, the pathogen may have to try many different keys before it can infect an entirely new host species. For instance, the keys a virus successfully uses to infect chickens and ducks may not work on cattle and humans. And because new keys can be made only through random mutation, the odds of obtaining all the right ones are very slim.

Given these evolutionary challenges, it is not surprising that pathogens often get stuck partway into the spillover process. A new variant of the pathogen might be transmissible from an animal only to a person who is either more susceptible due to preexisting illness or more likely to be infected because of extended exposure to the pathogen.

Even then, the pathogen might not be able to break out of its human host and transmit to another person. This is the current situation with H5N1. For the past year, there have been many animal outbreaks in a variety of wild and domestic animals, especially among birds and cattle. But there have also been a small number of human cases, most of which have occurred among poultry and dairy workers who worked closely with large numbers of infected animals.

Epidemiologists call this situation viral chatter: when human infections occur only in small, sporadic outbreaks that appear like the chattering signals of coded radio communications — tiny bursts of unclear information that may add up to a very ominous message. In the case of viral chatter, the message would be a human pandemic.

Sporadic, individual cases of H5N1 among people suggest that human-to-human transmission may likely occur at some point. But even so, no one knows how long or how many steps it would take for this to happen.

Influenza viruses evolve rapidly. This is partly because two or more flu varieties can infect the same host simultaneously, allowing them to reshuffle their genetic material with one another to produce entirely new varieties.

These reshuffling events are more likely to occur when there is a diverse range of host species. So it is particularly concerning that H5N1 is known to have infected at least 450 different animal species. It may not be long before the viral chatter gives way to larger human epidemics.

Reshaping the trajectory

The good news is that people can take basic measures to slow down the evolution of H5N1 and potentially reduce the lethality of avian influenza should it ever become a common human infection. But governments and businesses will need to act.

People can start by taking better care of food animals. The total weight of the world's poultry is greater than all wild bird species combined. So it is not surprising that the geography of most H5N1 outbreaks track more closely with large-scale housing and international transfers of live poultry than with the nesting and migration patterns of wild aquatic birds. Reducing these agricultural practices could help curb the evolution and spread of H5N1.

People can also take better care of themselves. At the individual level, most people can vaccinate against the common, seasonal influenza viruses that circulate every year. At first glance this practice may not seem connected to the emergence of avian influenza. But in addition to preventing seasonal illness, vaccination against common human varieties of the virus will reduce the odds of it mixing with avian varieties and giving them the traits they need for human-to-human transmission.

At the population level, societies can work together to improve nutrition and sanitation in the world's poorest populations. History has shown that better nutrition increases overall resistance to new infections, and better sanitation reduces how much and how often people are exposed to new pathogens. And in today's interconnected world, the disease problems of any society will eventually spread to every society.

For more than 10,000 years, human behaviors have shaped the evolutionary trajectories of infectious diseases. Knowing this, people can reshape these trajectories for the better.

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

In the days after President Trump ordered a pause on nearly all U.S. foreign aid, Secretary of State Marco Rubio suggested that scrutiny on the money the U.S. spends abroad is a matter of plain self-interest.

"Every dollar we spend, every program we fund, and every policy we pursue must be justified with the answer to three simple questions," Rubio said in a State Department press release. "Does it make America safer? Does it make America stronger? Does it make America more prosperous?"

One may take issue with such a narrow view of the value of foreign development assistance, which is essential to the survival of millions of people in regions affected by war, poverty and the impacts of human-caused climate change. But even by this narrow standard, the Trump administration's reckless dismantling of U.S. foreign aid programs makes no sense. In fact, it fails all three of Rubio's tests, making America weaker, less safe, and more prone to shocks that could cripple our economy.

Nowhere is the short-sightedness of the administration's strategy clearer than in the havoc it has brought on the U.S. Agency for International Development. USAID provides development assistance in more than 120 countries, funding projects that bring health services, education, food and clean water to vulnerable communities across the globe. From building schools to aiding in recovery from natural disasters, its work contributes in important ways to the health and economic development of regions that are prone to poverty, conflict, displacement and the political extremism that can often accompany social and economic disparity.

In terms of direct and tangible benefits to the U.S., one of USAID's most critical functions is to fight the spread of infectious diseases that have the capacity to spark a global pandemic. In 2014, for example, USAID deployed teams in West Africa to coordinate the response to a fast-growing Ebola outbreak. A significant part of that response was the establishment of screening protocols for people traveling from the affected region, a key measure in preventing an Ebola crisis in the U.S., which recorded only 11 Ebola cases in that year.

Such pandemic threats have not gone away. Ebola cases are rising in Uganda, and Tanzania recently experienced a deadly outbreak of Marburg virus, which causes severe hemorrhagic fever. Last August, an outbreak of mpox in the Democratic Republic of the Congo triggered the World Health Organization to declare an international public health emergency, signaling renewed concern about a virus that spread to 122 countries in a 2022 outbreak.

Related: Trump executive order calls mental health prescriptions a 'threat' — why?

In other parts of the world, USAID is a critical player in efforts to identify novel forms of avian influenza and other pathogens that have the potential to cause a future pandemic. As part of maintaining this global early warning system, the agency has funded labs and surveillance protocols in more than 30 countries, an investment of more than $900 million in 2023.

While much of this work is carried out far from the U.S., infectious diseases know no borders, and we have seen countless instances of viruses that arise in one part of the world but quickly find their way to other countries. The best way to prevent an epidemic in our own country is to control it at its source.

What is disappearing is our ability to react to such global health threats. USAID had been leading efforts to respond to the mpox crisis in the DRC, committing more than $55 million to orchestrate efforts to screen for the virus and distribute vaccines. However, among the many devastating impacts of President Trump's foreign aid freeze is that this work has stopped. All but six of USAID's 50 staff dedicated to global outbreaks have been fired, and on-the-ground disease response teams have been sent home.

The abrupt withdrawal of staff and financial support has left underresourced health systems such as the DRC's on the brink of collapse, unable to provide even basic health services. These disruptions continue to affect even the programs permitted to continue under the administration's narrow waivers for life-saving interventions.

The administration's announced order to cancel more than 90% of USAID's foreign contracts, effectively cutting nearly $60 billion in assistance, will only deepen these risks. According to USAID documents obtained by Propublica, discontinuation of the agency's services is predicted to lead to surges in cases of malaria and drug-resistant tuberculosis. One million more children will suffer severe malnutrition, and 200,000 more will be paralyzed by polio, according to the report.

In dozens of countries around the world, clinics that provide antiretroviral medications to 20 million people living with HIV — most of which rely on USAID for administrative and logistical support through PEPFAR (U.S. President's Emergency Plan for AIDS Relief) — have been shuttered. According to our research, even just a 90-day interruption in these services will lead to an additional 100,000 HIV-related deaths this year, threatening more than two decades of progress toward ending the global epidemic of HIV and AIDS.

For decades, U.S. leaders on both sides of the political spectrum have recognized the strategic value of these efforts. President John F. Kennedy, who launched USAID in 1961, described foreign aid as "a very powerful source of strength" for the U.S., allowing the country "to exert influence in the maintenance of freedom." Four decades later, President George W. Bush made historic investments in global health a centerpiece of his national security agenda, launching both PEPFAR, the largest commitment to fight a disease in our history, and the President's Malaria Initiative.

These presidents, like countless other leaders over the years, understood that working to secure the health and prosperity of other countries is, in fact, a direct investment in our own national health and prosperity. By contrast, what we see today is a haphazard retreat that will inevitably result in a world that is sicker, less stable and perilously exposed to threats such as climate change or a future infectious disease outbreak. We need only to look at the COVID-19 pandemic to understand how a health crisis that emerges in one part of the world can impact lives and economies across the globe. It is a dangerous strategy, and one for which we all may pay dearly.

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 close relative of the deadly Nipah and Hendra viruses has been detected in North America for the first time — specifically, in the U.S. state of Alabama.

The pathogen, which scientists have named Camp Hill virus, was detected in four northern short-tailed shrews (Blarina brevicauda). The animals were caught in 2021 near a town of the same name in Tallapoosa County, Alabama. After being captured for a study, the animals had been dissected and their organs frozen for later analyses; it was in those analyses that the virus was discovered.

Camp Hill virus is a type of henipavirus, a broad group of viruses that typically infect bats but have been known to "spill over" into various mammals, including humans. In people, henipaviruses can cause severe respiratory illness and a type of inflammation of the brain known as encephalitis.

Prominent henipaviruses known to infect humans include Hendra virus and Nipah virus. The former virus was first detected in Australia in 1994 and has a case-fatility rate of around 60%. The latter germ has caused disease outbreaks across Southeast Asia since being initially detected in Malaysia in 1998, and it kills between 40% and 70% of people infected.

Related: Deadly Nipah virus kills boy in India, prompts worries over outbreak

The detection of Camp Hill virus is significant because it marks the first time a henipavirus has been detected in North America. That's according to the scientists who discovered it, who released a paper Jan. 17 in the journal Emerging Infectious Diseases.

The discovery raises concerns that henipaviruses may be more widespread than once thought. In particular, it provides evidence that B. brevicauda shrews — which can be found across central and eastern North America — can harbor these types of viruses, along with other germs already confirmed to cause human disease. It's possible that Camp Hill virus may pose a risk to humans, perhaps spreading through direct contact with infected animals or their feces and urine, the researchers suggested.

However, despite these possible concerns, the authors of the new paper have cautioned against leaping to such conclusions.

"There is no evidence to suggest that the provisionally named Camp Hill virus has infected humans, and the likelihood of it doing so remains unknown but is likely low," lead study author Rhys Parry, a molecular virologist at the University of Queensland in Australia, told Live Science in an email.

Although Camp Hill virus belongs to the same genus as Hendra and Nipah viruses — called Henipavirus — it is genetically distinct from both of them, he emphasized. By comparison, Camp Hill virus is more closely related to other shrew-borne henipaviruses seen in Southeast Asia and Europe than bat-borne henipaviruses like Hendra and Nipah, he said.

This distinction is key because bat-borne henipaviruses tend to infect a wider range of hosts and cause them more harm, and they've been known to cause severe disease outbreaks in people, he said.

So far, only one other shrew-borne henipavirus has been identified, and that is Langya virus, Parry said. This virus infected 35 people in China between 2018 and 2021, causing symptoms such as fever, fatigue and cough and in rarer cases, impaired liver and kidney function. But importantly, no deaths were reported.

It's currently unknown whether the B. brevicauda shrews in North America are able to spread Camp Hill virus to humans. They usually inhabit woodland areas where direct encounters with humans would be somewhat rare, the study authors wrote.

Notably, B. brevicauda shrews have been found to carry other viruses that can potentially spill over to people, but these have never made the leap from these critters to humans.

"Given that B. brevicauda shrews already host other zoonotic viruses, such as Powassan virus and Camp Ripley virus, and that veterinary professionals already handle them with appropriate biosafety measures, no additional precautions are required," Parry said.

Future research should instead focus on trying to isolate the Camp Hill virus and decipher how many types of animals it can and has infected, he said. This information could then be used to better assess the potential risk of a spillover to humans.

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

A strain of bird flu never seen before in the United States has been detected among poultry at a California farm.

The virus, called highly pathogenic H5N9, is a type of avian influenza, otherwise known as "bird flu." This is not the same type of bird flu that's already been spreading on dairy cow and poultry farms in the U.S., causing at least several dozen infections in humans. That virus is called H5N1.

So what is H5N9? How does it differ from H5N1, and should we be equally concerned about it?

Related: Bird flu strikes 1st child in the US — CDC says infection source unknown

What is H5N9?

H5N9 is a highly pathogenic avian flu (or bird flu) virus that bears some structural similarities to H5N1.

"Low pathogenic" H5N9 viruses have previously been detected in birds in the U.S. and elsewhere in the world, dating back to the 1960s. However, these infections are usually associated with less-severe symptoms than "highly pathogenic" strains are. This is the first time highly pathogenic H5N9 has been seen in the U.S., and these deadlier strains are also fairly uncommon worldwide.

How did H5N9 emerge?

New subtypes and strains of influenza can emerge if viruses pick up random genetic mutations as they multiply, as well as if multiple viruses swap genetic information with one another. This latter process is known as genetic reassortment, and it usually happens when an organism is infected with at least two different viruses at the same time.

Some experts suspect that H5N9 may have emerged among the ducks in California due to genetic reassortment occurring between circulating H5N1 viruses and other flu viruses containing the N9 protein. ("H5" and "N9" are two proteins found on the surface of the virus that give the bird flu subtype its name.)

H5N1 was also detected in the birds at the farm, so this could be plausible, according to a Jan. 24 report from the World Organisation for Animal Health (WOAH), which monitors disease outbreaks in animals worldwide.

Such reassortment can lead to "unpredictable new viruses," Angela Rasmussen, a virologist at the University of Saskatchewan in Canada, wrote on X.

She added that ducks may be great host animals for genetic reassortment to take place because, unlike chickens, they don't get very sick from many avian flu viruses. Therefore, while an infected chicken would quickly die, ducks can survive and continue to spread the disease to new hosts.

Related: How to avoid bird flu

What's happening at the farm where H5N9 was detected?

In the Jan. 24 report, the WOAH announced that H5N9 had been identified at a duck farm in Merced County, California. The current outbreak, which the report says was confirmed on Jan. 13, is being closely monitored by officials.

"The USDA Animal and Plant Health Inspection Service (APHIS), in conjunction with State Animal Health and Wildlife Officials, are conducting comprehensive epidemiological investigations and enhanced surveillance in response to the HPAI [highly pathogenic avian influenza] related events," the WOAH wrote in the report.

To prevent further spread of the infection, all of the nearly 119,000 birds at the farm have now been culled. These bird flu viruses are known as "highly pathogenic" because they are extremely deadly to certain poultry — like chickens — and culling an exposed flock is typically considered the best way of preventing additional flocks from getting sick.

Why is bird flu concerning?

Scientists have recently expressed increasing concern that a strain of bird flu could mutate into a form that easily spreads among humans, sparking a pandemic. This happened during historic pandemics, such as the "Spanish flu" in 1918 and the "Asian flu" in 1957.

Humans can become infected with avian influenza if the virus gets into their eyes, nose or mouth, or if it is inhaled in the form of droplets in the air. However, not all bird flu viruses are equipped to efficiently infect people and then spread between them. When given more chances to spread to new animals, the viruses have a higher chance of picking up that ability and harming humans.

Notably, over the past couple of years, H5N1 has spread to new countries, including the U.S. It's been widely infecting wild birds and poultry and has also jumped into various mammals, including cattle and domestic cats. Since its discovery, H5N1 has infected more than 900 people globally, and in the past year, at least 67 people in the U.S. have been infected. In December 2024, a woman in Louisiana became the first person in the U.S. to die as a result of an H5N1 infection.

Related: Bird flu could become deadlier if it mixes with seasonal flu viruses, experts warn

How does H5N9 differ from H5N1?

Avian influenza viruses come in different subtypes, which are named according to subtle variations in the structure of two key proteins on the surface of the virus: hemagglutinin (H) and neuraminidase (N). So H5N9 and H5N1 have the same hemagglutinin protein, but a different neuraminidase protein.

A virus's specific combination of H and N proteins determines a range of important traits, such as how good it is at spreading from one animal to another, how deadly it is, and whether it is resistant to antiviral treatment.

Besides the difference in their neuraminidase proteins, H5N9 differs from H5N1 in several other ways.

For example, H5N1 infections are more common among humans and are believed to be the deadliest of all the highly pathogenic avian influenza strains in humans and chickens.

Does H5N9 pose a risk to humans?

As of yet, little is known about whether H5N9 could spread to humans and potentially cause a pandemic.

On its website, the Centers for Disease Control and Prevention (CDC) currently states that the public health risk from H5 bird flu is "low" but that the agency is "watching the situation carefully and working with states to monitor people with animal exposures." The CDC's primary focus on that webpage is H5N1, but the agency is monitoring H5 viruses broadly, using its flu surveillance systems to watch for any cases in humans.

As of Jan. 18, there has been no evidence of H5 bird flu spreading from one human to another in the U.S.

"The combination H5N9 is not new and other versions, like H5N5 also exist," Florian Krammer, a professor of vaccinology at the Icahn School of Medicine at Mount Sinai in New York, told CBS News. "Just because this was now detected, doesn't mean trouble necessarily," he emphasized.

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

Before the COVID pandemic, the World Health Organization (WHO) had made a list of priority infectious diseases. These were felt to pose a threat to international public health, but where research was still needed to improve their surveillance and diagnosis. In 2018, "disease X" was included, which signified that a pathogen previously not on our radar could cause a pandemic.

While it's one thing to acknowledge the limits to our knowledge of the microbial soup we live in, more recent attention has focused on how we might systematically approach future pandemic risks.

Former US Secretary of Defense Donald Rumsfeld famously talked about "known knowns" (things we know we know), "known unknowns" (things we know we don't know), and "unknown unknowns" (the things we don't know we don't know).

Although this may have been controversial in its original context of weapons of mass destruction, it provides a way to think about how we might approach future pandemic threats.

Influenza: a 'known known'

Influenza is largely a known entity; we essentially have a minor pandemic every winter with small changes in the virus each year. But more major changes can also occur, resulting in spread through populations with little pre-existing immunity. We saw this most recently in 2009 with the swine flu pandemic.

However, there's a lot we don't understand about what drives influenza mutations, how these interact with population-level immunity, and how best to make predictions about transmission, severity and impact each year.

The current H5N1 subtype of avian influenza ("bird flu") has spread widely around the world. It has led to the deaths of many millions of birds and spread to several mammalian species including cows in the United States and marine mammals in South America.

Human cases have been reported in people who have had close contact with infected animals, but fortunately there's currently no sustained spread between people.

While detecting influenza in animals is a huge task in a large country such as Australia, there are systems in place to detect and respond to bird flu in wildlife and production animals.

It's inevitable there will be more influenza pandemics in the future. But it isn't always the one we are worried about.

Attention had been focused on avian influenza since 1997, when an outbreak in birds in Hong Kong caused severe disease in humans. But the subsequent pandemic in 2009 originated in pigs in central Mexico.

Related: Never-before-seen antibodies can target many flu viruses

Coronaviruses: an 'unknown known'

Although Rumsfeld didn't talk about "unknown knowns", coronaviruses would be appropriate for this category. We knew more about coronaviruses than most people might have thought before the COVID pandemic.

We'd had experience with severe acute respiratory syndrome (SARS) and Middle Eastern respiratory syndrome (MERS) causing large outbreaks. Both are caused by viruses closely related to SARS-CoV-2, the coronavirus that causes COVID. While these might have faded from public consciousness before COVID, coronaviruses were listed in the 2015 WHO list of diseases with pandemic potential.

Previous research into the earlier coronaviruses proved vital in allowing COVID vaccines to be developed rapidly. For example, the Oxford group's initial work on a MERS vaccine was key to the development of AstraZeneca's COVID vaccine.

Similarly, previous research into the structure of the spike protein — a protein on the surface of coronaviruses that allows it to attach to our cells — was helpful in developing mRNA vaccines for COVID.

It would seem likely there will be further coronavirus pandemics in the future. And even if they don't occur at the scale of COVID, the impacts can be significant. For example, when MERS spread to South Korea in 2015, it only caused 186 cases over two months, but the cost of controlling it was estimated at US$8 billion (A$11.6 billion).

The 25 viral families: an approach to 'known unknowns'

Attention has now turned to the known unknowns. There are about 120 viruses from 25 families that are known to cause human disease. Members of each viral family share common properties and our immune systems respond to them in similar ways.

An example is the flavivirus family, of which the best-known members are yellow fever virus and dengue fever virus. This family also includes several other important viruses, such as Zika virus (which can cause birth defects when pregnant women are infected) and West Nile virus (which causes encephalitis, or inflammation of the brain).

The WHO's blueprint for epidemics aims to consider threats from different classes of viruses and bacteria. It looks at individual pathogens as examples from each category to expand our understanding systematically.

The US National Institute of Allergy and Infectious Diseases has taken this a step further, preparing vaccines and therapies for a list of prototype pathogens from key virus families. The goal is to be able to adapt this knowledge to new vaccines and treatments if a pandemic were to arise from a closely related virus.

Pathogen X, the 'unknown unknown'

There are also the unknown unknowns, or "disease X" — an unknown pathogen with the potential to trigger a severe global epidemic. To prepare for this, we need to adopt new forms of surveillance specifically looking at where new pathogens could emerge.

In recent years, there's been an increasing recognition that we need to take a broader view of health beyond only thinking about human health, but also animals and the environment. This concept is known as "One Health" and considers issues such as climate change, intensive agricultural practices, trade in exotic animals, increased human encroachment into wildlife habitats, changing international travel, and urbanization.

This has implications not only for where to look for new infectious diseases, but also how we can reduce the risk of "spillover" from animals to humans. This might include targeted testing of animals and people who work closely with animals. Currently, testing is mainly directed towards known viruses, but new technologies can look for as yet unknown viruses in patients with symptoms consistent with new infections.

We live in a vast world of potential microbiological threats. While influenza and coronaviruses have a track record of causing past pandemics, a longer list of new pathogens could still cause outbreaks with significant consequences.

Continued surveillance for new pathogens, improving our understanding of important virus families, and developing policies to reduce the risk of spillover will all be important for reducing the risk of future pandemics.

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

Pandemics — the global spread of infectious diseases — seem to be making a comeback. In the Middle Ages we had the Black Death (plague), and after the first world war we had the Spanish flu. Tens of millions of people died from these diseases.

Then science began to get the upper hand, with vaccination eradicating smallpox, and polio nearly so. Antibiotics became available to treat bacterial infections, and more recently antivirals as well.

But in recent years and decades pandemics seem to be returning. In the 1980s we had HIV/AIDS, then several flu pandemics, SARS, and now COVID (no, COVID isn't over).

So why is this happening, and is there anything we can do to avert future pandemics?

Related: 32 diseases you can catch from animals

Unbalanced ecosystems

Healthy, stable ecosystems provide services that keep us healthy, such as supplying food and clean water, producing oxygen, and making green spaces available for our recreation and wellbeing.

Another key service ecosystems provide is disease regulation. When nature is in balance — with predators controlling herbivore populations, and herbivores controlling plant growth — it's more difficult for pathogens to emerge in a way that causes pandemics.

But when human activities disrupt and unbalance ecosystems — such as by way of climate change and biodiversity loss — things go wrong.

For example, climate change affects the number and distribution of plants and animals. Mosquitoes that carry diseases can move from the tropics into what used to be temperate climates as the planet warms, and may infect more people in the months that are normally disease free.

We've studied the relationship between weather and dengue fever transmission in China, and our findings support the same conclusion reached by many other studies: climate change is likely to put more people at risk of dengue.

Biodiversity loss can have similar effects by disrupting food chains. When ranchers cleared forests in South America for their cattle to graze in the first half of the 20th century, tiny forest-dwelling, blood-feeding vampire bats suddenly had a smörgåsbord of large sedentary animals to feed on.

While vampire bats had previously been kept in check by the limited availability of food and the presence of predators in the balanced forest ecosystem, numbers of this species exploded in South America.

These bats carry the rabies virus, which causes lethal brain infections in people who are bitten. Although the number of deaths from bat-borne rabies has now fallen dramatically due to vaccination programs in South America, rabies caused by bites from other animals still poses a global threat.

As urban and agricultural development impinges on natural ecosystems, there are increasing opportunities for humans and domestic animals to become infected with pathogens that would normally only be seen in wildlife — particularly when people hunt and eat animals from the wild.

The HIV virus, for example, first entered human populations from apes that were slaughtered for food in Africa, and then spread globally through travel and trade.

Meanwhile, bats are thought to be the original reservoir for the virus that caused the COVID pandemic, which has killed more than 7 million people to date.

Ultimately, until we effectively address the unsustainable impact we are having on our planet, pandemics will continue to occur.

Targeting the ultimate causes

Factors such as climate change, biodiversity loss and other global challenges are the ultimate (high level) cause of pandemics. Meanwhile, increased contact between humans, domestic animals and wildlife is the proximate (immediate) cause.

In the case of HIV, while direct contact with the infected blood of apes was the proximate cause, the apes were only being slaughtered because large numbers of very poor people were hungry — an ultimate cause.

The distinction between ultimate causes and proximate causes is important, because we often deal only with proximate causes. For example, people may smoke because of stress or social pressure (ultimate causes of getting lung cancer), but it's the toxins in the smoke that cause cancer (proximate cause).

Generally, health services are only concerned with stopping people from smoking — and with treating the illness that results — not with removing the drivers that lead them to smoke in the first place.

Similarly, we address pandemics with lockdowns, mask wearing, social distancing and vaccinations — all measures which seek to stop the spread of the virus. But we pay less attention to addressing the ultimate causes of pandemics — until perhaps very recently.

A planetary health approach

There's a growing awareness of the importance of adopting a "planetary health" approach to improve human health. This concept is based on the understanding that human health and human civilisation depend on flourishing natural systems, and the wise stewardship of those natural systems.

With this approach, ultimate drivers like climate change and biodiversity loss would be prioritised in preventing future pandemics, at the same time as working with experts from many different disciplines to deal with the proximate causes, thereby reducing the risk overall.

The planetary health approach has the benefit of improving both the health of the environment and human health concurrently. We are heartened by the increased uptake of teaching planetary health concepts across the environmental sciences, humanities and health sciences in many universities.

As climate change, biodiversity loss, population displacements, travel and trade continue to increase the risk of disease outbreaks, it's vital that the planetary stewards of the future have a better understanding of how to tackle the ultimate causes that drive pandemics.

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

Dozens of people in the United States have caught bird flu from animals this year, but there's no evidence that the viral disease has spread from one person to another. However, a single mutation in the virus could make human-to-human spread possible, a new study finds.

This genetic change would make the virus a much better "match" for cells in humans' airways; it would enable a protein on the surface of the virus to fit snugly into a receptor found on human cells. That would allow the virus to infect those cells more easily — and make it more likely to spark a pandemic.

"In order to get sufficient infection, the virus needs to very efficiently attach to the cells in the airway," said Jim Paulson, a biochemist at The Scripps Research Institute in La Jolla, California, and co-senior author of the study. "In fact, it's believed that transmission [between people] cannot occur until the virus has acquired the human-type receptor specificity."

Currently, the circulating bird flu virus — called H5N1 — is a much better match for bird receptors. The new study, published Thursday (Dec. 5) in the journal Science, essentially explored what it would take for the virus to switch its preference to people.

Related: How to avoid bird flu

Pandemic potential

As of Dec. 4, the Centers for Disease Control and Prevention has confirmed 58 H5N1 infections among people in the U.S. The virus has also been circulating among wild birds, poultry and cattle in the country. Most of the confirmed human infections — about 60% — have been linked to exposure to infected cattle, while 36% have been associated with birds. The two remaining infections have no known source, but they're also suspected to have originated in animals.

So far, the human cases in the U.S. have been mild, triggering eye redness or a cough, at most. However, a teen infected in Canada has had more severe symptoms, and historically, H5N1 infections have been deadly in hundreds of cases. So there's a concern that the strain circulating in the U.S. could evolve to become deadlier, more transmissible, or both.

But how is H5N1 infecting people now, if it's not a good match for humans? "When the virus is coming from an infected animal, like birds or from cows, it's a very high concentration of virus," Paulson told Live Science. So, even if the virus is not a perfect match, the sheer number of viral particles entering the person's body can still lead to infection, he said.

To then jump to another person, though, the virus would need to be a better match. That's because, when a respiratory virus spreads between people, it's typically passed in tiny droplets expelled from the infected person's mouth. These droplets carry a relatively low concentration of virus.

Related: Bird flu strikes 1st child in the US — CDC says infection source unknown

To probe how H5N1 might become a good match, the researchers looked at the genetic code of the virus that infected the first person ever known to catch bird flu from a cow. They zeroed in on the code for hemagglutinin (HA), a protein the virus needs to infect cells.

"What we're looking at is a protein that comes from a virus, but it's isolated," said co-senior author Ian Wilson, a structural biologist at Scripps. The team didn't work with whole viruses in the lab, he clarified.

When the researchers looked at how well the isolated HA protein plugged into bird receptors compared with human ones, they found that the existing version had "strong avian-type specificity." They then introduced mutations, triggering changes in the part of HA that directly interacts with receptors.

They found that a single mutation — called the Gln226Leu substitution — can "completely switch" the virus's preference, making it a match for humans instead of birds. The mutant virus still didn't bind to human cells quite as well as it had to bird cells, but the switch in its preference was "nevertheless clear and pronounced" across different tests. Adding a second mutation — Asn224Lys — did tighten the virus's grip, though.

That Gln226Leu mutation had been flagged in previous studies of H5N1, which also hinted that it could boost the virus's ability to infect humans. However, most previous studies found that the HA would need multiple mutations to completely switch its preference, the researchers noted in their report. In this case, it seems just one mutation is sufficient.

The switch to human receptors is a major factor that could give an animal virus the potential to spark a human pandemic, the authors noted. For that reason, scientists should look out for the Gln226Leu mutation as they continue to track the spread of H5N1, the study suggests.

Related: H5N1 bird flu is evolving to better infect mammals, CDC study suggests

For now, "the particular mutation that we're reporting in this paper has not yet been reported in a database," Wilson said. The recent Canadian case may have some notable mutations in the HA protein, at least according to informal discussions among scientists on social media, Paulson said. For now, though, "it's a little premature to talk about that particular case," he added.

Ultimately, more human H5N1 infections would make the Gln226Leu mutation more likely to crop up. "The more people that get infected, the more likelihood is that … that mutation will get selected for," Wilson told Live Science. "When there's very few people infected, there's less likelihood of that mutation coming up."

The study didn't consider all of the factors that could give H5N1 pandemic potential. A second viral protein, called neuraminidase, also plays an important role, as does the pH that the virus needs to fuse to and get inside cells. With the Northern Hemisphere's flu season ramping up, there's a possibility that H5N1 could infect a person who is already infected with seasonal flu. From there, those two viruses could swap genes, thus opening the door for H5N1 to pick up genes that might help it adapt to humans.

"Genes from the previous human virus — they're already adapted to humans," Paulson said. "Therefore, the mutation of the hemagglutinin becomes a key factor in the success of the virus."

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H5N1 bird flu is getting better at spreading between mammals but does not yet spread as easily as seasonal flu, a Centers for Disease Control and Prevention (CDC) study suggests.

H5N1 has been detected in at least 46 people in the U.S. this year, causing only mild illnesses so far. The CDC maintains that the virus still poses little risk to the general public, but as a precaution, scientists have explored whether the avian virus has adapted to infect mammals.

H5N1 has been detected in about 50 mammal species, including cattle. The question is how adept the avian virus is at infecting mammals, and how easily it can spread when it jumps into a new species, like humans. In the ongoing outbreak, researchers haven't found any examples of human-to-human transmission, but they're watching out for signs.

In the new study, published Oct. 28 in the journal Nature, the CDC used ferrets because the animals are susceptible to human influenza and display similar symptoms.

Related: 'Playing Russian roulette with your health': Officials warn that social media trend of consuming raw milk will not protect you from bird flu

"Because they expel virus into the air, they have been used as a model system to study airborne transmission," said Seema Lakdawala, an influenza virologist at Emory University who was not involved with the study but collaborates with the CDC on other projects. The lungs of humans and ferrets bear a similar distribution of receptors that the virus can use to enter cells, Lakdawala noted.

The study showed H5N1 transmits easily between ferrets under certain circumstances, suggesting it could spread between other mammals.

"It doesn't mean that because the virus transmits in ferrets, it will transmit in humans," said Troy Sutton, a veterinary researcher at Penn State who was not involved with the study. Rather, it shows that the virus may be gaining in its ability to spread between mammals, he clarified.

Deadly disease

The CDC researchers used an H5N1 virus sampled from a dairy farmworker in Texas, who caught one of the first human cases this year. This virus bore a mutation called E627K, which has been linked to the flu pandemics that took place in 1918, 1957 and 1968, Sutton told Live Science.

E627K changes a protein that helps the virus replicate, enabling it to do so more efficiently at colder temperatures, Sutton explained. Human body temperature tends to be a few degrees Celsius lower than birds', so this mutation plays a role in helping bird flu viruses infect humans.

Surveillance has not found any further cases in humans or mammals involving this mutation, Lakdawala said. But the CDC has studied its effects on ferrets in case it reappears.

When scientists deposited H5N1 directly into ferrets' noses, the animals developed severe symptoms — such as diarrhea, difficulty breathing and fever — and, in some cases, they died. By contrast, the infections among people in the U.S. have been quite mild, with minor symptoms, like eye redness.

Related: 21-year-old student dies of H5N1 bird flu in Vietnam

One possible explanation is that researchers administered millions of virus particles to the ferrets, which Sutton said is standard practice for flu studies in ferrets.

"It is probably higher than what a person would receive if they were exposed in a room to somebody with human influenza," he said. However, he added that a milliliter of unpasteurized cow milk can carry 100 times more virus than the ferrets received, so it's possible that farmworkers may be exposed to higher doses.

Humans also have preexisting immunity to related flu strains that afford them some protection, whereas the ferrets in this study grew up on flu-free farms. In a paper that hasn't yet been peer-reviewed, Lakdawala found that ferrets with immunity to the 2009 H1N1 virus — better known as "swine flu" — show some immunity to H5N1.

Efficient transmission

Scientists aren't certain how farmworkers catch the virus. It could be through the direct handling of animals, airborne transmission, or contact with contaminated surfaces, like milking equipment. The CDC studied all three possibilities in ferrets.

By pairing an infected ferret with a healthy ferret in the same cage, they studied direct contact. "Ferrets are very social animals. They nuzzle each other and snuggle," Lakdawala said. They tested direct contact for three ferret pairs and found that transmission and severe disease occurred in each case.

By moving a healthy ferret to a cage previously occupied by an infected one, the researchers explored transmission from contaminated surfaces, such as cage walls, bedding, food and water. To test airborne spread, they placed infected and healthy ferrets in adjacent cages separated by a perforated wall that allowed airborne viruses through. Neither of these routes of transmission were as efficient as direct contact, with a fraction of the ferrets remaining uninfected.

This study provides insight into the potential severity and transmission of H5N1. However, Lakdawala noted that it doesn't account for the complexities of the human immune system or human behavior, nor do these types of cage experiments assess the possibility of spread over both long and short distances.

She said it will be important to study H5N1 viruses collected from other human patients to see if the behavior of the virus changes as its genetics do.

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In my research focused on early farmers of Europe, I have often wondered about a curious pattern through time: Farmers lived in large dense villages, then dispersed for centuries, then later formed cities again, only to abandon those as well. Why?

Archaeologists often explain what we call urban collapse in terms of climate change, overpopulation, social pressures or some combination of these. Each likely has been true at different points in time.

But scientists have added a new hypothesis to the mix: disease. Living closely with animals led to zoonotic diseases that came to also infect humans. Outbreaks could have led dense settlements to be abandoned, at least until later generations found a way to organize their settlement layout to be more resilient to disease. In a new study, my colleagues and I analyzed the intriguing layouts of later settlements to see how they might have interacted with disease transmission.

Earliest cities: Dense with people and animals

Çatalhöyük, in present-day Turkey, is the world's oldest farming village, from over 9,000 years ago. Many thousands of people lived in mud-brick houses jammed so tightly together that residents entered via a ladder through a trapdoor on the roof. They even buried selected ancestors underneath the house floor. Despite plenty of space out there on the Anatolian Plateau, people packed in closely.

For centuries, people at Çatalhöyük herded sheep and cattle, cultivated barley and made cheese. Evocative paintings of bulls, dancing figures and a volcanic eruption suggest their folk traditions. They kept their well-organized houses tidy, sweeping floors and maintaining storage bins near the kitchen, located under the trapdoor to allow oven smoke to escape. Keeping clean meant they even replastered their interior house walls several times a year.

These rich traditions ended by 6000 BCE, when Çatalhöyük was mysteriously abandoned. The population dispersed into smaller settlements out in the surrounding flood plain and beyond. Other large farming populations of the region had also dispersed, and nomadic livestock herding became more widespread. For those populations that persisted, the mud-brick houses were now separate, in contrast with the agglomerated houses of Çatalhöyük.

Was disease a factor in the abandonment of dense settlements by 6000 BCE?

At Çatalhöyük, archaeologists have found human bones intermingled with cattle bones in burials and refuse heaps. Crowding of people and animals likely bred zoonotic diseases at Çatalhöyük. Ancient DNA identifies tuberculosis (TB) from cattle in the region as far back as 8500 BCE and TB in human infant bones not long after. DNA in ancient human remains dates salmonella to as early as 4500 BCE. Assuming the contagiousness and virulence of Neolithic diseases increased through time, dense settlements such as Çatalhöyük may have reached a tipping point where the effects of disease outweighed the benefits of living closely together.

Related: Skeletons of Incan kids buried 500 years ago found marred with smallpox

A new layout 2,000 years later

By about 4000 BCE, large urban populations had reappeared, at the mega-settlements of the ancient Trypillia culture, west of the Black Sea. Thousands of people lived at Trypillia mega-settlements such as Nebelivka and Maidanetske in what's now Ukraine.

If disease was a factor in dispersal millennia before, how were these mega-settlements possible?

This time, the layout was different than at jam-packed Çatalhöyük: The hundreds of wooden, two-story houses were regularly spaced in concentric ovals. They were also clustered in pie-shaped neighborhoods, each with its own large assembly house. The pottery excavated in the neighborhood assembly houses has many different compositions, suggesting these pots were brought there by different families coming together to share food.

This layout suggests a theory. Whether the people of Nebelivka knew it or not, this lower-density, clustered layout could have helped prevent any disease outbreaks from consuming the entire settlement.

Archaeologist Simon Carrignon and I set out to test this possibility by adapting computer models from a previous epidemiology project that modeled how social-distancing behaviors affect the spread of pandemics. To study how a Trypillian settlement layout would disrupt disease spread, we teamed up with cultural evolution scholar Mike O'Brien and with the archaeologists of Nebelivka: John Chapman, Bisserka Gaydarska and Brian Buchanan.

Simulating socially distanced neighborhoods

To simulate disease spread at Nebelivka, we had to make a few assumptions. First, we assumed that early diseases were spread through foods, such as milk or meat. Second, we assumed people visited other houses within their neighborhood more often than those outside of it.

Would this neighborhood clustering be enough to suppress disease outbreaks? To test the effects of different possible rates of interaction, we ran millions of simulations, first on a network to represent clustered neighborhoods. We then ran the simulations again, this time on a virtual layout modeled after actual site plans, where houses in each neighborhood were given a higher chance of making contact with each other.

Based on our simulations, we found that if people visited other neighborhoods infrequently — like a fifth to a tenth as often as visiting other houses within their own neighborhood — then the clustering layout of houses at Nebelivka would have significantly reduced outbreaks of early foodborne diseases. This is reasonable given that each neighborhood had its own assembly house. Overall, the results show how the Trypillian layout could help early farmers live together in low-density urban populations, at a time when zoonotic diseases were increasing.

The residents of Nebilevka didn't need to have consciously planned for their neighborhood layout to help their population survive. But they may well have, as human instinct is to avoid signs of contagious disease. Like at Çatalhöyük, residents kept their houses clean. And about two-thirds of the houses at Nebelivka were deliberately burned at different times. These intentional periodic burns may have been a pest extermination tactic.

New cities and innovations

Some of the early diseases eventually evolved to spread by means other than bad foods. Tuberculosis, for instance, became airborne at some point. When the bacterium that causes plague, Yersinia pestis, became adapted to fleas, it could be spread by rats, which would not care about neighborhood boundaries.

Were new disease vectors too much for these ancient cities? The mega-settlements of Trypillia were abandoned by 3000 BCE. As at Çatalhöyük thousands of years before, people dispersed into smaller settlements. Some geneticists speculate that Trypillia settlements were abandoned due to the origins of plague in the region, about 5,000 years ago.

The first cities in Mesopotamia developed around 3500 BCE, with others soon developing in Egypt, the Indus Valley and China. These cities of tens of thousands were filled with specialized craftspeople in distinct neighborhoods.

This time around, people in the city centers weren't living cheek by jowl with cattle or sheep. Cities were the centers of regional trade. Food was imported into the city and stored in large grain silos like the one at the Hittite capital of Hattusa, which could hold enough cereal grain to feed 20,000 people for a year. Sanitation was helped by public water works, such as canals in Uruk or water wells and a large public bath at the Indus city of Mohenjo Daro.

These early cities, along with those in China, Africa and the Americas, were the foundations of civilization. Arguably, their form and function were shaped by millennia of diseases and human responses to them, all the way back to the world's earliest farming villages.

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

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.

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Computer scientists have created an artificial intelligence (AI) program that can predict the onset of catastrophic tipping points — and they want to use it to forecast ecological collapse, financial crashes, pandemics and power outages.

"If an upcoming critical transition can be forecast then we can prepare for the shift or perhaps even prevent the transition, and thus mitigate damage," senior study author Gang Yan, a professor of computer science at Tongji University in China, told Live Science. "This motivated us to develop an AI approach to predict the onset of such sudden transitions far before it happens."

The researchers published their findings July 15 in the journal Physical Review X

Tipping points are sudden shifts beyond which a localized system, or its environment, changes to an undesirable state from which it is difficult to return. For instance, if the Greenland ice sheet were to collapse, it would also reduce snowfall in the northern part of the island, drastically raising sea levels and making large parts of the sheet irretrievable.

Yet the science behind these dramatic transformations is poorly understood and often based on oversimplified models, making accurate predictions difficult. Previously, scientists used statistics to gauge the diminishing strength and resilience of systems by their growing fluctuations. But the results from studies that use such statistical methods are controversial.

Related: Would you prefer AI to make major life decisions for you? Study suggests yes — but you'd be much happier if humans did

To search for a more precise way to predict dangerous transitions, the researchers behind the new study combined two different types of neural networks, or algorithms that mimic the way information is processed in the brain. The first broke down complex systems into large networks of interacting nodes before tracking the connections between the nodes; and the second followed how individual nodes changed over time.

"For example, in a financial system, a node could be a single company; in an ecological system, a node could stand for a species; in a social media system, a node could denote a user, and so forth," Yan said.

Because tipping points are hard to predict, knowing where to look for them is equally difficult, making real-world data on abrupt critical transitions scarce. To train their model, the researchers instead turned to tipping points within simple theoretical systems — including model ecosystems and out-of-sync metronomes that, given enough time, begin to swing together.

Once their neural network had guzzled enough data, the researchers gave it a problem from the real world: the transformation of tropical forests into savannah. Taking more than 20 years of satellite data from three regions in Central Africa that made this sudden transition, the scientists fed the algorithm information on rainfall and tree coverage in two of the regions.

From that data the AI accurately predicted what happened in the third region, even when 81% percent of the systems' nodes (in this case chunks of land) went unobserved, the researchers said.

Having successfully predicted one tipping point, the researchers are now looking for ways to deconstruct the algorithm's black box to find the patterns it spotted. They then hope to apply their model to other systems such as wildfires, pandemics and financial crashes.

One challenge in predicting systems involving humans is that we learn about and react to our own forecasts, feeding our predictions back into our behavior in complex ways.

"For instance, consider urban transportation: while it may be straightforward to identify congested roads, announcing real-time congestion information to all drivers can lead to chaos," Gang said. "Drivers may immediately alter their routes in response to the information, which might relieve congestion on some roads but simultaneously create congestion on others. This dynamic interaction makes prediction particularly complex."

To get around this problem, the researchers say they will instead focus on parts of human systems that are seemingly unaffected by our intentions. In the road network example, this could be done by looking at routes that are congested more because of their fundamental design rather than how drivers behave in them.

"Using AI to capture these fundamental signals can be valuable for making predictions," Yan said. "Although predicting such systems is challenging, it is worthwhile because critical transitions in human-involved systems can have even more severe consequences."

The COVID-19 pandemic heralded a 35% drop in hospital admissions for heart attacks in the U.S. — but even now, that rate is continuing to fall. Why?

New research suggests that, although people avoiding medical care during the pandemic contributed to the decline in the short term, better heart-attack prevention is the bigger reason for this downward trend.

A heart attack, or acute myocardial infarction (AMI), happens when there's a blockage of blood flow to the heart that causes some of the heart's muscle tissue to die. The symptoms — including chest pain, arm or shoulder pain, shortness of breath, tiredness and nausea — are fairly well known, and most people are aware that heart attacks need immediate medical care in a hospital setting.

However, the pandemic came with an unusual dip in AMI hospitalizations.

Related: Young women may be likelier to die after heart attacks than men

Since 2020, researchers have debated the reasons for this drop. For instance, did patients who were experiencing heart-attack symptoms avoid medical care? Or did patients who might have otherwise had a heart attack die of COVID-19 first?

To investigate these questions, researchers analyzed 7.5 years of Medicare claims data collected between January 2016 and June 2023. They looked at the rates of AMI-related emergency room visits and hospitalizations and the characteristics of the affected patients.

The study, published July 31 in the journal JAMA Cardiology, found that AMI visits and hospitalizations were lowest when the pandemic was at its peak, as measured by COVID-19 death rates. The same was true for other urgent or painful conditions, such as kidney stones. This suggests that people who normally might have sought care chose to stay home when COVID-19 infection risk was high.

The scientists tried correcting for factors such as excess COVID-19 deaths, meaning those over and above the number of deaths that would be expected under typical conditions. However, that adjustment didn't explain the drop in hospital visits, so the researchers concluded that care avoidance was the main cause of the pandemic-related reduction.

"Although there were more deaths overall during the pandemic, we have to appreciate that only some of those patients would have had an AMI over the same time period," said study first author Andrew Wilcock, an assistant professor at the University of Vermont Larner College of Medicine and a visiting fellow at Harvard Medical School.

The effects of excess deaths or changes in Medicare enrollment were "so slight on expected [AMI] rates that they could not explain the shortfalls we observed," Wilcock told Live Science in an email.

But even after pandemic-related restrictions were lifted, AMI visits and hospitalizations stayed lower than they had been before the pandemic. This reflects a broader and sustained decline in heart-attack rates. The researchers propose a combination of reasons for this trend, including that fewer people are smoking, people may be eating healthier, and there is better treatment for underlying conditions such as high cholesterol and high blood pressure.

"It's not just one thing, but a constellation of factors," Wilcock said. "Lifestyle changes and better drugs are compelling explanations for the downward trend in AMI hospitalizations."

There's still room for progress, though.

"We've made improvements, but we still have a lot to do in terms of smoking cessation, exercise, diet, blood pressure and cholesterol control, and so forth," said Dr. Robert Bonow, a professor of cardiology at Northwestern University who was not involved in the research. "Cardiovascular disease remains the leading cause of death worldwide. It would be nice to see it drop to number two."

The study authors noted that their research had some limitations. For instance, using Medicare claims meant that most of the data came from people with disabilities or chronic illnesses, or who were 65 or older. As a result, AMIs in younger people or those with different health care coverage weren't included in the numbers.

In addition, the authors noted that they lacked data on patients' longer-term outcomes. For example, they can't say whether the drop in AMI-related health care visits at the height of the pandemic led to higher rates of heart attack-related disabilities down the line.

"Although AMIs returned to their expected trends, overall hospitalization incidence hasn't returned to pre-pandemic levels," Wilcock said. "The new, post-pandemic normal in use of the hospital is something we would like to understand better."

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Most flu viruses enter human cells through a single entryway — but new research has revealed a "back door" some germs can use to more easily infect cells and jump between species.

Seasonal influenza viruses infect about 1 billion people each year. Typically, these flu viruses enter our cells by binding to sugar molecules, called sialic acids, on the surfaces of cells. This triggers a process that moves the virus into the cell, where it can then replicate.

Like human flu viruses, many flu viruses that infect animals use sialic acids to enter host cells. However, some use a different entryway, called the major histocompatibility complex class II (MHC-II). Scientists had speculated that there might be flu viruses that could use both these routes, but none had ever been discovered — until now.

In a study published July 15 in the journal Nature Microbiology, researchers examined several subtypes of flu viruses to see whether any of them showed an ability to use both routes. They used two types of human cells: one with no detectable surface MHC-II expression and one with high levels of expression. "Expression" refers to the process by which cells make proteins.

Related: H5N1: What to know about the bird flu cases in cows, goats and people

The scientists exposed the cells to virus-like particles designed to resemble three different subtypes of flu viruses that have previously caused flu epidemics in humans: H1N1, H3N1 and H2N2.

The researchers saw that 10 times as many H2N2 lookalikes were able to enter cells with MHC-II than could enter MHC-II-deficient cells. That's despite both these cell types' having the same levels of sialic acids on their surfaces.

Next, the researchers wanted to double check that MHC-II complexes were actually an entry route for the viruses. They used gene editing to remove the cells' ability to make sialic acids, thus eliminating the route most flu viruses take. The H1N1 and H3N1 lookalikes were unable to infect the cells that lacked sialic acids. But the H2N2 particles could bind and enter those cells almost as efficiently as they could infect cells with normal sialic acid expression.

Finally, the researchers looked at different H2N2 strains to see which could use this alternate route. They identified three amino acids — building blocks of proteins — in the viral structure that are essential for binding to the "back door" receptor.

Interestingly, they also found that these viruses could replicate faster and reach higher levels in human lung cells than viruses that only use the "front door." In theory, this could make those viruses more likely to cause disease in and spread between humans.

A major concern is that not just human flu viruses enter our cells this way — it's that animal flu viruses can use the same route. Avian H2N2, for example, is a bird flu virus that caused a pandemic in the 1950s after it swapped genes with a human H1N1 virus.

"Today, H2N2 viruses no longer circulate in humans, but reside in the avian reservoir," study author Umut Karakus, a postdoctoral research scientist at the University of Zürich, told Live Science in an email. "Given that people born after 1968 were not exposed to H2N2 viruses and therefore do not have immunity against them, avian H2 viruses are of particular interest for pandemic preparedness."

H2 viruses can infect pigs, mice and ferrets, along with a variety of birds. This ability to move between species and exchange genes with other flu viruses increases the likelihood that, someday, H2N2 could transmit "zoonotically" from animals to humans. If such viruses pick up the ability to spread easily between people, they can spark pandemics.

So, how great is the threat of zoonotic infection from viruses that can use this "back door" into our cells?

"We need to understand how relevant that entry route is in jumping between species," said Richard Webby, director of the World Health Organization Collaborating Center for Studies on the Ecology of Influenza in Animals and Birds.

"Do viruses actually use that route? What is the relative contribution of MHC-II versus sialic acid?" said Webby, who was not involved in the study. "These questions are a good way to assess the risk that 'super viruses' circulating in animals might eventually jump over to humans."

With a better understanding of how these viruses behave in the wild, scientists can make more accurate judgements about where the greatest risks lie, and how we can best prevent the next flu pandemic.

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A third human case of bird flu has been linked to the ongoing outbreak in cows on U.S. dairy farms — and this one came with respiratory symptoms, such as cough, the Centers for Disease Control and Prevention (CDC) reported May 30.

Officials first became aware of bird flu spreading among U.S. dairy cows in March, and since then, the viral disease has been detected among cattle on farms in nine states. The type of bird flu spreading is known as H5N1, which has sporadically infected individual humans in the past but has never spread widely from person to person. However, these rare human infections can sometimes be fatal, and there's concern about the virus picking up the necessary mutations to spread easily through the populace.

Prior to the outbreak in cows, only one person in the U.S. had ever been infected with H5N1, as far as we know. Now, since the outbreak began, three people have likely been infected via exposure to sick cows. The first person infected by a cow was in Texas, and the second was in Michigan; both are dairy-farm workers and developed only eye infections from the virus before recovering.

The third, newly reported case linked to cow exposure was also in Michigan but on a different farm. The person was given treatment and is now isolating at home as their symptoms resolve. This infection is notable because it is the first human H5N1 case in the U.S. associated with respiratory symptoms. 

Related: H5N1: What to know about the bird flu cases in cows, goats and people 

"This is the first human case of H5 in the United States to report more typical symptoms of acute respiratory illness associated with influenza virus infection, including A(H5N1) viruses," the CDC reported. "The patient reported upper respiratory tract symptoms, including cough without fever, and eye discomfort with watery discharge." 

In humans, bird flu viruses, including H5N1, can cause both mild symptoms — including pink eye, cough, sore throat, runny nose and body aches — as well as severe ones, such as pneumonia, difficulty breathing and seizures. If severe, the infections can be fatal, but antiviral drugs available for seasonal flu can help treat the disease.

Finding another case of human H5N1 infection is "not surprising," given the extent of the spread of this virus in dairy cows, the CDC says. H5N1 was also already known to cause respiratory symptoms — however, seeing this is still concerning because, generally, symptoms like coughing and sneezing can make it easier for a virus to spread between people, The New York Times reported.

Each time the virus jumps to people, it gains an opportunity to pick up mutations that make it capable of spreading sustainably between humans — a chain of events that, in the worst scenario, could precipitate a pandemic. 

With that possibility in mind, the CDC continues to closely monitor for unusual flu activity across the country. So far, "there has been no sign of unusual influenza activity in people, including no increase in emergency room visits for influenza and no increase in laboratory detection of human influenza cases," the agency reported. 

Scientists are also looking to see if the virus has picked up any mutations that would raise the risk of spread, although thus far, there's no evidence of person-to-person transmission. 

Based on the available information, the risk of spread to the general public remains low, the CDC noted. As always, health authorities still recommend against drinking raw milk. Dairy-farm workers currently face the highest risk of exposure, the agency emphasized. 

Some experts have argued that federal officials should be screening many more workers for H5N1 and offering optional experimental bird flu vaccines, The New York Times reported. At this point, only about 40 farm workers have consented to being tested for H5N1, while a few hundred are being monitored for possible symptoms, according to news reports.

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

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Annual deaths from drowning in the U.S. have increased for the first time in decades, new data released by the Centers for Disease Control and Prevention (CDC) reveals. 

More than 4,500 people died due to unintentional drowning each year between 2020 and 2022 — an increase from 2019, when about 4,000 people died from drowning. The biggest increase in deaths occurred in groups who were already at a higher risk of drowning; these include children below age 4 and adults over 65 of all races and ethnicities, as well as Black people of all ages. 

Broken down by age group, the highest overall drowning rates occurred among children between 1 and 4 years old. Drowning is the leading cause of death in that age group. By race and ethnicity, the highest rates were seen among Black and Native American or Alaska Native people. 

The recent surge in deaths may be tied to disruptions to infrastructure caused by the COVID-19 pandemic, researchers suggested in a report published online on May 14. Namely, access to lifeguards, swimming lessons and supervised swimming settings decreased as people spent more free time in or near water, they said.  

"I've seen firsthand the effects of drowning: families forced to say goodbye to their loved ones too soon," Dr. Debra Houry, chief medical officer for the CDC, said in a statement. "Understanding the barriers people face to accessing basic swimming and water safety skills training can help us better understand how to address those barriers, decrease drowning rates, and save lives."

Related: COVID pandemic knocked 1.6 years off global life expectancy, study finds

To get the new figures, the researchers analyzed data from the National Vital Statistics System, which contains the most complete record of U.S. deaths and their causes. For the new report, CDC researchers compared the unintentional drowning death rates reported in 2019, before the pandemic began, with those recorded in 2020, 2021 and 2022. 

Compared with 2019, children ages 1 to 4 saw a roughly 28% jump in drowning deaths in 2021 and 2022, the researchers found. Adults ages 65 and older had the second-highest drowning rate in all the years and also experienced significant upticks compared to 2019. For instance, people ages 65 to 74 years old were 19% more likely to drown in 2022 than in 2019, and those over age 85 had a nearly 50% higher chance of drowning in 2021 than 2019. 

People ages 15 to 34 experienced the biggest surge in drowning deaths between 2019 and 2020. Based on prior data, the researchers suspect alcohol use may have factored into this uptick, although alcohol use wasn't specifically accounted for in the new study.

Drowning rates among Native American or Alaska Native people didn't increase between 2020 and 2022, but these individuals were still more likely to drown than any other race or ethnicity, as has been seen in past reports, the CDC found. The second-highest drowning rates by race were among Black people — with a 28% increase in 2021 compared with 2019. 

The CDC also assessed people's swimming ability with a national survey. The agency estimates that around 40 million U.S. adults don't know how to swim, based on 15.4% of survey respondents saying they didn't know how to do so. More than 50% of respondents said they have never taken a swimming lesson. 

Social and structural barriers still limit people's access to training in swimming and water safety, the CDC wrote in the report. This lack of access reflects disparities in drowning rates — for example, more Black adults than white adults report not knowing how to swim or having never taken a swimming lesson. Addressing these barriers could help reduce drowning rates, the CDC said. 

In the meantime, the agency recommended several ways in which people can protect themselves and their loved ones from drowning, such as installing four-sided pool fencing, ensuring that children are always supervised while in the water and using life jackets while boating. 

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

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Editor's note: This is a developing story and will be updated.

A bird flu virus called H5N1 recently infected animals that it had never been seen in before: goats and cows. Now, it's suspected that four people have picked up the infection after being exposed to infected cows, or potentially their bodily fluids or bedding.

Here's what we know so far about these unusual cases of H5N1 in the U.S.

Related: 21-year-old student dies of H5N1 bird flu in Vietnam

What is H5N1 bird flu?

H5N1 is a subtype of avian influenza A, a broad group of related bird flu viruses. It's categorized as a form of "highly pathogenic" avian influenza, or HPAI, because it causes severe and fatal disease in poultry. For example, H5N1 and other "H5" bird flu viruses can rapidly cause organ damage in chickens and kill up to 90% to 100% of chickens they infect, often within 48 hours, according to the Centers for Disease Control and Prevention (CDC). H5N1 has been responsible for the major bird flu outbreaks seen on U.S. poultry farms and on farms in other countries since 2022.

Although HPAI viruses are known for devastating domestic bird populations, H5N1 also infects wild birds and occasionally infects various mammals, including people. In non-avian species, it can still cause fatal disease, but some cases are mild or asymptomatic.

H5N1 infections in mammals, in general, raise concern that the virus could evolve to infect humans more easily and perhaps spread widely between people, sparking a pandemic, according to the World Health Organization (WHO). But scientists haven't seen any changes in the virus that suggest that's happening at this point.

Which animals can H5N1 infect?

H5N1 most often infects domestic and wild birds, although some wild birds act as "reservoirs" for the virus, meaning they can carry and spread it without getting sick. These carriers include waterfowl, such as ducks, geese and swans; and shorebirds, such as plovers and sandpipers, the CDC says.

In the past 20 years or so, H5N1 has also been detected in at least 48 mammal species across 26 countries. These include foxes, bears, seals, sea lions and polar bears, as well as pet cats and dogs and farmed mink. The U.S. Department of Agriculture (USDA) maintains a map of where different mammals have been infected in the U.S.

This year, for the first time, H5N1 was detected in goats and cows. This marks the first time H5N1 has been found in ruminants, which include hooved, cud-chewing mammals like cows, goats and sheep.

The infections among goats were reported in mid-March on a Minnesota farm where ducks and chickens had previously tested positive for the virus. The first infections in cattle were reported a week later among dairy cows in Texas and Kansas, which also likely got the virus from birds.

Related: 'Novel' swine flu virus sickens Pennsylvania child in 1st case of the year

Where has H5N1 been detected in cows?

After being detected in cows in Texas and Kansas, H5N1 infections were also confirmed in cows in Idaho, Michigan and New Mexico, according to the USDA's Animal and Plant Health Inspection Service. As of June 14, the USDA has reported that 92 dairy cow herds in 12 U.S. states have confirmed cases of infection. 

Early data suggest that the specific strain of H5N1 infecting cows matches one introduced to the U.S. by wild birds — known as clade 2.3.4.4b — back in 2021. Before that, the strain had spread mostly in Europe, Asia and Africa.

"[H5N1] could have been infecting dairy cattle a year ago. We just never thought about looking … for it," Dr. David Swayne, a bird flu expert who is now a private consultant after having worked for the USDA, told STAT. Experimental data published in 2008 suggested that at least one H5N1 strain can infect baby cows, so it's not totally unexpected to see the virus in cattle.

The recently infected cows have been reported to produce less milk, show poor appetite, develop cold-like symptoms and become lethargic. There have been no reported deaths among the cows.  

Can H5N1 infect people, and how dangerous is it?

H5N1 can occasionally infect people and can lead to death, with about 50% to 60% of reported cases resulting in fatal disease. More than 880 human cases of H5N1 have been reported worldwide since the late 1990s, according to the CDC.

Most often, human H5N1 infections occur after a person had close or lengthy unprotected contact — without gloves, a face mask or eye protection — with infected birds or with objects contaminated with sick birds' saliva, mucus or poop. These cases have not been tied to sustained human-to-human spread of the virus, but there's been some evidence of very limited spread between people.

Although H5N1 infections can be fatal, some people show no symptoms or only mild symptoms. Mild symptoms might include eye infections, such as conjunctivitis (pink eye), and upper respiratory symptoms, like sneezing and coughing. Severe cases can lead to life-threatening pneumonia.

Bird flu can be treated with antiviral drugs used for seasonal flu. The CDC also has several candidate vaccines prepared for manufacturing, just in case this or a closely related virus were to suddenly spread between people; seasonal flu vaccines do not protect against H5N1.

There have been five human cases of H5N1 in the U.S. The first was in 2022, in a person in Colorado who'd had direct exposure to infected poultry. It's possible that this case wasn't a full-blown infection but rather remnants of the virus being detected in the person's nasal passages. 

The second case was in April 2024, when a person in Texas caught the virus after likely being exposed to infected cows; this person's only reported symptom was pink eye. The third was reported in Michigan in May 2024, also in connection with infected cows on a farm. This third individual also only showed eye-related symptoms. The fourth case was reported later in May 2024, when a worker at a different Michigan dairy farm developed mild respiratory symptoms, including cough. The fifth was reported in July 2024, in a dairy worker in Colorado who developed only eye symptoms.

Related: 1st-known 'highly pathogenic' bird flu cases in Antarctic could threaten penguins

Should you worry about H5N1 in cows?

Finding H5N1 in cows is interesting to scientists because it hasn't been seen before, but as of now, it poses a low risk to the general public.

As for cows, there's some early hints that the virus can spread among cattle — the cows in Idaho reportedly became sick after being exposed to cows shipped from Texas, Science reported, and the Michigan cases were also thought to be tied to cows from Texas, the CDC reported. However, H5N1's ability to spread among cows still needs to be confirmed.

In regards to people, "initial testing has not found changes to the [H5N1] virus that would make it more transmissible to humans," the USDA noted in an April statement. "While cases among humans in direct contact with infected animals are possible, this indicates that the current risk to the public remains low."

The CDC also reported that there have been no changes to the virus that would make it less vulnerable to Food and Drug Administration (FDA)-approved antiviral drugs for the flu.

Nevertheless, the CDC recommends that people avoid sick or dead animal carcasses, including wild birds, poultry and cattle. They should also avoid raw milk, poop, litter or other materials contaminated by animals with suspected H5N1 infections, and they should avoid uncooked and undercooked food products from such animals.

Is the milk and beef supply safe?

The discovery of H5N1 in cows does not threaten the country's milk supply, the USDA noted. Dairies are required to send only milk from healthy animals into processing for human consumption, and the commercial milk supply is pasteurized before going to market, which kills viruses. Unpasteurized milk always carries a risk of causing dangerous infections, but the likelihood of H5N1 infection from raw milk is not yet known.

Related: H5N1 bird flu can remain infectious in raw milk for at least an hour, study finds

Since March 25, shortly after news of the cow infections came to light, weekly sales of raw milk have increased by as much as 21% compared with previous years. But experts have warned that consuming raw milk could expose individuals to dangerous pathogens, alongside increasing the likelihood of H5N1 gaining the necessary mutations to jump to and spread between humans. 

Notably, there isn't yet enough evidence to know whether drinking raw milk contaminated with H5N1 could result in a human infection.

More information on milk safety given the current situation can be found on the FDA's website.

So far, H5N1 has been found in dairy cows, but the USDA also emphasized that the beef supply is safe and that cooking meat properly kills viruses.

Editor's note: This article was updated on July 5 to note an additional human case of H5N1. The original article was posted on April 4.

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 person in Texas has tested positive for bird flu after being in contact with dairy cows that were likely infected with the virus, health officials announced on Monday (April 1).

The individual's only reported symptom was eye redness, likely caused by an infection of the eye called conjunctivitis. The person is now isolating and being treated with an antiviral drug for influenza, according to the Centers for Disease Control and Prevention (CDC).

This is the second reported case of a human in the U.S. being infected with a type of "highly pathogenic" avian influenza virus called A(H5N1) and the first person to likely be infected by cows. The first human case in the U.S. was in 2022 and involved a prisoner in Colorado who had been culling infected poultry at a commercial farm as part of a pre-release employment program.

H5N1 is a subtype of highly pathogenic avian influenza (HPAI), a type of flu that can cause severe disease and death in birds. The virus causes outbreaks in both poultry and wild birds but can also spread to mammals. In the past few years, the virus has been reported in more than 48 mammal species, including foxes, skunks, raccoons, seals and polar bears.

Now, the virus has made its way to cows. The announcement of a person likely catching H5N1 from cattle comes one week after dairy cows in Texas and Kansas tested positive for the virus, and two weeks after the disease was found in goats for the first time. H5N1 has since been detected in cows in New Mexico, Michigan and Idaho.

Health officials say the risk of humans being infected remains low and that, as milk is pasteurized before being sold, dairy products remain safe. The meat supply is also safe, and cooking meat to safe internal temperatures kills viruses like influenza.

Nonetheless, the spread of H5N1 among mammal species is concerning scientists, especially if it's a sign that the virus is now capable of mammal-to-mammal transmission.

"Mammal-to-mammal transmission has been suspected for a while, but not confirmed. If sequencing confirms this, it would be a pretty worrying step in the evolution of the virus," Deepti Gurdasani, a clinical epidemiologist and statistical geneticist at the Queen Mary University of London, wrote on X, formerly known as Twitter. "If mammal-to-mammal transmission can occur, that raises the possibility of the potential of human to human transmission."

About 860 human cases of H5N1 have previously been reported worldwide. The mortality rate is around 60%, according to the World Health Organization (WHO), although the CDC notes some cases cause no or few symptoms. Symptoms can include a cold, cough and fever, and the infections are typically treated with the same antivirals used for seasonal flu.

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

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The Doomsday Clock, whose hypothetical hands strike the minutes and seconds left until a human-made apocalypse destroys the world as we know it, has remained at just 90 seconds to midnight.

The clock moved to 90 seconds to midnight for the first time ever last year, after hovering at 100 seconds to midnight for three consecutive years as the world teetered on the "doorstep of doom." The clock's hands remain in this critical position mainly because of the existential risk posed by climate change and nuclear escalation in Russia's ongoing assault on Ukraine, representatives of the Bulletin of the Atomic Scientists (BAS) announced on Tuesday (Jan. 23). The BAS is a non-profit organization of scientists and policy-experts that sets the time of the Doomsday Clock. 

Representatives also cited disruptive technologies — including cutting-edge bioresearch and vectors for misinformation — as dangers contributing to our dash toward self-destruction.

The time of the Doomsday Clock is decided by the BAS's Science and Security Board (SASB), which this year featured science educator Bill Nye, and the organization's board of sponsors, which includes 15 Nobel laureates.

"The Bulletin SASB took into account developments across many different domains, including a broad range of events or factors that relate to the possibility of nuclear war, to climate change, to biological threats such as pandemics or biological weapons, and to emerging technologies that may prove disruptive to peace and stability," Herbert Lin, a senior research scholar at the Center for International Security and Cooperation at Stanford University who sits on the SASB, told Live Science in an email. 

Related: Catastrophic climate 'doom loops' could start in just 15 years, new study warns

Chief among these potentially world-ending new technologies is artificial intelligence (AI), Lin said. AI technology progressed by leaps and bounds last year, but 2024 may be the year it changes our lives. 

The BAS created the Doomsday Clock in 1947 to warn against the existential threat posed by nuclear weapons, initially setting it to seven minutes to midnight. The clock jumped to three minutes to midnight two years later, following the first successful Soviet atomic bomb test during the Cold War between the U.S. and the Soviet Union. It lurched another minute closer to midnight in 1953, after the detonation of the first hydrogen bombs but was again set to seven minutes in 1960. Its hands can and have moved even further backward — in 1991, they moved to 17 minutes to midnight after the collapse of the Soviet Union and the signing of the Strategic Arms Reduction Treaty that agreed to reduce the number of long-range nuclear weapons in the U.S. and former Soviet Union.

The clock re-entered the two-minute-warning zone in 2018 for the first time since 1960 due to "reckless language in the nuclear realm" and a world "on the cusp of a new arms race," BAS president and CEO Rachel Bronson wrote in a statement at the time.

Over the past six years, the clock has gradually crept closer to midnight.

The decision to move the clock forward last year was largely based on humanity's inaction on climate change and fears over the war in Ukraine. But there were a number of other factors. "For many years we have also considered various disruptive technologies from online misinformation to new bioresearch," Bronson said in a statement shared with Live Science. "This year, the technology conversation must also include the recent rapid advancements in AI."

New technologies pose dangers of their own, but they also have the power to exacerbate existing challenges. "We also call attention to the threat of the corruption of the global information environment that acts as a threat multiplier," Lin said. "The abundance of mis and disinformation about nuclear, climate, and pandemic threats makes those problems enormously harder to solve because it works against the political consensus needed to tackle them seriously."

The Bulletin's board members hope the new announcement will galvanize governments into action, Lin said.

"There is some progress, ranging from early-stage nuclear diplomacy between the U.S. and China to record-breaking investments in renewables [and] emerging national and international policy frameworks around technologies like AI and biological research," Bronson said. "But none of these efforts are moving forward quickly enough."

In mid-November, news broke of an outbreak of respiratory illness in China, raising concerns that another pandemic like COVID-19 might emerge. Now, scientists say the pathogens behind the surge are actually quite common. 

The worries of another pandemic started Nov. 13, when China's National Health Commission announced a nationwide increase in respiratory infections, mainly in children, according to the World Health Organization (WHO). Then, on Nov. 21, various media outlets reported clusters of cases of "undiagnosed pneumonia" in children in northern China, notably in Beijing and Liaoning province. The Program for Monitoring Emerging Diseases (ProMED), an international network for disease surveillance, also amplified similar news reports. 

This prompted the WHO to investigate, and on Thursday (Nov. 23), the organization confirmed that the reported increase in infections and hospitalizations among children is actually being caused by several known pathogens. 

These pathogens include the bacterium Mycoplasma pneumoniae, respiratory syncytial virus (RSV), adenoviruses and influenza. M. pneumoniae can cause bacterial pneumonia, while RSV, adenoviruses and influenza can cause viral pneumonia in severe cases.    

Chinese health authorities also told the WHO that they haven't detected any "unusual or novel pathogens or unusual clinical presentations, including in Beijing and Liaoning." In other words, this rise in infection is being caused by multiple known culprits, not a mysterious monster bug. 

Related: Who should get the new COVID vaccines? What to know about the 2023-2024 shots

"This is not an indication of a novel pathogen; This is expected," Maria Van Kerkhove, acting director of the WHO's department of epidemic and pandemic preparedness and prevention, told STAT News.  

"This is what most countries dealt with a year or two ago," when they began to lift restrictions enacted in the early pandemic, she said. China only loosened its quarantining and testing policies in December 2022.

Now that pandemic restrictions have been eased, children are more likely to catch bugs this winter that they were sheltered from before. This also means that their immune systems have not been exposed to many common viruses, and as a result, they have not yet acquired protective immunity against them — something known as an "immune deficit," Dr. Ben Marais, director of the Sydney Infectious Diseases Institute at the University of Sydney, told the Australian Science Media Centre (SMC). Children are also more likely to develop severe RSV infection and to be infected by M. pneumoniae than adults.

In addition, respiratory infections normally surge in winter. 

"This is a typical 'winter surge'' in acute respiratory infections," Benjamin Cowling, a professor of epidemiology at the University of Hong Kong, told Nature. "It is happening slightly earlier this year, perhaps because of increased population susceptibility to respiratory infections resulting from three years of COVID measures," he said. 

China also recently enhanced its disease surveillance systems, Paul Arbon, a professor at Flinders University in Australia who researches health emergencies and health system strengthening, told the Australian SMC. 

"There has been an uptick in the rates but it is that time of year and China has implemented a new national reporting system that has, as it should, picked up cases that were not reported under the old system," he said. The WHO also noted that these enhancements "may have contributed to the observed increase in detection and reporting of respiratory illness in children." 

Other countries saw similar waves of respiratory infections in children during the first winter after lifting lockdown restrictions, Francois Balloux, a professor of computational systems biology at University College London, told the U.K. SMC. In the U.S., for example, more people were hospitalized with flu in November 2022 than at any point since 2010, according to the Centers for Disease Control and Prevention (CDC). 

The WHO is still closely monitoring the outbreak in China and remains in contact with local health authorities, according to the Nov. 23 statement.

The WHO recommends that people in China follow standard measures to reduce the risk of infection, such as getting vaccinated as appropriate, wearing face masks and maintaining a safe distance from people who are ill. 

As for the rest of the world, the WHO currently advises against travel or trade restrictions, and it hasn't introduced any specific measures for people traveling to China. However, anyone who develops symptoms of respiratory illness while traveling should seek medical attention, the WHO recommends.

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!

The 1918 flu was one of the deadliest pandemics in history, killing at least 50 million people worldwide. It was long believed that young, healthy adults were just as likely to die from the illness as those who were older, sick or frail — but a new study has turned this idea on its head.

Scientists examined skeletons of people who died before and during the 1918 pandemic. Signs of stress in the bones suggest that, regardless of their ages, people who were already frail or unhealthy were more likely to die during the crisis than those who weren't.

The findings, published Monday (Oct. 9) in the journal PNAS, are perhaps not surprising, but they're a reminder of how individuals' attributes can shape their susceptibility to disease, the authors said.

"Even in a novel pandemic — one to which no one is supposed to have prior immunity — certain people are at a greater risk of getting sick and dying, and this is often shaped by culture," Amanda Wissler, lead author of the study and an assistant professor of anthropology at McMaster University in Ontario, told Live Science in an email. In other words, people who are already disadvantaged in terms of their health or socioeconomic status tend to be more vulnerable to outbreaks, she said.

Related: 1918 flu mutated to become deadlier in later waves, century-old lungs reveal

The 1918 flu spread so fast that doctors originally believed that healthy young adults were as likely to die as older people who were already frail and babies with immature immune systems. The pattern of flu deaths across age groups was "W-shaped," with peaks at very young and very old ages, and another peak among young adults. Most flu outbreaks have "U-shaped" death curves, with peaks on both ends of the age spectrum.

The W-shaped curve highlighted an unusual trend among young people, but it didn't take their preexisting conditions into account. Evidence of rampant death among healthy young adults was mainly anecdotal and had no concrete scientific backing, the study authors wrote in their paper. Historical documents, such as census data and life insurance records, contained scant details on the people's health conditions and socioeconomic pressures.

In the new study, scientists examined the skeletons of 81 people who died when the flu struck Cleveland between September 1918 and March 1919 and those of 288 people who died before the pandemic. They looked at the ages of death and for bumps, or "lesions," on the people's shinbones, which served as markers of physical stress and underlying health conditions. When the body is stressed as a result of physical trauma, infection or nutritional deficiencies, inflammation triggers healing and the formation of new bone.

People who had active shinbone lesions were considered the frailest, and compared with people with healed lesions, they were more likely to die before and during the pandemic. During the pandemic, their risk of death was 2.7 times greater than that of people who had healed lesions.

Young people were not an exception to this trend. Regardless of their age of death, those who had evidence of stress in their bones were more likely to have died from the flu than those who started out healthier.

The study had several limitations: It only included skeletons from Cleveland, meaning the results can't necessarily be applied to other places. And the shinbone technique is great for looking at general patterns of frailty but can't explain the exact causes of the lesions. Nevertheless, the findings may reflect how health and social disparities tend to drive death rates in pandemics — similar to trends seen in the COVID-19 pandemic, or even the Black Death.

"We saw during COVID-19 that people who were socially and economically minoritized had a greater risk of getting sick and dying, and I suspect a similar thing happened in the 1918 flu," Wissler told Live Science.

The misconception that healthy adults were equally likely to die during the 1918 pandemic as frailer people may reflect the fact that young adults, in general, were at greater risk in the 1918 flu than in previous outbreaks, the authors wrote in the paper. Scientists have since proposed theories for this — perhaps a virus similar to the pandemic flu circulated before those young adults were born, leaving them especially susceptible once the 1918 virus emerged.

It would have been surprising to see lots of young people dying, which probably made the trend stand out, the authors concluded.

The Food and Drug Administration (FDA) has authorized a new formulation of the COVID-19 vaccine made by the Maryland-based pharmaceutical company Novavax, the agency announced Tuesday (Oct. 3). The newly updated "nanoparticle" vaccine joins the Pfizer and Moderna COVID-19 vaccines already cleared for use in the U.S.  

The Novavax shot now includes a spike protein — a pointy structure found on the virus's surface — from a version of the virus that is currently circulating, called XBB.1.5. The widespread subvariant branched off of the omicron family tree. Compared to its old formula, the new Novavax shot is expected to provide better protection against both XBB.1.5 and its close relatives that stem from the same branch. 

The shot has been authorized for use in people ages 12 and older.  

"Today's authorization provides an additional COVID-19 vaccine option that meets the FDA's standards for safety, effectiveness and manufacturing quality needed to support emergency use authorization," Dr. Peter Marks, director of the FDA's Center for Biologics Evaluation and Research, said in the agency's announcement. "As we head into the fall season and transition into 2024, we strongly encourage those who are eligible to consider receiving an updated COVID-19 vaccine to provide better protection against currently circulating variants."

Related: Who should get the new COVID vaccines? What to know about the 2023-2024 shots 

Updated COVID-19 vaccines from Pfizer-BioNTech and Moderna were approved in September, but the Novavax shot is based on different technology. 

The Pfizer-BioNTech and Moderna shots contain mRNA, a genetic molecule that carries instructions for human cells to build the spike protein once the vaccine enters the body. In contrast, the Novavax vaccine contains nanoparticles made out of lab-made spike proteins — so the spike proteins are made by cells in a lab, rather than inside the human body. 

In addition, the Novavax shot contains an "adjuvant," a substance that revs up the immune system to mount a stronger response to the vaccine.

The FDA says that individuals who have previously been vaccinated for COVID-19 can get one dose of the updated Novavax shot, provided that their last shot was given at least two months ago. People who have never been vaccinated against COVID-19 can get two doses of Novavax, spaced three weeks apart. People with weakened immune systems can consider getting a second dose of the updated vaccine two months after their first.

Additional doses "may be administered at the discretion of the healthcare provider, taking into consideration the individual's clinical circumstances," the FDA noted.

During the worst waves of the COVID-19 pandemic, between 30% and 46% more people in the U.S. were dying each week than would have under typical circumstances. But in the past few months, we've seen this "excess death rate" fall, and now, it's hovering near zero. 

Does that mean America has seen the end of the COVID-19 pandemic? And that the coronavirus can now be considered "endemic" to the country? Experts told Live Science that, yes, it's reasonable to declare the pandemic over in the U.S. — but that doesn't mean U.S. residents no longer face any risk of harm from COVID-19.

Related: 'Face blindness' could be rare long COVID symptom, case report hints

What are 'excess deaths'?

Essentially, the excess death rate is the number of actual deaths recorded, of any cause, minus the number of deaths that would have been expected over a given time period, based on historical data. 

"[Excess death rate] is always going to be based on mathematical models. It's always going to be flawed," Dr. Shira Doron, chief infection control officer for Tufts Medicine in Massachusetts, told Live Science. She said it's very difficult to establish a baseline for what death rates "should" be, given that past mortality rates may have been shaped by unique public health threats, and the emergence of new medical treatments may now be improving survival rates for different illnesses. 

But despite its flaws, "it was a metric that was useful during COVID because of the concern that we may not be capturing all COVID deaths," Doron said. Rather than only relying on death certificates that list "COVID-19" as a primary or contributing cause of death, excess death rates can capture the pandemic's wider impact and help determine the number of people who died both directly and indirectly of the disease. 

Such a metric is helpful, in part, because some COVID-related deaths may have been overlooked due to a lack of testing and underdiagnosis of the disease during the pandemic's early days. The excess death rate also captures deaths that were not caused by COVID-19 itself, but rather the rippling effects the pandemic had on society. 

Related: Genetic quirk could explain why not everyone shows symptoms of COVID-19

For example, homicides in the U.S. surged by more than 30% from 2019 to 2020, while deaths involving alcohol spiked 25.5% over the same time period, likely due to a rise in stress and anxiety. While the healthcare system buckled and people avoided hospitals during each COVID-19 wave, many people did not receive adequate care for existing conditions, which is partially what led to an uptick in deaths related to health issues like heart disease, for instance. 

Due to these combined factors, excess death rates in the early pandemic were harrowing, consistently exceeding 20% in 2020 and 2021. From March 2020 to March 2022, the country's excess deaths totaled more than 1.1 million, which is 15% higher than the official COVID-19 death toll reported over that same time period, according to the Centers for Disease Control and Prevention (CDC). 

But in 2023, the U.S. turned a corner.

Starting in January, excess death rates began to plummet, falling from about 17% at the end of December to 2% by January's end. Since then, the rates haven't exceeded 3% and have often lingered around zero.

Some estimates suggest that COVID-19 deaths are still being undercounted. However, based on national data from the CDC and the Human Mortality Database, which is compiled by the University of California, Berkeley, and the Max Planck Institute for Demographic Research in Germany, the recent fall in excess death rates likely reflects a return to pre-pandemic levels of mortality.

One sobering reason why these excess death rates have dipped is because COVID-19 has already claimed the lives of many of the people most vulnerable to the disease, particularly those aged 65 and older, which accounted for more than 75% of total coronavirus deaths in the U.S. leading up to October 2022, according to the Kaiser Family Foundation.

Related: COVID-19 is no longer a global health emergency, WHO says

However, one of the main explanations for the excess death rate bottoming out is that the vast majority of the U.S. has now gained some immunity to SARS-CoV-2, the virus that causes COVID-19. By 2022, more than 95% of U.S. residents had COVID-19 antibodies coursing through their veins, whether from being infected, receiving a vaccine or both, which means we've likely "realized a community immunity" across the country, Doron said.

And while individuals with immunity can still contract COVID-19, they are much less likely to die from it, according to a study published in March in the journal The Lancet. Additionally, effective treatments for COVID-19, including the antiviral Paxlovid, became more widely accessible last year and help reduce the disease's severity, The New York Times reported.

So, is the pandemic over?

The federal Public Health Emergency for COVID-19 was ended in May, meaning the government no longer considers the disease a national emergency but still regards it a public health priority. The excess death rate data reflects that transition out of a state of emergency, according to Dr. Paul Monach, the chief of rheumatology at the VA Boston Healthcare System. 

"I think that we're in a state where, in putting all these data together and not seeing much excess death overall, that it's reasonable to say yes, the pandemic is over," he told Live Science. "But I think it's still important to figure out who is still at risk." 

For the majority of immunocompromised people, vaccines are effective at preventing severe COVID-19 infections, Doron said. But some groups remain vulnerable, including those age 65 and older and people who have received organ transplants, who must take immune-suppressing drugs. 

And although more than 80% of people in America have received at least one dose of the vaccine, there are still a lingering few who have refrained. And getting just one dose of the original vaccine does not protect as well against now-circulating coronavirus variants, which could lead to more severe infections, according to the CDC. 

"There remain pockets and enclaves of individuals, particularly in rural America, that are unvaccinated or under-vaccinated and who either have limited access to treatments or are unaware of options who are still vulnerable," Andrew Stokes, an assistant professor at the Boston University School of Public Health, told Live Science. 

While excess death rates are currently low, in July alone, about 30 to 70 people in the U.S. have died of COVID-19 each week, according to preliminary CDC data. And there is always the risk of a new, immunity-evading coronavirus variant emerging in the coming years and causing spikes in mortality, Monach told Live Science. 

As the initial pandemic winds to a close, it will be important to remain vigilant to these changing circumstances.

Fever, shortness of breath and cough are all key COVID-19 symptoms we've been told to look out for throughout the pandemic. However, at least 1 in 5 people who test positive for the virus don't develop any symptoms, and the reason why has remained a mystery — until now. 

In a new study published Wednesday (July 19) in the journal Nature, scientists report a possible explanation for why some people don't develop symptoms after catching SARS-CoV-2, the virus that causes COVID-19, and it boils down to variation in a key gene involved in our immune response to viral infection. 

After analyzing data from nearly 30,000 people, they found that people who carried a gene variant called HLA-B*15:01 were more than twice as likely to be asymptomatic following SARS-CoV-2 infection than those without the variant. Those with two copies of the variant showed even greater protection, with a more than eightfold greater likelihood of being asymptomatic. 

The study authors propose that this variant guards against COVID-19 symptoms by tapping into the body's existing immunity against seasonal, cold-causing coronaviruses.

Related: A version of this gene doubles the risk of dying from COVID-19

Variations in the human leukocyte antigen (HLA) complex, a set of genes that help the immune system to detect disease-causing microorganisms like bacteria and viruses, shape how people react to viral infections, such as HIV and hepatitis B. However, scientists are still uncovering how HLA variations affect people's reactions to COVID-19. 

To plug this gap, the authors recruited about 29,950 people for a smartphone-based study that tracked symptoms and outcomes of COVID-19. Focusing on 1,428 people who were unvaccinated and had caught the disease by the end of April 2021, the team identified 136 people who had not experienced symptoms for at least two weeks before and after testing positive for the virus. 

Of these asymptomatic people, 1 in 5, or 20%, were found to carry the HLA-B*15:01 gene variant, compared to 9% of people who reported symptoms of the disease. Similar trends in variant frequency were also seen in two additional, independent cohorts investigated by the team. 

To explain why the HLA-B*15:01 variant may be protective, the team studied T cells, a type of immune cell, that were collected before the pandemic from a separate group of donors carrying the variant. Despite having not yet been exposed to SARS-CoV-2, these T cells were reactive to a protein fragment from the virus, as well as to similar fragments from seasonal coronaviruses. The authors therefore suggest that the absence of symptoms in people with HLA-B*15:01 could be explained by their cells being primed for the virus. 

"We were able to show that when a piece of the SARS-CoV-2 virus is bound to this HLA, it looks remarkably similar at a molecular level to a piece of seasonal cold virus bound to that HLA," Jill Hollenbach, senior author and professor of neurology at the University of California, San Francisco, told Live Science in an email. 

"Therefore, the T cells that are tasked with identifying infected cells are seeing essentially the same thing, making them highly cross-reactive," she explained.

The authors highlighted several limitations of their research, most notably that their analysis was restricted to people who self-identified as "white" due to an absence of data from other ethnic groups. Relying on self-reported symptoms also meant that they couldn't be certain that those who said that they were asymptomatic were completely free of symptoms.

Francois Balloux, a professor of computational systems biology at University College London who was not involved in the study, praised the findings but urged caution regarding any incorrect interpretation of their meaning.

"The study makes a really convincing case that this allele [gene variant] is protective," he told Live Science. But that doesn't mean that people with one or two copies of the variant will never have symptomatic COVID-19, he cautioned. "It is just that they're less likely to and other factors may be at play."

Going forward, "we think that this observation can help inform next generation vaccine design, and help us to understand how to prevent symptoms even when people do become infected," Hollenbach said. "In future work we hope to learn more about whether the same mutation is important in individuals from diverse ancestries and to gain a better understanding of why these cross-reactive T cells from HLA-B*15:01 individuals are so remarkably effective at controlling the virus."  

"It would be interesting to know whether these findings extend to other HLA," types, Edd James, a professor in cancer immunology at the University of Southampton who was not involved in the study, told Live Science in an email. Other scientists have reported cross-reactivity between other HLAs, COVID-19 and seasonal coronaviruses, he noted. 

"If so, can vaccinations be designed to harness this cross-reactivity," he said.

A sudden and deadly epidemic sweeping across the Red Sea has killed an entire species of sea urchin, stripping their flesh and turning them into skeletons. 

Just two months ago, thousands of black sea urchins (Diadema setosum) lived in the Gulf of Aqaba, in the northern tip of the Red Sea, keeping the corals there healthy by snacking on excess algae. Now, only their skeletons remain, after their tissue was consumed by a mysterious pathogen. 

"It's a fast and violent death: within just two days a healthy sea urchin becomes a skeleton with massive tissue loss," Omri Bronstein, a senior lecturer in Zoology at Tel Aviv University, said in a statement. "While some corpses are washed ashore, most sea urchins are devoured while they are dying and unable to defend themselves, which could speed up contagion by the fish who prey on them."

Related: Red Sea dolphins slather their skin in coral mucus, because nature is wonderfully gross

Researchers spotted the first signs of the urchin plague in the Mediterranean Sea at the beginning of the year, when an invasive species of urchin began falling sick in waters around Greece and Turkey. From there, the disease appears to have spread southward through the Suez Canal to the Red Sea. 

Scientists are unsure of the exact disease causing the mass die-off, but they suspect it is a pathogenic ciliate parasite — a single-celled microorganism — which in 1983 eliminated the Caribbean’s entire sea urchin population. Before the parasite plague, the Caribbean was home to thriving tropical reefs, but since losing the sea urchins the reefs have been smothered by algal blooms that multiplied unchecked, blocking out sunlight and destroying around 90% of the region’s coral. 

The disease was only identified after a second wave hit the Caribbean in 2022, an event which gave scientists a second opportunity to study it.

"The sea urchins are the reef's 'gardeners' — they feed on the algae and prevent them from taking over and suffocating the corals that compete with them for sunlight," Bronstein said. "Unfortunately, these sea urchins no longer exist in the Gulf of Eilat [Aqaba] and are quickly disappearing from constantly expanding parts of the Red Sea further south."

The imperilment of the region’s corals is significant on both a local and global level. The Gulf of Aqaba is known for its numerous diving spots and is a popular tourist destination. And because the corals there evolved to high temperatures and salinity over millions of years, they are more resistant to climate change-driven temperature fluctuations that are killing off other coral reefs around the world. 

"It must be understood that the threat to coral reefs is already at an all-time peak, and now a previously unknown variable has been added," Bronstein said. "This situation is unprecedented in the entire documented history of the Gulf of Eilat [Aqaba]."

Bronstein says that to prevent the entire sea urchin populations of the Red Sea and the Mediterranean from being eradicated, urgent action is needed to establish uninfected broodstock populations of the urchins so that they can be returned to the oceans once the epidemic is over.

"We must understand the seriousness of the situation: in the Red Sea, mortality is spreading at a stunning rate, and already encompasses a much larger area than we see in the Mediterranean," Bronstein said. "In the background there is still a great unknown: What is actually killing the sea urchins? Is it the Caribbean pathogen or some new unfamiliar factor?"

"Either way, this pathogen is clearly carried by water, and we predict that in just a short time, the entire population of these sea urchins, in both the Mediterranean and the Red Sea, will get sick and die," Bronstein added.

The researchers published their findings May 24 in the journal Royal Society Open Science.

COVID-19 is no longer a global health emergency, the World Health Organization (WHO) has declared.

The United Nations agency's announcement, made after a Thursday (May 4) meeting of the WHO's International Health Regulations (IHR) Emergency Committee, means that COVID-19 is no longer considered a "public health emergency of international concern" (PHEIC), the highest alert level the body can issue. 

WHO Director-General Tedros Adhanom Ghebreyesus said at a May 5 news conference that it was "with great hope that I declare COVID-19 over as a global health emergency." However, he cautioned "that does not mean COVID-19 is over as a global health threat."

The WHO's announcement ends a designation made by the agency on Jan. 30, 2020. In the more than three years that have followed, the coronavirus has swept across the world, resulting in more than 765 million confirmed cases and just under 7 million deaths, as of May 3, 2023. Tedros said that this death toll is a significant underestimates and that the true death toll is likely closer to 20 million.  

Related: Brain shrinkage linked to COVID-19 

The WHO's guidelines are legally binding for 196 countries, including 194 WHO member states, that signed up to the International Health Regulations (IHR), which were first adopted in 1969. PHEIC status is assigned to extraordinary events that, due to the international spread of a disease, pose a public health risk to the whole world that requires a coordinated international response. 

The global COVID-19 weekly death rate has fallen dramatically since its peak at the height of the pandemic, from more than 100,000 weekly deaths in January 2021 to around 4,000 per week in April 2023, according to WHO data. 

"For more than a year, the pandemic has been on a downward trend, with population immunity increasing from vaccination and infection, mortality decreasing and the pressure on health systems easing," Tedros said. "This trend has allowed most countries to return to life as we knew it before COVID-19." 

The declaration of a PHEIC creates an agreement among U.N. member states around the world to follow WHO recommendations for managing the health emergency, which are used as guidelines to build each country's emergency response. With the virus's PHEIC status removed, it is now up to individual nations to decide how they will manage the virus.

The removal of PHEIC status doesn't mean that SARS-CoV-2, the virus that causes COVID-19, is no longer around or that the infrastructure built to fight the virus should be rolled back, Tedros cautioned.

"The worst thing any country can do now is to use this news as a reason to let down its guard, to dismantle the systems it has built, or to send the message to its people that COVID-19 is nothing to worry about," he said. Tedros said that if deaths or infections from COVID-19 rose significantly in the future, he would not hesitate to call another emergency meeting and reassign its PHEIC status.

During the May 4 news conference, Dr. Mike Ryan, executive director of WHO's Health Emergencies Programme, said COVID-19 still poses a public health threat and that the virus still has the potential to evolve into new variants that could exacerbate those risks.

"We fully expect that this virus will continue to transmit, but this is the history of pandemics," Ryan said. "It took decades for the final throes of the pandemic virus of 1918 to disappear. In most cases, pandemics truly end when the next pandemic begins. I know that’s a terrible thought but that is the history of pandemics."

The COVID-19 pandemic has not damaged people's mental health on a wide scale, new research finds. 

Overall, people reported being about as prone to depression, anxiety and other mental health symptoms both before and during 2020, when SARS-CoV-2 first exploded. But why didn’t the pandemic have wide-reaching mental health impacts, given just how much it disrupted people’s lives?

In some ways, the results are unsurprising, experts told Live Science. 

Just as in past disasters, people showed they were resilient and could adapt to the threat of COVID-19, said Bruria Adini, head of the department of emergency management and disaster medicine at Tel Aviv University, who has tracked the impact of the pandemic over time in Israel but was not involved in the new analysis.

"Adversities do not cause most people over time to be incapacitated," Adini said. 

However, there were nuances in the results, with some groups, such as parents and sexual and gender minorities, faring worse than the general population, overall.

COVID's mental health impacts

The study, published March 8 in the British Medical Journal, analyzed 137 studies that looked at the same people's mental health before January 2020 and later in 2020, although one study revisited participants in 2021. In total, these studies included tens of thousands of people from at least 32 countries, most of which were middle-to-high income. 

The meta-analysis found no overall differences in the rate of self-reported depression or anxiety symptoms, or in general mental health symptoms, which can include things like fatigue or changes in appetite or sleep, in the population. Some subgroups, including women, parents, and sexual and gender minorities saw mental health declines, but these declines were relatively small, nothing like the "tsunami" of mental health problems some predicted. 

The findings triggered a wave of skepticism on social media, with users pointing out the ways they'd cracked up during the lockdown era of COVID-19. 

"I built my cat a mech suit out of cardboard," tweeted comedy writer Jesse McLaren, alongside photos of a nonplussed cat on top of a cardboard robot creation. Meanwhile quantum computing specialist Anna Hughes tweeted photos of her quarantine project of cooking "increasingly unsettling eggs." 

This genre of tweet inadvertently reveals part of what might be behind the apparent lack of mental health catastrophe: People are adaptable and find creative ways to cope and connect, even in trying situations. For that reason, some psychologists weren't surprised that the pandemic didn't trigger huge spikes in negative mental health symptoms. 

"People are considerably more resilient than is commonly assumed, so I did not anticipate substantial mental health effects," said Anthony Mancini, a clinical psychologist at Pace University who was not involved in the current study but who published similar findings in the journal Psychological Medicine in 2021. Lockdowns may have cut both ways on mental health, Mancini added. Although they ripped people from their daily routines and increased isolation, they also cut down on stressful day-to-day hassles like commuting. 

But there is more nuance to the findings. Both Mancini's work and the new study found variation in how people responded. Study coauthor Danielle Rice, a clinical psychologist at McMaster University in Canada and her colleagues found that there was a small-to-medium decline in general mental health and a small worsening of anxiety for parents after the pandemic began. Older adults, university students and sexual and gender minorities all experienced some small increases in depression symptoms. On the other hand, people who had existing mental health conditions saw some small improvements in general mental health and depression symptoms. 

Some of these findings make logical sense, Rice told Live Science. For instance, women are overrepresented in the healthcare field and thus may have experienced more work-related stressors in the early pandemic. Parents had to navigate school closures and childcare disruptions. 

But those results should also be taken with a grain of salt, because each subgroup was small enough that the estimates are uncertain, she said. And the meta-analysis included a limited set of studies, each with weaknesses, said Roxane Cohen Silver, a psychologist at the University of California, Irvine, who was not involved in the research.

"There are serious limitations in most of the research that they're including," Silver told Live Science.

Study limitations

Rice and her team selected studies that provided comparisons of mental health in the same people before and after the pandemic began. That's a valid choice, Silver said, but leaves out many studies that began after the pandemic started. Silver and her colleagues conducted nationally representative research in the U.S. that did show increases in acute stress and depressive symptoms in the early months of 2020. But those studies would not meet the criteria to be included in the new analysis, because they started in March.

While the studies may have had the advantage of pre- and post-pandemic measurements, they had other limitations. Most didn't capture a representative sample of society, and many participants in these studies didn’t answer follow-up surveys over time. Those drawbacks should temper the conclusions of the meta-analysis, Silver said. 

The studies were done around the world, with 38% focusing on Europe and Central Asia, 34% on East Asia and the Pacific region, 20% on North America and 8% on the rest of the globe. The vast majority, however, were done in upper- and middle-income nations, and 76% focused on adults, with most of the rest focusing on adolescents. Very few children under the age of 10 were included.

Rice and her colleagues focused on analyzing depression, anxiety, and general mental health symptoms because these were the most common questions asked in the studies they included. These symptoms are also important because they can indicate that a person might need clinical treatment, Rice said.

But people may have felt other things, such as loneliness, stress, or distress, that the surveys didn’t focus on. Silver's work suggests that the degree of mental health struggles people experienced had a lot to do with their personal experience of the pandemic. Those who lost a loved one to COVID-19, who had the disease themselves in early 2020, or who consumed a lot of COVID-related news coverage fared the worst, according to her research published in 2022 in the journal Health Psychology. 

Adini agreed that individual differences mattered a lot. Her studies have shown that people's stress, perceptions of threat, and mental health symptoms fluctuated over the first two years of the pandemic, and that it wasn't always the disease itself that caused the distress, but also economic and national security worries.

COVID-19 was the top infectious disease killer for kids and teens in the U.S. between August 2021 and July 2022, a new analysis shows. It also ranked among the leading causes of death for any reason for U.S. children and teens in the same time period, the researchers determined.

The research, published Monday (Jan. 30) in the journal JAMA Network Open, utilized data from the Centers for Disease Control and Prevention (CDC) Wide-Ranging Online Data for Epidemiologic Research (WONDER) database, which includes mortality statistics drawn from the death certificates. 

The analysis took into account only deaths where COVID-19 was listed as the underlying, or primary, cause of death, as opposed to a contributing factor. In the study timeframe, 821 people ages 19 and younger died of the disease; that's an overall death rate of about one COVID-19 death per 100,000 people in the age group. 

"COVID-19 deaths constituted 2% of all causes of death in this age group," the researchers reported.

To put this death toll in context, the team pulled child and teen mortality data from 2019, before the pandemic began. In doing so, they checked the National Center for Health Statistics' ranked list of causes of death, where the causes are ordered by the frequency at which they're reported. 

Related: The 'Kraken' COVID subvariant: What to know about quickly rising omicron descendant 

Placed within this list, the rate of COVID-19 deaths in the study period exceeded the rate of influenza and pneumonia deaths in 2019 — reported at 0.6 deaths per 100,000 people — and fell just short of deaths caused by heart disease — 1.1 deaths per 100,000 people. That placed COVID-19 eighth out of the 10 ranked causes of death. 

If the team excluded deaths unrelated to disease, meaning those caused by unintentional injuries, assault or suicide, COVID-19 ranked fifth out of the remaining causes of death. (Unintentional injuries initially ranked second, at 9.1 deaths per 100,000 people, and assaults and suicides ranked fourth and fifth, respectively, at about 3.4 deaths per 100,000 people.)

"Our study period, August 1, 2021, to July 31, 2022, coincides with substantial infection waves of the COVID-19 Delta and Omicron variants," the researchers noted in their report. 

Finally, the researchers looked at the 10 leading causes of death dating back to 2015. They found that the rankings had remained largely unchanged between 2015 and 2021, with the exception of COVID-19 making the list in 2021.

"In this study, COVID-19 was a leading cause of death among individuals aged 0 to 19 years in the US," the study authors concluded. "Our findings underscore the public health relevance of COVID-19 to CYP [children and young people]."

The Black Death ravaged Europe between 1347 and 1353, killing millions. Plague outbreaks in Europe then continued until the 19th century.

One of the most commonly recited facts about plague in Europe was that it was spread by rats. In some parts of the world, the bacterium that causes plague, Yersinia pestis, maintains a long-term presence in wild rodents and their fleas. This is called an animal "reservoir."

While plague begins in rodents, it sometimes spills over to humans. Europe may have once hosted animal reservoirs that sparked plague pandemics. But plague could have also been repeatedly reintroduced from Asia. Which of these scenarios was present remains a topic of scientific controversy.

Our recent research, published in the Proceedings of the National Academy of Sciences (PNAS), has shown that environmental conditions in Europe would have prevented plague from surviving in persistent, long-term animal reservoirs. How, then, did plague persevere in Europe for so long?

Our study offers two possibilities. One, the plague was being reintroduced from Asian reservoirs. Second, there could have been short- or medium-term temporary reservoirs in Europe. In addition, the two scenarios might have been mutually supportive.

However, the rapid spread of the Black Death and subsequent outbreaks of the next few centuries also suggest slow-moving rats may not have played the critical role in transmitting the disease that is often portrayed.

European climate

To work out whether plague could survive in long-term animal reservoirs in Europe, we examined factors such as soil characteristics, climatic conditions, terrain types and rodent varieties. These all seem to affect whether plague can hold on in reservoirs.

For example, high concentrations of some elements in soil, including copper, iron, magnesium, as well as a high soil pH (whether it is acidic or alkaline), cooler temperatures, higher altitudes and lower rainfall appear to favour the development of persistent reservoirs, though it is not entirely clear why, at this stage.

Based on our comparative analysis, centuries-long wild rodent plague reservoirs were even less likely to have existed from the Black Death of 1348 to the early 19th century than today, when comprehensive research rules out any such reservoirs within Europe.

This contrasts sharply with regions across China and the western US, where all the above conditions for persistent Yersinia pestis reservoirs in wild rodents are found.

In central Asia, long-term and persistent rodent reservoirs may have existed for millennia. As ancient DNA and textual evidence hints, once plague crossed into Europe from central Asia, it appears to have seeded a short- or medium-term reservoir or reservoirs in European wild rodents. The most likely place for this to have been was in central Europe.

However, as local soil and climatic conditions did not favour long-term and persistent reservoirs, the disease had to be re-imported, at least in some instances. Importantly, the two scenarios are not mutually exclusive.

Radical difference

To go deeper into the role of rats in spreading plague in Europe, we can compare different outbreaks of the disease.

The first plague pandemic began in the early sixth century and lasted until the later eighth century. The second pandemic (which included the Black Death) began in the 1330s and lasted five centuries. A third pandemic began in 1894 and remains with us today in places such as Madagascar and California.

These pandemics overwhelmingly involved the bubonic form of plague, where the bacteria infect the human lymphatic system (which is part of the body’s immune defences). In pneumonic plague, the bacteria infect the lungs.

The plagues of the second pandemic differed radically in their character and transmission from more recent outbreaks. First, there were strikingly different levels of mortality, with some second pandemic outbreaks reaching 50%, while those of the third pandemic rarely exceeded 1%. In Europe, figures for the third pandemic were even lower.

Second, there were different rates and patterns of transmission between these two plague epochs. There were massive differences in the frequency and speed of transporting goods, animals, and people between the late middle ages and today (or the late 19th century). Yet the Black Death and many of its subsequent waves spread with astonishing speed. Over land, it raced almost as fast each day as the modern outbreaks do over a year.

As described by contemporary chroniclers, physicians, and others – and as reconstructed quantitatively from archival documents – the plagues of the second pandemic spread faster and more widely than any other disease during the middle ages. Indeed they were faster than in any period until the cholera outbreaks from 1830 or the great influenza of 1918-20.

Regardless of how the various European waves of the second pandemic began, both wild and non-wild rodents – rats, first and foremost – move much slower than the pace of transmission around the continent.

Third, the seasonality of plague also shows wide discrepancies. Plagues of the third pandemic (except for the rare ones, principally of pneumonic plague) have closely followed the fertility cycles of rat fleas. These rise with relatively humid conditions (although lower rainfall is important for plague reservoirs to first become established) and within a temperature band between 10°C and 25°C.

By contrast, plagues of the second pandemic could cross winter months in bubonic form, as seen across the Baltic regions from 1709-13. But in Mediterranean climes, plague from 1348 through the 15th century was a summer contagion that peaked in June or July – during the hottest and driest months.

This deviates strikingly from plague seasons in these regions in the 20th century. Because of the low relative humidity and high temperatures, these months were then the least likely times for plague to break out among rats or humans.

These differences raise a crucial question about whether the bubonic form of the plague depended on slow-moving rodents for its transmission when instead it could spread much more efficiently directly, from person to person. Scientists have speculated that this could have occurred because of ectoparasites (fleas and possibly lice), or through people’s respiratory systems and through touch.

Questions such as the precise roles played by humans and rats in past plague pandemics need further work to resolve. But as shown by this study, and others, major steps forward can be made when scientists and historians work together.

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

You may have heard the term "endemic" used to describe diseases, often in comparison with the terms "epidemic" and "pandemic." Many health officials say that COVID-19 is likely transitioning from pandemic to endemic status in many countries. But what does that mean? 

More broadly, the term "endemic" refers to an organism that's found in a specific region. In ecology, that means a species that lives only in one geographical area, like a plant or animal limited to an island, according to the U.S. Geological Survey. However, in the context of public health, "endemic" refers to a disease with a constant presence or "usual" number of infections in a specific area, according to the Centers for Disease Control and Prevention. 

"The technical definition is a disease that's at a steady state. It's there all the time," Dr. Christopher J. Gill, a professor of global health at Boston University, told Live Science. "It's not really causing outbreaks, and it's not dying away."

That concept, in turn, depends on the idea of an "epidemic" disease — one with greater-than-normal levels of infection in a population, Gypsyamber D'Souza, an epidemiology professor at the Johns Hopkins Bloomberg School of Public Health, told Live Science. (An epidemic disease becomes "pandemic" if it spreads over several countries or the globe.)

Related: The worst epidemics and pandemics in history

Endemic status also depends on the impacts a disease has on society in a particular region, D'Souza said. "It means that there is enough immunity in the population that we have learned to live with that infection," she said. "We don't have surges of disease … that disrupt daily life."

Not every epidemic disease becomes endemic, however; many just disappear. "If you have an epidemic and you successfully contain and treat it and you are able to drive it to zero infections, you can prevent it from becoming endemic," D'Souza said. Examples include the 2005 H5N1 bird flu and the 2002-2004 severe acute respiratory syndrome (SARS) outbreaks.

A host of diseases have become endemic in the U.S., including respiratory illnesses such as flu and respiratory syncytial virus (RSV), as well as many childhood diseases. "Measles, mumps, rubella, chickenpox, group A strep [Streptococci], pink eye — all of these things are just constantly circulating," Gill said. At the beginning of the COVID-19 pandemic, experts wondered whether the disease would rise quickly in prevalence and disappear or eventually become endemic, though most predicted an endemic route, Gill said. At nearly three years into the pandemic, many experts said COVID-19 was endemic in the U.S. or soon to become so, as most people had some immunity from vaccination or exposure, D'Souza said. 

The timing of that transition could vary according to the expert, however, as they evaluated how far infection and death levels had fallen. "It's not an exact science," she said. "We're not going to say this exact day is when we have transitioned." Meanwhile, epidemic infection levels may continue in other parts of the world even as a disease becomes endemic in another region. 

Experts caution that becoming endemic doesn't necessarily mean less-severe disease, although "generally, we expect pathogens to become less pathogenic over time," Gill said. Similarly, endemicity doesn't mean a disease has ceased to be a public health problem, virologist and immunologist Matt Koci said in a North Carolina State University post. "Smallpox was an endemic disease that consistently killed 1 out of every 3 people it infected," he said.

Rarely, endemic diseases — particularly influenza — can return to epidemic status, Gill said. "Occasionally, the influenza virus can mutate radically into something almost completely unseen by the population," he said. "And then you can have a totally disastrous influenza pandemic," as happened in the 1918 influenza outbreak, in which a new flu strain killed roughly 50 million people.

Since the COVID variant omicron emerged in late 2021, it has rapidly evolved into multiple subvariants. One subvariant, BF.7, has recently been identified as the main variant spreading in Beijing, and is contributing to a wider surge of COVID infections in China.

But what is this new variant, and should we be worried? Although reports from China about this variant's characteristics are concerning, it doesn't appear to be growing too much elsewhere in the world. Here's what we know.

BF.7, short for BA.5.2.1.7, is a sub-lineage of the omicron variant BA.5.

Reports from China indicate BF.7 has the strongest infection ability out of the omicron subvariants in the country, being quicker to transmit than other variants, having a shorter incubation period, and with greater capacity to infect people who have had a previous COVID infection, or been vaccinated, or both.

To put this into context, BF.7 is believed to have an R0, or basic reproduction number, of 10 to 18.6. This means an infected person will transmit the virus to an average of 10 to 18.6 other people. Research has shown omicron has an average R0 of 5.08.

The high transmission rate of BF.7, taken with the risk of hidden spread due to the many asymptomatic carriers, is understood to be causing significant difficulty in controlling the epidemic in China.

Read more: China could face a catastrophic COVID surge as it lifts restrictions – here’s how it might play out

The symptoms of an infection with BF.7 are similar to those associated with other omicron subvariants, primarily upper respiratory symptoms. Patients may have a fever, cough, sore throat, runny nose and fatigue, among other symptoms. A minority of people can also experience gastrointestinal symptoms like vomiting and diarrhoea.

BF.7 may well cause more serious illness in people with weaker immune systems.

BF.7's mutations

As omicron has evolved, we've seen the emergence of new subvariants better able to escape immunity from vaccination or prior infection. BF.7 is no different.

BF.7 carries a specific mutation, R346T, in the spike protein of SARS-CoV-2 (a protein on the surface of the virus that allows it to attach to and infect our cells). This mutation, which we also see in BF.7's "parent" variant BA.5, has been linked with enhancing the capacity of the virus to escape neutralising antibodies generated by vaccines or previous infection.

A recent study examined the neutralisation of BF.7 in sera (a component of blood that should contain antibodies) from triple-vaccinated healthcare workers, as well as patients infected during the omicron BA.1 and BA.5 waves of the pandemic. BF.7 was resistant to neutralisation, driven partly by the R346T mutation.

BF.7 around the world

BF.7 has been detected in several other countries around the world including India, the U.S., the U.K. and several European countries such as Belgium, Germany, France and Denmark.

Despite BF.7's immune-evasive characteristics, and worrying signs about its growth in China, the variant seems to be remaining fairly steady elsewhere. For example, in the U.S. it was estimated to account for 5.7% of infections up to December 10, down from 6.6% the week prior.

While the U.K. Health Security Agency identified BF.7 as one of the most concerning variants in terms of both growth and neutralisation data in a technical briefing published in October (it accounted for over 7% of cases at that time), the most recent briefing says BF.7 has been de-escalated due to reduced incidence and low growth rates in the U.K.

Read more: XBB and BQ.1: what we know about these two omicron 'cousins'

We don't know exactly why the situation looks different in China. BF.7's high R0 might be due in part to a low level of immunity in the Chinese population from previous infection, and possibly vaccination too. We should, of course, be cautious about the data from China as it's based on reports, not peer-reviewed evidence yet.

An evolving virus

Since the emergence of SARS-CoV-2 three years ago, the virus has continued to evolve, acquiring genetic mutations more rapidly than expected.

The emergence of BF.7 and other new variants is concerning. But vaccination is still the best weapon we have to fight COVID. And the recent approval by the U.K. drugs regulator of bivalent boosters, which target omicron alongside the original strain of SARS-CoV-2, is very promising.

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

Believing in COVID-19 conspiracies may make people likelier to believe in other conspiracy theories down the road, a new study suggests.

The researchers, who published their findings Oct. 26 in the journal PLOS One, suggested that thinking the number of COVID-19 deaths was exaggerated, or that China deliberately released or engineered the virus for nefarious purposes, is a kind of gateway drug to other conspiracy theories.

Conspiracy theories hold that shadowy groups are secretly masterminding large-scale plots that affect the public. They range from the belief that aliens on UFOs create crop circles to the wild and unfounded idea that the moon landing was faked.  

Conspiracist beliefs tend to be rooted in a feeling of losing control or being uncertain, Live Science previously reported. 

RELATED: When did Democrats and Republicans switch parties?

Therefore, the COVID-19 pandemic was the perfect storm for generating conspiracy theories, the research authors suggested.

"The widespread damage created by the COVID-19 pandemic has heightened people's anxiety, uncertainty, feelings of powerlessness, and has created friction between members of different social groups," the researchers wrote in the study. "Such conditions represent a near perfect recipe for the proliferation of conspiracy theories."

In the new study, the researchers looked at two surveys. In the first, they surveyed roughly 500 people in the U.S. in June 2020, asking participants about their conspiracist beliefs in general and their belief in COVID-19 conspiracy theories in particular. The study authors then followed up with those people six months later. 

The participants who believed that "COVID-19 was intentionally brought into the world for dark purposes" or that "the severity of COVID-19 was exaggerated" were more likely to believe that the 2020 U.S. presidential election was riddled with fraud or to espouse other theories, such as that “some UFO sightings and rumors are planned or staged in order to distract the public from real alien contact.” This correlation held even when the researchers controlled for baseline political orientation.

In the second survey, the researchers asked more than 2,000 people in the U.K. to rate how much they agreed with the following statement: “I think that many very important things happen in the world, which the public is never informed about,” as a proxy for their tendency to believe in conspiracy theories. At a second point in time, they asked people to endorse their belief in COVID-19 conspiracy theories.

They then asked participants the first question in several waves over time. Just as in the first survey, belief in COVID-19 conspiracy theories predicted a later rise in general conspiracist thinking.

The findings support the notion that conspiracy theories about COVID-19 can act as a gateway to additional outlandish beliefs, but further research should assess if the same effect holds true for other conspiracy theories, such as the notion that the 9/11 attacks were faked, the study authors noted.

Boston University scientists have created a hybrid version of the coronavirus that causes COVID-19. Their experiments sparked controversy, with heated headlines claiming that the researchers made the virus more lethal and university officials denouncing these claims as "false and inaccurate."

The new omicron spike-carrying virus — built by attaching the spike protein from an omicron version of the virus to the original SARS-CoV-2 virus — killed 80% of lab mice infected with it, making it more severe than the original omicron variant which didn’t kill any infected mice. Yet the hybrid virus was still less deadly than the original Wuhan variant of the virus, which killed 100% of infected lab mice. 

Scientists at Boston University's National Emerging Infectious Diseases Laboratories (NEIDL) created the chimeric virus to study how omicron versions of the virus, which first appeared in 2021, evade immunity built up against past strains and yet cause a lower rate of severe infections. After exposing mice either to the chimeric virus or to the naturally-occuring omicron BA.1 virus, the researchers found that the mutated spike protein of the omicron virus did enable it to dodge immunity, but that the mutated spike wasn't responsible for making omicron less severe. 

The researchers published their findings Oct. 14 on the preprint database bioRxiv, so it has yet to be peer-reviewed.

Related: 21 of the worst epidemics and pandemics in history

"Consistent with studies published by others, this work shows that it is not the spike protein that drives Omicron pathogenicity, but instead other viral proteins. Determination of those proteins will lead to better diagnostics and disease management strategies," lead author Mohsan Saeed, an assistant professor at NEIDL, said in a statement, according to STAT..

Although the research was conducted properly in a biosecurity level 3 laboratory and approved by an internal biosafety review committee and Boston's Public Health Commission, controversy is swirling around the study because the researchers did not clear the work with the National Institute of Allergy and Infectious Diseases (NIAID), which was one of its funders, STAT reported. 

The scientists also didn't divulge to NIAID if their experiments could create an enhanced pathogen of pandemic potential (ePPP), according to STAT. To be awarded federal funding for research on viruses with pandemic potential, proposals have to pass through a committee process, called a P3CO framework, that assesses the pros and cons of the work.

"What we would have wanted to do is to talk about exactly what they wanted to do in advance, and if it met what the P3CO framework defines as enhanced pathogen of pandemic potential, ePPP, we could have put a package forward for review by the committee that's convened by HHS, the office of the assistant secretary for preparedness and response, Emily Erbelding, director of NIAID's division of microbiology and infectious diseases told STAT. "That's what the framework lays out and that's what we would have done." Eberling said that NIAID would have "conversations over upcoming days" with the researchers.

The mistake may have emerged from an ambiguity in the P3CO framework's rules. For a virus to be defined as an ePPP, it has to be reasonably expected to produce pandemic potential results in humans. The mice used by the researchers for the study, however, might not have seemed to them to be a close enough analogue. 

Boston University has pushed back against media reports, most notably an article published by the U.K.'s Daily Mail, which claimed the research had created a more dangerous variant.

"We want to address the false and inaccurate reporting about Boston University COVID-19 research, which appeared today in the Daily Mail," Boston University said in a statement. "First, this research is not gain-of-function research, meaning it did not amplify the Washington state SARS-CoV-2 virus strain or make it more dangerous. In fact, this research made the virus replicate less dangerous." (The "Washington state SARS-CoV-2 strain" refers to a sample of the original Wuhan strain gathered in Washington in the early pandemic.)

Ronald B. Corley, the director of NEIDL, said in the statement that the Daily Mail report "sensationalized the message" and misrepresented "the study and its goals in its entirety."

"The animal model that was used was a particular type of mouse that is highly susceptible, and 80 to 100 percent of the infected mice succumb to disease from the original strain, the so-called Washington strain," Corley said. "Whereas Omicron causes a very mild disease in these animals."

As of Sept. 21, the current monkeypox outbreak has infected 62,532 people across 105 countries. Still, the World Health Organization (WHO) has not yet classified the current caseload as a pandemic.

But could that change? Given its spread, could monkeypox become a pandemic? 

The answer to that question depends on the definition of "pandemic." A pandemic is a "worldwide epidemic," in which there are high numbers of cases or outbreaks in many countries, Rachel Roper, a professor of microbiology and immunology at East Carolina University in Greenville, North Carolina, told Live Science in an email.

"I think it's a matter of opinion as to just how many cases you have to have in how many countries," Roper said. The Centers for Disease Control and Prevention (CDC) defines pandemic as "a disease event in which there are more cases of a disease than expected spread over several countries or continents, usually involving person-to-person transmission and affecting a large number of people."

There's always a chance that something, such as the virus's genetic code, could change, but several factors reduce the chances that monkeypox will become a pandemic. Even if it does, monkeypox will not exact anywhere near the toll of the COVID-19 pandemic, experts told Live Science.

Historically, monkeypox has not been terribly contagious, and outbreaks have been small

Monkeypox (sometimes abbreviated as MPXV or MPX) "is much less contagious than COVID," Roper said. Typically the transmission chain of monkeypox was short — one case of MPXV transmitted to about seven people maximum before dying out, so outbreaks have been short lived in the past, Roper said. Monkeypox was first documented to infect humans in 1970, and outbreaks since then, excluding the current pandemic, were "kind of small," she said. In countries where it is endemic, monkeypox is always present in animal hosts and typically spreads between humans only when they catch it from animals and start transmitting it to other people. 

But an analysis of monkeypox genomes from the current epidemic, published June 24 in the journal Nature Medicine, suggests that the version of the virus that is currently circulating has been passing from human to human in an uninterrupted transmission chain since 2017. This indicates that the average transmission chain is increasing, Roper said.

Still, for monkeypox, the reproductive number (R0), or the number of people directly infected by each person with the disease, has historically been less than 1, meaning any epidemic would burn out eventually even without active disease control measures (In contrast, the R0 for the currently circulating omicron variants of SARS-CoV-2, the virus that causes COVID-19, is estimated to be between six and 10, according to The Conversation.) But researchers don't know the R0 for the version of monkeypox currently circulating, according to a June 2022 paper in the journal The Lancet Infectious Diseases. 

It's hard to say why monkeypox is infecting so many people now, she added. It may be because mutations have made it more transmissible, or it may be because it has entered new populations that as a whole, have different behaviors or risk factors that increase transmission rates, Roper said. 

For example, in the African countries where monkeypox is endemic, the virus has not previously been known to spread via men having sex with men, Roper said. But the current outbreak is primarily affecting men who have sex with men and spreading through sexual and other close physical contact, according to the World Health Organization (WHO).

Monkeypox mutates pretty slowly

Monkeypox is a virus made of DNA, as opposed to being made up of single-stranded ribonucleic acid (RNA). This matters because DNA replication involves fewer mistakes than copying RNA does, so monkeypox mutates more slowly than counterparts such as SARS-CoV-2 or HIV.  This gives monkeypox viruses fewer opportunities to evolve to become more transmissible than RNA viruses would, according to the American Society for Microbiology. 

Still, for a poxvirus, monkeypox is developing mutations quickly, according to the June Nature Medicine genome analysis. Compared with strains circulating in 2018 and 2019, the currently circulating virus has 50 mutations, most likely picked up while circulating in humans, according to the paper. That's six to 12 times the number of mutations expected based on the typical mutation rate for poxviruses, the paper authors noted.

Not a lung virus

The virus that causes COVID-19 is "majorly respiratory," Roper said. "Its main target organ is the lungs." SARS-CoV-2 spreads when an infected person sneezes, coughs, or even just breathes, Roper said. In contrast, monkeypox is spread primarily by "direct contact with monkeypox rash, scabs, or body fluids from a person with monkeypox," according to the Centers for Disease Control and Prevention (CDC). The virus can also spread when a person touches objects and surfaces that have been used by someone infected with monkeypox.

"Monkeypox is so inefficient in how it's spread," Rodney Rohde, a professor and chair of clinical laboratory science at Texas State University, told Live Science. "You've got to be really close, skin-to-skin contact, or maybe with fomites like bed linen or clothing. And it actually takes kind of a long time, so several hours of contact, for it to occur, whereas [for] an aerosolized virus, it might be instantaneous — somebody sneezes or coughs in a room and you inhale it, and maybe 8, 10, 12 people get it."

We already have vaccines and treatments for monkeypox

Two vaccines, JYNNEOS and ACAM2000, are approved for use against monkeypox in the U.S., as Live Science previously reported. 

While there are no treatments specifically for monkeypox, according to the CDC, antiviral drugs that were developed to fight smallpox, such as tecovirimat (TPOXX), may be recommended for people with weakened immune systems. 

Given the existence of vaccines and treatments, combined with other factors, such as the low mortality rate of the monkeypox strain that's currently circulating, it should be possible to slow the rate of infection and limit deaths, Rohde said. The mortality rate for the type of monkeypox circulating in the current epidemic has historically been about 1%, according to the CDC. But the current outbreak may be much less deadly; based on  WHO numbers from late September, the fatality rate is 0.04%. While those numbers are still a rough estimate, they do suggest the toll of monkeypox is likely to be much, much lower than that of COVID-19, even if monkeypox does become a pandemic. "It could be deemed a pandemic at some point due to the number of countries that have cases and kind of the linear rise in cases that we're seeing," Rohde said. "But I do not believe it will be the type of global mortality crisis that we saw with COVID."

Originally published on Live Science.

Since the emergence of SARS-CoV-2, the coronavirus that causes COVID-19, the pathogen has given rise to a slew of descendants.

By picking up mutations in their genetic code, some of these descendants, known as coronavirus variants, have gained the ability to spread more easily between people, outwit the immune system or trigger more severe disease. These abilities give the variants a competitive edge over their relatives, and in time, the advantaged variants outcompete the disadvantaged for hosts and eventually drive them to extinction.

The omicron variant first emerged in November 2021 and gained global prominence in March 2022. And as of August 2023, the direct descendents of omicron — known as omicron subvariants — only have each other left to compete against, as all other versions of the coronavirus have dwindled away.             

The World Health Organization (WHO) ranks circulating SARS-CoV-2 variants in three categories: variants of concern (VOC), variants of interest (VOI) and variants under monitoring (VUM). As of March 15, 2023, there are no circulating VOCs, and all the VOIs and VUMs are different subvariants of omicron.

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

Here's a look at the science of the SARS-CoV-2 variants, including both omicron and past variants that have fallen from prominence.

Currently circulating variants 

Omicron variant (B.1.1.529)

Where did the variant emerge? The original version of omicron, formally known as B.1.1.529, was first identified in South Africa in November 2021. The WHO labeled omicron as a variant of concern on Nov. 26, 2021, but it's since been downgraded.

Where is it now? Omicron quickly spread around the world, causing a surge of COVID-19 cases in December 2021 and January 2022. By mid-March 2022, omicron was the dominant coronavirus variant in the world, accounting for 99.9% of coronavirus genome sequences from recent COVID-19 cases in the global database GISAID.

What are key mutations? The original version of omicron had more than 30 mutations in the genes that code for its spike protein, with 10 of those genes coding for parts of the "receptor binding domain," or the part of the spike protein that latches onto human cells. 

Some of omicron's other mutations have also shown up in previous variants of concern. For example, omicron has the N501Y mutation, which is also found in the alpha variant, and is thought to make the virus more contagious, according to The New York Times.

The original omicron, B.1.1.529, has since fallen out of circulation, but not before spawning dozens of its own descendents. Each of these offspring comes with its own genetic quirks. 

As of August, the WHO's list of VOIs includes XBB.1.5 and XBB.1.16, two branches that stem from the broader XBB lineage of omicron. The majority of VUM are also XBB subvariants, with the exception of BA.2.75 and its offspring CH.1.1. 

Why is the variant concerning? Omicron has many mutations in the spike protein that appear to make it more transmissible and allow it to at least partially evade vaccines. Some studies estimated that omicron's BA.1 subvariant is four times more transmissible than the delta variant, according to CNBC. And BA.2 is more contagious still — it's estimated to be 1.5 times more transmissible than BA.1, CNBC reported. 

Do vaccines work? Most COVID-19 vaccines, including those used in the U.S., prime the immune system against the spike protein. Because of the high number of mutations that omicron has on its spike protein, scientists expected that vaccines would be less effective against omicron compared with previous variants. 

And indeed, there has been an increased number of breakthrough infections with omicron compared with earlier variants. A study published in March in The New England Journal of Medicine found that the vaccine effectiveness of two doses of the Pfizer vaccine was 65%, but this fell to about 9% more than 25 weeks after vaccination. However, with an additional vaccine dose, the shot's effectiveness rose to 67%, and then fell to about 45% after about 10 weeks, the researchers found. A CDC report published in January 2022 also found that an extra dose provided 90% protection against hospitalization with omicron.

In fall 2022, two updated COVID-19 vaccines were released that targeted the omicron subvariants BA.4 and BA.5, as well as the original version of SARS-CoV-2. At the time, these two flavors of omicron were responsible for the majority of new COVID-19 cases in the U.S. In 2023, the vaccines will get another update, this time to guard against the XBB lineage of omicron, whose members are currently causing the majority of cases. 

(The XBB lineage includes EG.5, which started dominating in the U.S. in late July 2023.)  

Previously circulating variants 

The following information was last updated in March 2022. Previous sections of this article were last updated in August 2023.

Delta variant (B.1.617.2)

Where did the variant emerge? The delta variant, formerly called B.1.617.2, was first identified in India in October 2020 and labeled as a variant of concern in May 2021, according to the WHO.

Where is it now? Delta rapidly became the dominant variant in the U.S. and worldwide in the summer of 2021, but it would largely be replaced by omicron in mid-December 2021, according to Yale Medicine. Besides omicron, delta remains the only other VOC with a notable level of global circulation, according to WHO. By mid-March 2022, delta accounted for 0.1% of coronavirus genome sequences from recent COVID-19 cases in the global database GISAID. 

What are key mutations? The delta variant has several important mutations in the spike protein, including T19R, del157/158, L452R, T478K, D614G, P681R, D950N mutations, according to outbreak.info. Two of these mutations — L452R and D614G — allow the variant to attach more firmly to ACE2 receptors, Live Science previously reported. Others, such as P681R, may allow delta to evade host immunity. 

Why is the variant concerning? The delta variant is potentially up to 60% more transmissible than the alpha variant and perhaps twice as transmissible as the original strain of coronavirus that emerged in Wuhan, China. In addition, some evidence suggests the variant can more easily evade existing vaccines than earlier variants of the coronavirus.

Do vaccines work? All the vaccines approved in the U.S. likely work against the delta variant, although exactly how well still isn't clear. For instance, Public Health England found the Pfizer vaccine was 88% effective against the delta variant, while health officials in Israel announced the Pfizer vaccine was only 64% effective against delta, The New York Times reported. However, Israel didn't control for differences in people who did and did not get vaccinated, making its data hard to interpret, according to The New York Times. The Pfizer vaccine remained strongly protective against severe disease and hospitalization. In a statement, Moderna said its vaccine neutralized the delta variant, and though it has not yet provided real-world data on infection, it is likely to work similarly to the Pfizer mRNA vaccine. Johnson & Johnson said their vaccine produced a strong neutralizing antibody response against the delta variant, but did not report on how much it reduces the odds of symptomatic disease, Live Science previously reported.

Alpha variant (B.1.1.7)

Where did the variant emerge? The alpha variant, formerly called B.1.1.7, was first seen in the United Kingdom in September 2020, according to WHO(WHO). By December 2020, the variant had shown up in the United States.

Where is it now? Alpha is virtually extinct worldwide. After its emergence in the U.K., the alpha variant soon spread around the world, and became the dominant variant in the U.S. in the spring of 2021, according to The New York Times. But the delta variant replaced alpha as the dominant strain in the U.S. in the summer of 2021, the Times reported.  Cases of the alpha variant have since faded in the U.S. and worldwide. By March 2022, few to no genetic sequences from alpha had been reported worldwide, and the variant was designated a "previously circulating VOC," according to WHO. 

What are key mutations? The alpha variant has 23 mutations compared with the original Wuhan strain, with eight of those in the virus's spike protein, according to the American Society for Microbiology. (ASM) Three of the spike-protein mutations are thought to be responsible for the biggest impact on the virus's biology: The N501Y mutation seems to boost how tightly the spike protein attaches to the ACE2 receptors — the main entry point into human cells; the 69-70del mutation could, in concert with N501Y, explain the variant's increased transmissibility, some scientists say; and the P681H mutation could also increase transmissibility, as it may be involved in how the virus merges its membrane with that of a human cell in order to deliver its genome into the cell, according to ASM.

Why is the variant concerning? The strain is about 50% more transmissible than the original form of the novel coronavirus, according to the Centers for Disease Control and Prevention (CDC).

Do vaccines work? Research to date suggests that the two mRNA COVID-19 vaccines (Pfizer and Moderna vaccines) are effective at preventing symptomatic infections with the alpha variant of the coronavirus. For instance, a study published June 28, 2021 in the journal Nature Communications found that the blood of health care workers who had been vaccinated with the Pfizer shot was effective at neutralizing B.1.1.7. A single dose of the Johnson & Johnson vaccine also stimulates neutralizing antibodies that protect against the alpha variant, J&J reported in July, 2021.

Beta variant (B.1.351)

Where did the variant emerge? The beta variant, formerly called B.1.351, was first detected in South Africa in October 2020 and was designated a variant of concern in December 2020, according to WHO.

Where is it now? Beta is also nearly extinct. It took off rapidly in South Africa in late 2020 and early 2021, and spread to over 30 countries, Live Science previously reported. But beta was never common in the U.S., and it was later replaced by delta in the places where it was once dominant, according to Nature News. Beta was also designated a "previously circulating VOC" in March 2022, according to WHO.. 

What are key mutations? The beta variant has eight distinct mutations that may affect how the virus binds to cells, Live Science previously reported. The most notable are N501Y, K417N and E484K. The N501Y mutation, also seen in the alpha variant, may allow the novel coronavirus to bind more tightly to the ACE2 receptor. The K417N mutation may change the shape of the spike protein, making antibodies primed for earlier strains less likely to recognize the spike. The third notable mutation, E484K, also seems to help the virus evade antibodies from the immune system, according to a February 2021 study in the British Medical Journal. 

Why is the variant concerning? The beta variant is about 50% more transmissible than the original strain of SARS-CoV-2 that emerged in Wuhan, according to the CDC. Some monoclonal antibodies don't work as well against the strain, according to the CDC. Vaccines are also less effective against the variant. And the variant may lead to slightly more severe disease and slightly higher risk of death than the original coronavirus, according to a July 2021 study in The Lancet Global Health.

Do vaccines work? Most vaccines work with lower efficacy against beta than was seen for earlier strains. For instance, the Pfizer vaccine had a 75% efficacy against the beta variant, which is lower than the 95% efficacy seen in clinical trials when earlier strains were dominant, according to a May 2021 study in The New England Journal of Medicine. The Johnson & Johnson and Novavax vaccines also showed lower efficacy against the beta variant. And the AstraZeneca vaccine did not prevent mild or moderate COVID-19 in trials in South Africa when beta was the dominant strain, according to the Global Virus Network. Data on how well the Moderna shot works against the beta variant is limited, but most experts suspect it will work similarly to Pfizer's mRNA vaccine.

Gamma variant (P.1)

Where did the variant emerge? The earliest documented samples of the gamma variant, also known as P.1, were collected in Brazil in November 2020, according to the WHO. Scientists first found the variant in Japan in early January 2021, when four travelers tested positive for the virus after a trip to Brazil; researchers then found evidence that the variant was already widespread in the South American country, The New York Times reported. Gamma was labeled as a variant of concern on Jan. 11, 2021. 

Where is it? Gamma is no longer circulating widely. In July, 2021, gamma had been reported in 74 countries worldwide, according to the United Nations. But cases faded with the rise of delta and omicron, with few to no genetic sequences from gamma reported worldwide by March 2022, according to WHO. Gamma was also designated a "previously circulating VOC" in March 2022.

What are key mutations? Gamma is closely related to beta (B.1.351), and the two variants share some of the same mutations in their spike proteins, the Times reported. These spike protein mutations include N501Y, which helps the virus bind tightly to cells and is also found in the alpha (B.1.1.7) lineage. The spike mutation K417T may also help gamma latch onto cells, while the E484K mutation likely helps the variant dodge certain antibodies. And according to the CDC, in addition to these three mutations, the variant carries eight additional sequence changes in its spike: L18F, T20N, P26S, D138Y, R190S, D614G, H655Y and T1027I.

Why is the variant concerning? Several studies suggest that gamma is about twofold more transmissible than its parent coronavirus lineage, B.1.1.28, and that gamma infections are associated with a significantly higher viral load than other variants. Compared with the original strain of SARS-CoV-2, gamma shows less susceptibility to several monoclonal antibody treatments, including bamlanivimab and etesevimab, according to the CDC. And according to a study, published May 12, 2021 in the journal Cell Host & Microbe, the variant also appears relatively resistant to neutralization by convalescent plasma and antibodies drawn from vaccinated people.

Do vaccines work? Moderna's COVID-19 vaccine produces neutralizing antibodies against gamma, although the shot is slightly less effective against the variant than it is against the original strain of the virus, the company announced on June 29. The Pfizer vaccine showed similar levels of protection against gamma in a recent study, Business Insider reported; and the single-dose Johnson & Johnson vaccine also produces neutralizing antibodies against the variant, according to a recent statement from the company.

Lambda variant (C.37)

Where did the variant emerge? The lambda variant, also known as C.37, was first detected in Peru in August 2020, according to WHO. On June 14, 2021, WHO designated C.37 a global variant of interest, and dubbed it lambda.

Where is it now? Lambda spread to a number of countries in the summer of 2021 and had high levels of spread in Peru and Chile, Live Science previously reported. But by March 2022, there was no circulation of the variant reported worldwide in the past 90 days, according to WHO.

What are key mutations? The variant has seven mutations in the virus's spike protein compared with the original strain of SARS-CoV-2 detected in Wuhan. Specifically, these mutations are known as G75V, T76I, del247/253, L452Q, F490S, D614G and T859N, according to the WHO.

Why is the variant concerning? Some of these mutations have the potential to increase transmissibility of the virus or to reduce the ability of certain antibodies to neutralize, or inactivate, the virus. For example, lambda has a mutation known as F490S located in the spike protein's receptor-binding domain (RBD), where the virus first docks onto human cells. A paper published in the July 2021 issue of the journal Genomics identified F490S as a likely "vaccine escape mutation" that could both make the virus more infectious and disrupt the ability of vaccine-generated antibodies to recognize the variant.

Do vaccines work? Data from the time when lambda was circulating did not show that the lambda variant caused more severe disease or reduced vaccine effectiveness, according to Public Health England.

Mu variant (B.1.621)

Where did the variant emerge? The mu variant, also known as B.1.621, was first detected in Colombia in January 2021, according to the WHO. On Aug. 30, WHO classified it as a "variant of interest," and named it mu.

Where is it now?  The mu variant caused some large outbreaks in South America and Europe in 2021, according to the WHO. But the mu variant did not out-compete the delta variant in terms of circulation, and by March 2022, there was no circulation of the variant reported worldwide in the past 90 days, according to WHO. 

What are key mutations?  Mu shares some concerning mutations with the beta variant, including mutations known as E484K and K417N, according to Medpage Today. 

Why is the variant concerning? The mu variant "has a constellation of mutations that indicate potential properties of immune escape," WHO officials said in August 2021. Early data in lab dishes show that antibodies generated in response to COVID-19 vaccination or previous infection are less able to "neutralize," or bind to and disable, the mu variant, the report said. However, this finding still needs to be confirmed by future studies.

Do vaccines work? According to Public Health England, there is "no real-world data on vaccine effectiveness" against mu. Studies in lab dishes have found a reduction in the ability of antibodies to neutralize the mu variant that is "at least as great as that seen with the beta variant,"  according to Public Health England. 

 Jeanna Bryner, Tia Ghose and Yasemin Saplakoglu contributed to this article. 

Editor's note: The introduction and omicron sections of this page were last updated on Aug. 8, 2023. The information about previously circulating variants was last updated on March 23, 2022. 

Originally published on Live Science.  

Editor's note: This article was last updated on March 22, 2022, by Live Science staff writer Nicoletta Lanese.

Dozens of coronavirus vaccines entered clinical trials during 2020, and now, more than 20 different shots are being administered to people around the world. Out of the five most widely used COVID-19 vaccines, three are cleared for use in the United States. 

Here's a guide to how those top five vaccines work, their common side effects and how well the shots protect against SARS-CoV-2, the virus that causes COVID-19:

Pfizer-BioNTech

As of March 2022, the COVID-19 vaccine developed by Pfizer and German biotechnology company BioNTech is in use in 156 countries, including the U.S., according to The New York Times coronavirus vaccination tracker. 

The vaccine was the first to be fully approved by the U.S. Food and Drug Administration (FDA), according to a statement from the agency. Full approval was granted on Aug. 23, 2021, roughly seven months after the shot had first been authorized for emergency use in the U.S. 

The full approval allows the vaccine to be used in individuals ages 16 and older; meanwhile, the vaccine can be given to children ages five to 15 under an emergency use authorization, as it's yet to be fully approved for this age group, according to the Centers for Disease Control and Prevention (CDC). 

Related: 11 surprising facts about the immune system

The Pfizer-BioNTech vaccine uses a molecule called messenger RNA (mRNA) as its base, the CDC notes. A molecular cousin of DNA, mRNA contains instructions to build specific proteins, and in this case, the mRNA in the vaccine codes for the coronavirus spike protein. 

To build the vaccine, scientists place the mRNA inside a small bubble of fat, called a lipid nanoparticle; the shot also contains several salts and sugars, to help keep the vaccine's ingredients stable while it's manufactured, frozen, shipped and stored. (The Pfizer-BioNTech vaccine must be stored at minus 94 F (minus 70 C) to remain viable, according to The New York Times.)

Once injected into the body, the vaccine instructs human cells to build the spike protein, and the immune system learns to recognize and attack it, according to the CDC.

The vaccine is administered in two doses given 21 days apart. In the U.S., everyone aged 12 and older is now recommended to get a booster shot at least five months after completing their Pfizer-BioNTech primary series. Individuals ages 12 to 17 can only get a Pfizer-BioNTech booster, but older people can get either Pfizer-BioNTech or Moderna, the CDC notes. (The Johnson & Johnson vaccine is also available as a booster, but Pfizer-BioNTech or Moderna would be recommended, the CDC states.)

Common side effects include pain, redness and swelling at the injection site; tiredness; headache; muscle pain; chills; fever; and nausea. Rarely, inflammation of the heart muscle (myocarditis) and inflammation of the saclike membrane surrounding the heart (pericarditis) have been reported in teens and young adults who received the shot. 

"These reports are rare, and the known and potential benefits of COVID-19 vaccination outweigh the known and potential risks, including the possible risk of myocarditis or pericarditis," the CDC notes. "The inflammation, in most cases, gets better on its own without treatment," according to Yale Medicine.

Late-stage clinical trials found that the vaccine was 95% effective at preventing laboratory-confirmed COVID-19 infections in people ages 16 and older, according to a report in the CDC journal Morbidity and Mortality Weekly Report (MMWR) published in December 2020. Later clinical trials suggested that the shots were similarly effective in children ages 5 to 15, according to the CDC. 

That said, there's been mixed data on whether the shot offers the same level of protection against infection with omicron to children ages 5 to 11 as it does to older children and adults, STAT reported. Real-world data from New York state hinted that the shots provide less protection to the youngest age group, potentially because those children receive a smaller dose of vaccine than older teens and adults. However, new data from 10 states suggests that the vaccine is similarly protective in both groups, regardless of this dosing difference. 

In general, data suggest that two doses of the vaccine provide about 70% protection against hospitalization and 33% protection against infection with the omicron variant, Healthline reported. A booster dose bolsters this protection, as early data suggest it's 70% to 75% effective against symptomatic infections and about 80% to 90% effective against severe disease. 

Moderna

The COVID-19 vaccine developed by U.S. biotech company Moderna and the National Institute of Allergy and Infectious Diseases is now being used in the U.S. and 87 other countries, according to The New York Times coronavirus vaccination tracker. 

It received full FDA approval on Jan. 31, 2022, for individuals ages 18 and older, according to the CDC. The FDA originally authorized the vaccine for emergency use on Dec. 18, 2020.

Like the Pfizer-BioNTech vaccine, the Moderna shot uses mRNA as its base and is administered in two doses. However, those doses are given four weeks apart, rather than three. People ages 18 and older should get a booster shot at least five months after completing their Moderna primary series, the CDC now recommends. In most instances, these individuals are recommended to get either a Pfizer-BioNTech or Moderna booster, rather than the Johnson & Johnson vaccine. 

The Moderna vaccine can be stored at minus 4 F (minus 20 C), rather than requiring deep-freezing like the Pfizer-BioNTech shots.

Common side effects include pain, redness and swelling at the injection site; tiredness; headache; muscle pain; chills; fever; and nausea. As with the Pfizer-BioNTech shots, rarely, young adults who get the Moderna shots have developed myocarditis or pericarditis. Again, the potential benefits of COVID-19 vaccination outweigh this small risk, the CDC states.

Clinical trials found that the vaccine was 94.1% effective at preventing laboratory-confirmed COVID-19 infection in people who received two doses. There's not much data on how the shots hold up against omicron, but early studies hint that a three-dose course of the vaccine (that is, the two initial shots, plus a booster) offers 88% to 99% protection against hospitalization from omicron, Healthline reported. The three-dose course was about 47% to 71% protective against symptomatic omicron infections in healthy adults, although again, these estimates rely on preliminary data.

Related: 20 of the worst epidemics and pandemics in history 

Oxford-AstraZeneca

The COVID-19 vaccine developed by the University of Oxford and pharmaceutical company AstraZeneca is now being used in 182 countries but not in the U.S., according to The New York Times coronavirus vaccination tracker. 

The vaccine contains a modified version of an adenovirus, which is a type of virus that causes the common cold; specifically, the virus used in the AstraZeneca vaccine naturally infects chimpanzees, according to the Vaccine Knowledge Project, an informational site managed by an academic research group in the Department of Paediatrics at the University of Oxford.

Related: 5 dangerous myths about vaccines

Scientists modified the adenovirus so that it cannot infect human cells. Instead, the virus acts as a vessel to carry a short stretch of DNA into the body. That DNA codes for the coronavirus spike protein, a pointed structure that the virus uses to enter and infect cells. Once inside the body, the vaccine enters human cells and delivers these spike protein genes, which the cells then use to build the spike protein itself. The presence of spike proteins then triggers an immune response that trains the immune system to recognize and destroy the spike. 

The Oxford-AstraZeneca vaccine is administered in two doses, spaced four to 12 weeks apart, the Vaccine Knowledge Project notes. In the U.K., people are now recommended to get a booster shot if three or more months have elapsed since their second dose of the vaccine. This recommendation applies to individuals ages 16 and older, plus children ages 12 to 15 who are at high-risk for severe COVID-19 or who live with an immunocompromised person. Most people in the U.K. receive either a Pfizer-BioNTech or Moderna shot for their booster, but some may be offered Oxford-AstraZeneca if they can't receive the other shots due to known allergies to the vaccines' ingredients, for instance.

Common side effects include pain near the injection site, chills, fever, joint pain, muscle aches, fatigue and headache. These flu-like symptoms typically occur in the few days following the injection. Very rarely, people who received the Oxford-AstraZeneca vaccine developed blood clots and low platelet counts, Live Science previously reported.

A large, late-stage clinical trial found that the Oxford-AstraZeneca vaccine is about 76% effective at preventing symptomatic COVID-19 infections, AstraZeneca reported in March 2021. In the same trial, the shot showed 100% efficacy against severe disease and hospitalization. At the time those results were published, the alpha, beta and gamma coronavirus variants had recently been named variants of concern, but the report didn't break down whether the shots were more or less protective against different variants.

In October 2021, the company also released real-world data on the vaccine's effectiveness; this new data took new coronavirus variants, such as delta, into account. According to the AstraZeneca statement, two doses of the vaccine are about 92% effective against severe disease or hospitalization due to the delta variant and about 70% effective against symptomatic delta infections. 

However, early data from the U.K. Health Security Agency suggested that the vaccine offered "significantly lower" protection against symptomatic infections due to omicron than those due to delta. However, after a booster shot, the vaccine's effectiveness against omicron rose to between about 70% and 75%.         

The vaccine can be stored at normal refrigerator temperatures and is expected to last for at least six months when stored at 36 to 46 degrees Fahrenheit (2.2 to 7.7 degrees Celsius), according to The Conversation. 

Johnson & Johnson

The COVID-19 vaccine developed by Johnson & Johnson's Janssen is used in the U.S. and 86 other countries, according to The New York Times coronavirus vaccination tracker. 

In clinical trials, the vaccine was about 72% effective at preventing symptomatic COVID-19 in the U.S., but across all the countries included in the trials, the vaccine was only 66% effective, according to Yale Medicine. This difference in protection was attributed to the highly contagious variants circulating in some countries at the time. Data later gathered in South Africa suggest that the shot is about 67% effective against hospitalization and about 82% effective against fatal disease from the delta variant, and the shot offered similar protection against beta. 

Early data hint that the Johnson & Johnson vaccine may offer a similar level of protection against omicron as the Pfizer-BioNTech and Moderna shots, The New York Times reported in March 2022. This conclusion was based on data from people who had not received booster shots but had completed their primary vaccine series. 

In addition, early data suggest that two doses of the Johnson & Johnson vaccine — meaning the primary dose plus a booster — offer a similar level of protection against symptomatic and severe omicron infections as three doses of an mRNA vaccine, according to the Times.  

The vaccine has not been fully approved by the FDA but is available under emergency use authorization, the agency's website notes. 

The single-dose vaccine is available both as a primary vaccination dose for individuals ages 18 and older and as a booster dose for individuals ages 18 and older who completed their primary vaccination at least two months prior. In general, the CDC recommends that people who received the Johnson & Johnson vaccine for their primary vaccination seek a Pfizer-BioNTech or Moderna shot as their booster.

"In most situations, Pfizer-BioNTech or Moderna COVID-19 vaccines are preferred over the J&J/Janssen COVID-19 vaccine for primary and booster vaccination due to the risk of serious adverse events [linked to the J&J vaccine]," the CDC states. 

The most common side effects of the vaccine are fairly mild, including redness and pain at the injection site; tiredness; headache; muscle pain; chills; fever; and nausea. However, "there is a plausible causal relationship" between the Johnson & Johnson shot and a rare but potentially fatal blood clotting disorder called thrombosis with thrombocytopenia syndrome, where people develop blood clots and low platelet counts. "It occurs at a rate of about 3.83 cases per million Janssen doses," the CDC notes. 

In July 2021, the FDA also issued a warning that there may be a link between the vaccine and Guillain-Barré syndrome (GBS), a neurological disorder in which the body’s immune system damages nerve cells. The available evidence hinted that there may be an increased risk of GBS after vaccination, but it was insufficient to establish a causal relationship, the FDA noted.

Like the Oxford-AstraZeneca vaccine, the Johnson & Johnson vaccine contains a modified adenovirus, which is filled with snippets of DNA, according to Nebraska Medicine. This particular adenovirus, called Ad26, has been modified such that it cannot replicate in cells and cause infection. Instead, the virus carries genetic instructions to build the coronavirus spike protein; once inside the body, the vaccine directs human cells to build the spike, which then provokes an immune reaction. 

Sinopharm-Beijing

Sinopharm, the state-owned China National Pharmaceutical Group, and the Beijing Institute of Biological Products developed a COVID-19 vaccine that is now in use in 88 countries but not the U.S., according to The New York Times coronavirus vaccination tracker.

Clinical trials suggested that the vaccine had an efficacy of 79% against symptomatic COVID-19 infection, The New York Times reported, and in May 2021, an analysis by the World Health Organization concluded that the vaccine had an efficacy of 78.1% against symptomatic infection. The vaccine showed about 79% efficacy against hospitalization in both analyses.

However, real-world data from Peru suggested that the two-dose vaccine was only 50.4% effective in preventing infections; this data was collected as the lambda and gamma variants of the coronavirus were surging in the country, Reuters reported.  And more recently, evidence emerged to suggest that the vaccine is much less protective against the delta and omicron variants, Quartz reported.

The vaccine is given in two doses spaced three to four weeks apart, according to Medical News Today. The WHO says that a booster shot can be given four to six months after this primary series. The booster shot can either be another dose of the Sinopharm vaccine or a different vaccine, although a study conducted in Bahrain suggested that getting a different vaccine might trigger a stronger immune response, the WHO notes.

Common side effects include headache, fatigue, fever, dizziness;, nausea, and redness and swelling at the injection site.

To make the vaccine, researchers took samples of the novel coronavirus from infected human patients and allowed the viruses to replicate in monkey kidney cells grown in bioreactor tanks, according to the Times. Then, they inactivated the viruses by applying a chemical called beta-propiolactone; once treated with this chemical, the viruses could no longer replicate but still carried all their characteristic proteins, including the spike.

The vaccine contains these inactivated viral particles and a substance called an adjuvant, which stimulates the immune system. Inside the body, specific immune cells gather up the dead viruses from the vaccine and display the viral proteins on their surfaces so that other immune cells can learn to recognize and attack the coronavirus.

Related: 11 (sometimes) deadly diseases that hopped across species

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Oliver, S. E., Gargano, J. W., Marin, M., Wallace, M., Curran, K. G., Chamberland, M., McClung, N., Campos-Outcalt, D., Morgan, R.  L., Mbaeyi, S., Romero, J. R., Talbot, H. K., Lee, G. M., Bell, B. P., & Dooling, K. (2020, December 18). The Advisory Committee on Immunization Practices’ Interim Recommendation for Use of Pfizer-BioNTech COVID-19 Vaccine — United States, December 2020. Centers for Disease Control and Prevention. Retrieved March 22, 2022, from https://www.cdc.gov/mmwr/volumes/69/wr/mm6950e2.htm?s_cid=mm6950e2_w

Pike, H. (2021, May 18). Sinopharm COVID-19 vaccine: Should you worry about the side effects? Medical News Today. Retrieved March 22, 2022, from https://www.medicalnewstoday.com/articles/sinopharm-covid-19-vaccine-should-you-worry-about-the-side-effects

Rochabrun, M., & Liu, R. (2021, August 13). Peru study finds Sinopharm COVID vaccine 50.4% effective against infections. Reuters. Retrieved March 22, 2022, from https://www.reuters.com/world/americas/peru-study-finds-sinopharm-covid-vaccine-504-effective-against-infections-2021-08-13/

SAGE Working Group on COVID-19 vaccines. (2021, April 29). Evidence Assessment: Sinopharm/BBIBP COVID-19 vaccine. World Health Organization. Retrieved March 22, 2022, from https://cdn.who.int/media/docs/default-source/immunization/sage/2021/april/2_sage29apr2021_critical-evidence_sinopharm.pdf?sfvrsn=3dfe32c1_5

Sakay, Y. N. (2022, March 14). By the Numbers: COVID-19 Vaccines and Omicron. Healthline. Retrieved March 22, 2022, from https://www.healthline.com/health-news/by-the-numbers-covid-19-vaccines-and-omicron#2-dose-Pfizer-vaccine-vs.-Omicron

Tseng, H. F., et al. (2022). Effectiveness of mRNA-1273 against SARS-CoV-2 Omicron and Delta variants. Nature Medicine. https://doi.org/10.1038/ s41591-022-01753-y

U.K. Health Security Agency. (2021, December 10). SARS-CoV-2 variants of concern and variants under investigation in England - Technical briefing 31. U.K. Health Security Agency. Retrieved March 22, 2022, from https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/1027511/Vaccine-surveillance-report-week-42.pdf

U.K. Health Security Agency. (2021, December 31). SARS-CoV-2 variants of concern and variants under investigation in England - Technical briefing: Update on hospitalisation and vaccine effectiveness for Omicron VOC-21NOV-01 (B.1.1.529) . U.K. Health Security Agency. Retrieved March 22, 2022, from https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/1027511/Vaccine-surveillance-report-week-42.pdf

U.S. Food and Drug Administration. (2020, December 11). FDA Takes Key Action in Fight Against COVID-19 By Issuing Emergency Use Authorization for First COVID-19 Vaccine. U.S. Food and Drug Administration. Retrieved March 22, 2022, from https://www.fda.gov/news-events/press-announcements/fda-takes-key-action-fight-against-covid-19-issuing-emergency-use-authorization-first-covid-19

U.S. Food and Drug Administration. (2020, December 18). FDA Takes Additional Action in Fight Against COVID-19 By Issuing Emergency Use Authorization for Second COVID-19 Vaccine. U.S. Food and Drug Administration. Retrieved March 22, 2022, from https://www.fda.gov/news-events/press-announcements/fda-takes-additional-action-fight-against-covid-19-issuing-emergency-use-authorization-second-covid

U.S. Food and Drug Administration. (2021, August 23). FDA Approves First COVID-19 Vaccine. U.S. Food and Drug Administration. Retrieved March 22, 2022, from https://www.fda.gov/news-events/press-announcements/fda-approves-first-covid-19-vaccine

U.S. Food and Drug Administration. (2021, July 13). Coronavirus (COVID-19) Update: July 13, 2021. U.S. Food and Drug Administration. Retrieved March 22, 2022, from https://www.fda.gov/news-events/press-announcements/coronavirus-covid-19-update-july-13-2021

U.S. Food and Drug Administration. (2022, March 10). Janssen COVID-19 Vaccine. U.S. Food and Drug Administration. Retrieved March 22, 2022, from https://www.fda.gov/emergency-preparedness-and-response/coronavirus-disease-2019-covid-19/janssen-covid-19-vaccine

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Originally published on Live Science. 

Scientists have discovered an alien hammerhead flatworm species that looks a bit like a miniature king cobra, or perhaps an itty-bitty snake with a moustache. The researchers found the tiny creatures hunting snails in France and Italy, and they’ve named the invaders after the COVID-19 pandemic, according to a new study. 

These new hammerhead flatworms are among two newly described species found in countries that researchers believe are not part of their native range so they were very likely introduced there by humans. 

Scientists dubbed the first soil-dwelling predator species Humbertium covidum, with covidum being a reference to COVID-19 as an "homage to the numerous casualties" of the pandemic and because much of the 55-page study was written during lockdowns. 

"Due to the pandemic, during the lockdowns most of us were home, with our laboratory closed. No field expeditions were possible," lead author Jean-Lou Justine, a professor at the Muséum National d'Histoire Naturelle (National Museum of Natural History) in Paris, said in a statement. "I convinced my colleagues to gather all the information we had about these flatworms, do the computer analyses, and finally write this very long paper." 

Related: 11 animals named after US presidents

Typically found in warm parts of Asia, hammerhead flatworms are often accidentally transported around the world by humans in soil from the plant trade. These flatworms can reproduce asexually, so one hammerhead flatworm can give birth to offspring without a mate, making it easier for them to establish themselves as an invasive species — organisms that cause ecological or economic damage to an environment where they are not native, Live Science previously reported. 

Humbertium covidum were discovered in two gardens in Pyrénées-Atlantiques in southwest France and a garden in Veneto in northern Italy, although the species likely originated in Asia. Some reports indicate the species may also be in Russia, China and Japan, according to the study. The researchers discovered the second species, which they named Diversibipalium mayottensis, on Mayotte, a French island off the east coast of Africa in the Indian Ocean. This species could have been introduced to Mayotte from Madagascar.

The researchers studied the anatomy and morphology of the flatworms and carried out genetic analysis to formally describe the new species. Diversibipalium mayottensis have a unique green-blue iridescence, and the researchers determined the species belongs to a hammerhead sister group, distinct from all other hammerhead flatworms. This species could therefore be important to understanding the evolutionary history of hammerhead flatworms.  

Both of the new species measure about 1.2 inches (3 centimeters) long. That's small for hammerhead flatworms, which can grow to be more than 15 inches (40 centimeters) long, and may explain why the new species have previously been overlooked by researchers, according to the statement. 

The findings were published Feb. 1 in the journal PeerJ.

Originally published on Live Science.

Omicron's explosive surge in the U.S. is a painful reminder that the pandemic is far from over. 

It also raises some questions. Will the pandemic ever end? And will we need more boosters to enter the "endemic" phase of transmission, in which COVID-19 case counts don't break records and hospitals aren't strained? 

"I think many of us working in infectious disease realized that after the first couple of surges, it wouldn't just go away completely, because that's not what viruses like this do," Dr. Shruti Gohil, associate medical director of epidemiology and infection prevention at the University of California, Irvine, told Live Science.

Related: 14 coronavirus myths busted by science

The pandemic phase of transmission will end, but to get to an endemic phase faster, we will probably need additional COVID-19 boosters that target different variants and keep the virus from causing large outbreaks, experts told Live Science. Eventually, a yearly or seasonal vaccine may be needed to keep case counts low and to make COVID-19 more of a nuisance than an existential threat — something that, for most people, would be like dealing with the common cold, Gohil said. 

A big factor in how long it takes to go from a pandemic to an endemic phase depends on how fast it takes to vaccinate more of the world and more of the U.S. population.

More shots are coming 

In a cloudy crystal ball, Dr. Sharon Nachman, chief of the Division of Pediatric Infectious Diseases at Stony Brook Children's Hospital in New York, sees boosters being given once a year. Several studies suggest that initial vaccines wane in effectiveness after about five to six months; protection against infection drops fairly quickly, while the dramatic reduction in hospitalization is more durable. Without yearly boosters, COVID-19 will be less manageable as surges of severe cases strain hospital resources. “But if COVID-19 turned endemic like the flu, we’re all going to get a cold and that’s really it,” Nachman said.

And because SARS-CoV-2 (the virus that causes COVID-19) can mutate into more infectious and/or immune-evading variants, as omicron has clearly shown, we will probably need to update vaccine formulations, Gohil said. 

In the more distant future, COVID-19 mRNA vaccines will likely target multiple variants of concern, Gohil said. She compared it to how vaccine makers design the flu vaccine each year to target two to four flu viruses circulating earlier in the year in the Southern Hemisphere, with the goal of stimulating the body to produce a mixture of antibodies that match currently circulating strains of flu.

But in the short term, we may need boosters targeting a specific variant. Vaccine manufacturers such as Pfizer-BioNTech and Moderna are working on creating omicron-specific boosters, according to Reuters. However, using variant-specific boosters is likely a temporary measure, Nachman said. Over time, she said, companies should develop and produce vaccines that stimulate an immune response to many different versions of the SARS-CoV-2 spike protein, which the virus uses to latch onto and infect cells. 

"I think our boosters will contain spike-protein sequencing from around the world so that when those viruses do change or they get close to us, we'll have cross-variant protection," Nachman told Live Science. Having one vaccine that induces cross-protective immunity would mean you'd get one vaccine a year rather than, say, four variant-specific ones.

Vaccinating everyone is key 

Reaching an endemic stage would mean the virus is circulating at low but steady levels. In that scenario, there are predictable patterns of infection, there are no record-breaking case counts and hospitals are not overwhelmed with surges of severe infections. 

However, endemicity will be elusive until there are higher rates of global vaccination, says Dr. Erica N. Johnson, chair of the Infectious Disease Board for the American Board of Internal Medicine and an assistant professor of medicine at the Johns Hopkins University School of Medicine. “There are a lot of places in the world that don't have the same vaccine availability. Until we solve that problem, I don't think we're going to get to a place where this becomes just another endemic virus.”   

Global access to vaccines is important because variants are fueled by the virus spreading and replicating, which occurs more easily in unvaccinated people or people who are immunocompromised. 

That means getting more of the population vaccinated is key to reaching endemicity. While past infection does provide immunity against infection — one study found immunity from a prior infection led to a 50% decrease in the risk of hospitalization—  that protection is fleeting and variable and works less well to prevent hospitalization, Live Science previously reported. A CDC study found that compared to vaccinated individuals, unvaccinated individuals who recovered from a past infection were 5.49-fold times more likely to get COVID-19 illness.  

For people who are unvaccinated, COVID-19 will be an ongoing concern, Nachman said.  "We're seeing that now as [unvaccinated people] who had coronavirus earlier are getting sick again," Nachman said. "And we're seeing them sicker than those who got a COVID-19 vaccine after having a prior illness."

In the future, SARS-CoV-2 will join a host of other viruses, such as respiratory syncytial virus (RSV) and influenza, that regularly circulate but do not upend daily life. 

Moreover, there are now antivirals that can prevent severe disease if they are taken in the first few days of COVID-19 infection. Early data published to the preprint database bioRxiv found the current antivirals were effective against omicron.

COVID-19 is here to stay, but it will eventually become a more manageable threat. To keep it that way, we may be looking at a future of annual boosters.

Originally published on Live Science.

The new year rode in on a wave of omicron cases, but will this be the last of the variants, or will a brand-new "variant of concern" emerge in 2022?

Experts told Live Science that they wouldn't be surprised if a troublesome new coronavirus variant crops up this year — but that it's difficult to predict how quickly that variant would spread, how well it would evade the human immune system or whether it would cause more severe disease than prior versions of the virus. 

The omicron variant gained an edge over delta both because it is highly transmissible and because it can evade the immune defenses of vaccinated and previously infected people. This has allowed the variant to infect part of the population that delta can't readily infect, Kartik Chandran, a virologist and professor of microbiology and immunology at the Albert Einstein College of Medicine in New York City, told Live Science. Similarly, to compete with omicron, future variants of concern would need to make similar gains in both transmissibility and immune evasiveness, Chandran said. 

Related: Coronavirus variants: Facts about omicron, delta and other COVID-19 mutants 

"There's no reason to believe that the virus has run out of room, genetically," he said. "I would expect that we're going to see more variants, and we're going to see similar types of wave-like behavior," meaning a surge in infection rates following a new variant's introduction.

But while the next problem variant may easily spread and outwit the immune system, the trajectory for its other traits, such as virulence — the severity of disease caused by the virus — remains unclear.

What could the next variant of concern be like? 

Given the current rate of coronavirus infection worldwide, and the mutation rate of SARS-CoV-2, "it is predictable that new variants will emerge," Karen Mossman, a professor of pathology and molecular medicine at McMaster University in Ontario, told Live Science in an email. But as we've learned over the last two years of the pandemic, not every new variant will be competitive enough to take over, she said. 

Future variants could gain a competitive edge via several routes. In theory, one of these potential trajectories could result in a virus that's more transmissible than omicron while causing less severe disease, Mossman said.

"Viruses need to propagate and spread to new hosts. The most successful viruses do this by rapidly spreading without causing symptoms," because the infected host can easily move about and pass the bug to additional hosts, Mossman said. "It is not advantageous to a virus to kill off its host before it can spread." 

Omicron may be less likely to cause severe disease than prior variants, Live Science previously reported. In part, that may be because it grows more easily in the upper airways and less well in the lungs — which may also help the variant spread more easily. In this case, it does seem like the virus may have evolved to be less virulent as a result of its increased ability to jump between hosts.

But there's no guarantee that the next variant of concern will make the same trade-off, Mossman noted. "A collection of mutations that provide a selective advantage may also induce more severe disease," she said. 

For instance, mutations that grant the virus the ability to replicate incredibly quickly, or escape the clutches of the antibodies that prevent it from entering cells, could also make the bug more likely to trigger severe infection. Delta showed such a combination of traits, in that it spread more easily than all previous coronavirus variants while still doubling the risk of hospitalization for unvaccinated people, as compared with alpha, The New York Times reported. HIV and Ebola are examples of viral diseases that have not evolved to be less severe despite being around for decades; smallpox was another example, prior to its eradication.

Related: 20 of the worst epidemics and pandemics in history

The idea that the virus might become less virulent over time is "certainly not unreasonable as a hypothesis," Chandran said, but he agreed with Mossman that such an outcome isn't assured. Often, as viruses replicate and pick up mutations, the individual mutations within the genome interact with each other and can produce unexpected traits, he noted. This phenomenon, called epistasis, makes the evolution and behavior of future variants incredibly difficult to predict.

Big unknowns 

In general, there are physical and genetic constraints that limit how much SARS-CoV-2 can evolve, Chandran noted. Some of these constraints prevent the virus from becoming infinitely more infectious, and for this reason, scientists expect that the transmissibility of the virus will eventually level off and stop increasing, Nature reported.

On a physical level, "viruses have to walk this fine line between stability and instability," and this balancing act limits their transmissibility, Chandran said. A virus is basically a microscopic box full of genetic material, and that box must be sturdy enough to keep the genetic material safe in the body and in the outside world. But to infect cells, the box must open to let the virus's genetic material out. Too stable, and the virus can't open up and infect cells as efficiently; too unstable, and the virus won't survive for long after being spewed out in someone's sneeze, Chandran said.

And on a genetic level, the virus can only accumulate so many mutations before it begins to malfunction, he said. 

For example, the virus needs its spike protein to fit snugly into a receptor on human cells in order to trigger infection. Spike mutations can help the microbe hide from antibodies to past variants; omicron carries about 30 mutations in its spike, some of which help the variant evade the immune system. But there's likely a limit to how many mutations the spike can accommodate before its ability to plug into human cells starts to falter, Chandran said.  

In this respect, the virus likely still has some genetic wiggle room. Based on a recent study, published Dec. 2 in the journal Science, SARS-CoV-2 can likely withstand a large number of escape mutations — those that help the bug dodge antibodies — while still retaining its ability to plug into human cells. "The great structural flexibility we saw in the SARS-CoV-2 spike protein suggests that omicron is not likely to be the end of the story for this virus," senior study author Dr. Jonathan Abraham, an assistant professor of microbiology at Harvard Medical School and an infectious disease specialist at Brigham and Women’s Hospital, told The Harvard Gazette.

Other unknowns make the future of SARS-CoV-2's evolution difficult to predict. One big question is where the next variant of concern will come from, since it may not descend from the omicron lineage, Chandran said. Omicron stemmed from a different branch of the coronavirus family tree than delta, even though delta was predominant at the time; the next variant may have a similar origin story. 

Meanwhile, animal hosts for the coronavirus are yet another wildcard. 

SARS-CoV-2 can infect a variety of animals, including mink, ferrets, cats, white-tailed deer and various primates, Nature reported. This has raised concerns that, while circulating in animals, the virus could pick up mutations that render the bug more infectious or lethal to humans, or else undermine the efficacy of our vaccines. For this scenario to unfold, the coronavirus would need to make the leap back to humans after infecting an animal, and in some cases, the virus might mutate so much that it can't hop back into people, Chandran noted. "The genetic trajectory of the virus could be quite different in these other hosts," he said. 

That said, cases of animal-to-human transmission were reported on mink farms early in the pandemic, and it's possible that other species could also pass the virus back to people, Live Science previously reported. For this reason, scientists should continue to track SARS-CoV-2 spread in both humans and animals, as animal reservoirs of the virus could definitely be an issue in the future, Chandran said.

Reducing the risk of problem variants 

Is there anything we can do to reduce the risk of new problem variants emerging?

"What we need to do is reduce … the space the virus has to replicate. And the way we're going to do that is by vaccinating people," Chandran said. As of Jan. 10, about 4.67 billion people worldwide have received at least one dose of a COVID-19 vaccine, which leaves nearly 40% of the world's population completely unvaccinated, according to The New York Times.

Even if vaccines offer only partial protection against a future variant, as they do with omicron, they would likely still reduce people's chances of catching and passing on the virus. However, vaccination would work best in combination with other measures, such as masking, physical distancing and frequent testing, Chandran said. But importantly, increasing the number of people vaccinated would also ease the strain on the health care system by preventing severe disease, he noted.

Early evidence, posted Jan. 3 to the preprint database medRxiv, suggests that even though the omicron variant can dodge some vaccine-induced antibodies, other immune defenses raised by the vaccine still block severe infections. The study, which has not been peer-reviewed, shows that the vaccines generate "durable responses" from helper T cells, which rev up the body's immune response upon sensing SARS-CoV-2, and killer T cells, which can kill infected cells. These T cells show cross-reactivity to both the delta and omicron variants, meaning they can recognize and target both versions of the virus for destruction, the study found. Similarly, these T cells could offer protection against potential future variants of concern.

Broadly speaking, "As more and more people become infected and/or vaccinated, particularly multiple times, they will build up higher levels of immunity, potentially against different variants," Mossman told Live Science. "As this general level of immunity increases within populations, and around the world, the overall evolution of SARS-CoV-2 will likely decline, and the pandemic will become endemic."

This is how the pandemic could end — but we'll likely have to face new variants of concern until then. 

Originally published on Live Science.

Officials have confirmed the first known omicron variant (B.1.1.529) case in the United States. 

The case was an individual who had returned to California from South Africa on Nov. 22 and tested positive for COVID-19 on Nov. 29, Dr. Anthony Fauci, the director of the National Institute of Allergy and Infectious Diseases said at a White House briefing on Wednesday (Dec. 1). None of the individual's close contacts have tested positive, he said. 

The individual was fully vaccinated and experienced mild COVID-19 symptoms that are improving, Fauci said. To his knowledge, the person hadn't received a booster shot.

Related:  Coronavirus variants: Here's how the SARS-CoV-2 mutants stack up

The University of California, San Francisco confirmed that the individual was infected with the omicron variant, after scientists at the university analyzed the individual's test samples. The CDC labs later confirmed the finding.

"We knew that it was just a matter of time before the first case of omicron would be detected in the United States," Fauci said during the briefing. 

Scientists in South Africa first report omicron to the World Health Organization on Nov. 24, and the WHO identified it as a "variant of concern" on Nov. 26, Live Science previously reported. Since the variant's discovery, dozens of other nations, including Canada and England, have confirmed cases of omicron. 

Scientists aren't sure yet whether the omicron variant is more transmissible or more severe than other coronavirus variants; and they don't yet know how effective current vaccines are at protecting against omicron. What is clear is that omicron has a lot of mutations to its spike protein, the arm the novel coronavirus uses to latch onto and invade human cells.

In two to three weeks, scientists should have answers to some of these questions, Fauci said during the briefing.

He noted that people should continue masking when indoors, congregate settings; Fauci also stressed the importance of getting a COVID-19 vaccine if you haven't already, and for those who have and it's been six months since your last dose of the Moderna or Pfizer-BioNTech vaccine, a booster shot is in order, he said. For those who received the Johnson & Johnson vaccine, a booster is recommended two months following that shot. 

Even though the vaccine isn't targeting specific variants such as the delta or omicron, when you get a high enough level of an immune response (such as from a booster), you get "spillover protection," Fauci said. 

"Even though we don't have a lot of data on it , there's every reason to believe that that kind of increase that you get with a boost would be helpful at least in preventing severe disease of a variant like omicron."

Originally published on Live Science.

During the COVID-19 pandemic, more than 28,000 tons (25,000 metric tons) of pandemic-related plastic waste, such as masks and gloves, have ended up in the ocean, according to a new study. 

That's more than 2,000 double-decker buses  worth of waste, The Guardian reported. And within a few years, a portion of those plastic gloves and packaging materials from pandemic purchases could be swirling around the North Pole.

The analysis found that 193 countries produced about 9.2 million tons (8.4 million metric tons) of pandemic-associated plastic waste from the start of the pandemic to mid-August 2021, according to The Guardian. 

The majority of the plastic — about 87.4% — was used by hospitals, while 7.6% was used by individuals. Packaging and test kits accounted for about 4.7% and 0.3% of the waste, respectively, the authors reported in a recent study, published online on Nov. 8 in the journal Proceedings of the National Academy of Sciences.

Related: Sea science: 7 bizarre facts about the ocean 

The team developed a model to predict how much of this plastic waste wound up in the ocean after being discarded. They predicted that, as of Aug. 23, about 28,550 tons (25,900 metric tons) of the plastic debris had already found its way into the oceans, transported there by 369 major rivers, according to The Guardian. 

In three years' time, the majority of the  debris will shift from the surface ocean to beaches and the seafloor, with more than 70% washing onto beaches by year's end, the authors wrote. 

While in the short-term, the trash will mostly impact coastal environments near its original sources, in the long-term, garbage patches may form in the open ocean, the model predicts. For instance, patches may accumulate in the northeast Pacific and the southeast Indian oceans. And plastic that gets swept toward the Arctic Circle will hit a dead-end, and much of it will then swiftly sink to the seabed, the model predicts. The researchers also predict that a so-called circumpolar plastic accumulation zone will form by 2025. 

And "at the end of this century, the model suggests that almost all the pandemic-associated plastics end up in either the seabed (28.8%) or beaches (70.5%), potentially hurting the benthic ecosystems," meaning the deepest regions of the ocean, the authors wrote.

"The recent COVID-19 pandemic has led to an increased demand for single-use plastic, intensifying pressure on this already out-of-control problem," the study authors wrote. "These findings highlight the hotspot rivers and watersheds that require special attention in plastic waste management." 

In particular, the study highlights a need for better systems for collecting, treatmenting and disposing of medical plastic waste in developing countries, to keep it out of rivers, and an overall need to limit the use of single-use plastics and increase the use of sustainable alternatives, where possible, the authors wrote. 

Read more about the new study in The Guardian. 

Originally published on Live Science.

Moderna's COVID-19 vaccine is safe and effective for children ages 6 to 12 years, the company announced on Monday (Oct. 25).

The findings are part of a clinical trial on the effectiveness and safety of the vaccine in around 5,700 children between the ages of 6 months and 12 years; More than 4,700 children between the ages of 6 and 12 years participated in the study and were given two doses of the vaccine 28 days apart, but at half the dose (50 µg) given to adults (100 µg). 

The researchers found that the vaccine at this dose was "well tolerated," and side effects were similar to what was seen in adolescents and adults, according to a statement. The majority of adverse events were mild or moderate; and the most common side effects were fatigue, headache, fever and injection site pain, the company said.

Related: 14 coronavirus myths busted by science

They also found that the vaccine prompted a "strong immune response" one month after the second dose; children in this age group had 1.5 times higher antibody levels than those observed in young adults, the company said.

Moderna previously submitted data to the Food and Drug Administration (FDA) to get authorization for use of its vaccine in people ages 12 to 17, but the agency hasn't yet responded to the request. The company now plans to also submit this new data to the FDA and other regulatory agencies around the world.

Meanwhile, the researchers will continue to monitor the participants for 12 months after their second dose to assess long-term protection and safety.

Currently, Moderna is approved for those who are 18 years or older, while Pfizer is approved for those 12 years and older. Pfizer has already submitted a request to the FDA to authorize its vaccine for children ages 5 to 11, Live Science previously reported.

The FDA's advisory committee will meet on Tuesday (Oct. 26) to discuss Pfizer's request.

Originally published on Live Science.

COVID-19 has now killed as many people in the U.S. as the 1918 flu pandemic, which is often cited as the most severe pandemic in recent history, according to the Associated Press.

As of Tuesday (Sept. 21), more than 676,200 people have died in the U.S. from COVID-19, according to the Johns Hopkins dashboard. The 1918-1919 flu pandemic is thought to have killed roughly 675,000 people in the U.S., according to the Centers for Disease Control and Prevention (CDC). 

But it's not exactly clear how many people died a century ago, due to incomplete records and poor understanding of the illness cause, according to the AP.

Related: 20 of the worst epidemics and pandemics in history

The worldwide mortality from COVID-19 — estimated at around 4.7 million deaths to date — is nowhere near global deaths brought by the 1918 flu, a number estimated to be more than 50 million.

Of course, an apples-to-apples comparison doesn't reveal the true picture of either pandemic, as there are many factors that have changed since a century ago. 

On one hand, the population of the U.S. was about a third of what it is today, which means that the 1918 flu wiped out a bigger part of the population than the COVID-19 pandemic has so far, according to the AP. (And the population of the world was about a fourth of what it is today.)

On the other hand, there have been significant scientific advances since a century ago, including three currently available vaccines against COVID-19 in the U.S. 

Not only were vaccines not available in 1918, but also they didn't have antibiotics to treat secondary bacterial infections at the time, according to the AP. The 1918 flu killed young, healthy adults in much bigger numbers than COVID-19, which has disproportionately targeted the older and more vulnerable population.

There are currently about 1,900 COVID-related deaths a day, on average in the U.S., and University of Washington projections suggest an additional 100,000 deaths related to the disease in the U.S. by Jan. 1, 2022, according to the AP.

About 64% of the eligible population in the U.S. (those 12 years of age or older) are now fully vaccinated against COVID-19. 

Only about 43% of the world population has received at least one dose of a COVID-19 vaccine, with only 2% of people in low-income countries who received one dose, according to our World in Data. (The vaccines are still not readily available in many countries around the world.)

COVID-19 would have been much less deadly in the U.S., where vaccines are readily available, if more people had quickly gotten vaccinated. "We still have an opportunity to turn it around," Dr. Jeremy Brown, director of emergency care research at the National Institutes of Health, told the AP. "We often lose sight of how lucky we are to take these things for granted."

How the COVID-19 pandemic will be remembered in comparison to the 1918 flu remains unclear. You'd like to say it won't be remembered the worst in human history, .

"We have a lot more infection control, a lot more ability to support people who are sick. We have modern medicine," Ann Marie Kimball, a retired University of Washington professor of epidemiology, told the AP. "But we have a lot more people and a lot more mobility. ... The fear is eventually a new strain gets around a particular vaccine target."

Read the original Associated Press story here. 

Originally published on Live Science.

The coronavirus delta variant may be as contagious as chickenpox and cause more severe illness than previous variants, according to an internal presentation from the Centers for Disease Control and Prevention (CDC). 

Vaccines continue to be highly effective, especially at preventing severe illness and death, but may be less effective at preventing infection or transmission of the delta variant, according to a CDC slide deck first obtained by The Washington Post. 

The slides were shared within the CDC and cite some of the data — both published and unpublished — that drove the recent shift in the CDC's masking recommendations. "Acknowledge the war has changed," the CDC wrote in the report. 

Related: Delta variant: Your questions answered

One major takeaway from the slides is that at current levels of vaccination in the U.S., delta will continue to spread exponentially without other mitigation measures in place, such as masking of vaccinated people. "Given higher transmissibility and current vaccine coverage, universal masking is essential to reduce transmission of the delta variant," according to the presentation. 

On Tuesday (July 27), the CDC updated its mask guidance to say that fully vaccinated people should resume wearing masks in public indoor spaces in areas with substantial coronavirus transmission, Live Science previously reported. The delta variant is "different from previous strains," according to the slides. It is "highly contagious," "likely more severe," and "breakthrough infections may be as transmissible as unvaccinated cases," according to the summary slide. 

There are currently about 35,000 symptomatic breakthrough infections (with any variant) per week among 162 million vaccinated Americans, according to the report. Currently, the risk of symptomatic disease is reduced eightfold and the risk of hospitalization and death is reduced 25-fold among those who are fully vaccinated versus those who are unvaccinated, those national estimates suggest.

However, the risk of infection with the delta variant is likely only reduced threefold in those who are vaccinated,  according to the slides.

The delta variant is more transmissible than the viruses that cause Middle East respiratory syndrome (MERS) and severe acute respiratory syndrome (SARS), Ebola, the common cold, seasonal flu, the 1918 flu and smallpox, and just as transmissible as chicken pox, according to the slides. 

What's more, people who are infected with the delta variant may carry a higher viral load than people infected with other variants (even in breakthrough cases) and shed virus —  thus being able to spread it — for longer, according to the slides. A small preliminary study found that people infected with delta may be carrying more than 1,000 times more virus particles and test positive two days earlier than those infected with the original virus, Live Science previously reported. 

More preliminary data from an outbreak of delta in Barnstable County, Massachusetts, suggests that there was no difference in viral load among those who were vaccinated but had a breakthrough case and those who were unvaccinated, which suggests that vaccinated breakthrough cases may be able to transmit the delta variant as easily as unvaccinated cases. (In contrast, previous variants could not easily spread from vaccinated people with breakthrough infections, according to The New York Times).

However it's not clear whether all of those virus particles are infectious, and whether the fraction that can infect others is the same for vaccinated versus unvaccinated people. 

The CDC slides say that the "delta variant may cause more severe disease than alpha or ancestral strains," according to published data from Canada, Singapore and Scotland. 

Data from England, Scotland, Canada and Israel suggests that the Pfizer-BioNTech vaccine is somewhere between 93% and 100% effective in preventing hospitalization or death but 64% to 88% effective in preventing symptomatic disease from the delta variant. 

What's more, breakthrough cases will occur more frequently in congregate settings and in groups for whom the vaccine works less robustly, including people who are immunocompromised or elderly, according to the slides. The risk of hospitalization and death is higher among older adults compared to younger populations, regardless of vaccination status, according to the presentation.

Originally published on Live Science.