Six years after COVID-19 first made headlines, an antiviral pill has finally been shown to stop users from developing the disease after being exposed to the virus.

The drug, called ensitrelvir, was originally approved for use in Japan as a treatment for COVID-19, and it has now been approved as a preventative treatment, too. Now, promising late-stage trial results have been published as regulators in the U.S. and Europe consider whether to follow suit, Nature reported.

While SARS-CoV-2 is no longer prompting global lockdowns, the virus still poses a significant threat to a large proportion of the population, especially older adults and people with compromised immune systems. But while antivirals like Pfizer's Paxlovid have been developed to reduce disease severity and viral load once an infection has started, nothing has so far proven effective at preventing the disease after exposure to the virus.

Now, ensitrelvir, developed by Japanese pharmaceutical company Shionogi, has been shown to significantly reduce the risk of developing the disease, according to research published Wednesday (May 13) in The New England Journal of Medicine.

The trial specifically focused on exposures from household contacts, a common source of SARS-CoV-2 spread. So if your roommate got sick, you could take ensitrelvir in addition to distancing yourself from them at home.

Ensitrelvir works by blocking a key enzyme that the virus relies on to make new copies of itself. This enzyme is also targeted by Paxlovid. But unlike Paxlovid, ensitrelvir was shown to significantly reduce the risk of developing COVID-19 symptoms compared to a placebo among those who had been exposed to the virus.

The newly published trial looked at more than 2,000 people who lived with people who got infected with SARS-CoV-2 between June 2023 and September 2024. Roughly half of the participants were given a five-day course of ensitrelvir while the other half were given a placebo. Neither the participants nor the researchers knew who had been given which pill, making the trial "double-blinded."

While 9% of those given the placebo within 72 hours of exposure developed COVID-19 symptoms, only 2.9% of those who took ensitrelvir became symptomatic.

The trial runners also tested participants for SARS-CoV-2 up to the tenth day out from exposure: Only 14% of those who received the drug tested positive — with or without symptoms — compared to 21.5% of those who received the placebo.

There was no real difference in side effects between the ensitrelvir and placebo groups; in fact, slightly fewer people in the ensitrelvir group reported adverse events (15.1% compared to 15.5%). Reported adverse effects included temporary and reversible reductions in "good" cholesterol and higher levels of fat in the blood.

The researchers note that their trial did not consider factors that might influence the degree of household transmissions, such as the size of the household and whether or not participants were social distancing. The medication was also not tested on pregnant women or those taking medications that could interact with the drug.

"This is really the first clear demonstration in a well-performed phase III placebo-controlled, double-blind trial that we actually have an agent that is easily administered orally and effective if taken in a timely fashion for protecting individuals who are exposed to COVID-19 in the household setting," first study author Frederick Hayden, a professor of medicine and pathology at the University of Virginia, told MedPage Today.

Beyond households, he said that the drug would likely also protect patients in the case of COVID-19 outbreaks at nursing homes and long-term care facilities. It's just that those uses weren't expressly included in the trial.

Ensitrelvir, known by the brand name Xocova, was approved by Japan's health ministry for treatment of mild-to-moderate COVID-19 infections in March 2024 and as a means of preventing the disease in March 2026. It has also been approved in Singapore.

Shionogi submitted the drug for U.S. Food and Drug Administration approval in September 2025. A decision by the U.S. regulator is expected in June, according to Medpage Today.

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

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.

Each fall, updated versions of the COVID-19 vaccines come out around the same time as the annual flu shot. And just like the flu shot, these updated COVID vaccines are formulated to protect against virus strains that people are more likely to encounter in the coming months, as opposed to strains that were rampant the year prior.

But this year, the hunt for an updated COVID vaccine may be fraught.

In August, the Food and Drug Administration (FDA) issued guidance limiting the groups that are recommended to get the updated shot: Only people ages 65 or older or those who are at least 6 months old with one underlying health condition that increases their risk of a severe COVID infection are covered. Those outside these two groups may have to consult a doctor to get a prescription before seeking a COVID shot, and even then, it might not be covered by their insurance. The situation is confusing, and the picture varies from state to state.

Typically, vaccine advisors to the Centers for Disease Control and Prevention (CDC) also weigh it with their own COVID vaccine recommendations, and that should happen next week (Sept. 18 to 19). But prominent opponents to vaccines have recently been added to that committee, so it's unclear how it will rule.

Some states are already breaking from the federal guidance. For instance, Minnesota and New York have issued executive orders to try and expand their residents' access to the shots, and New Jersey's health department has issued a directive with the same intent. Oregon, Washington, California and Hawaii have formed an alliance to provide their residents with unified recommendations on vaccines, although they've yet to issue details on the 2025-2026 COVID shots.

Have you tried to get a COVID vaccine this year? If so, how did it go? Tell us in the poll below, and if you've encountered specific issues while getting this year's COVID vaccine, let us know what they were in the comments. Live Science will publish additional guidance on the 2025-2026 COVID vaccine next week, so stay tuned for that article, too.

Related: COVID-19 vaccines for kids are mired in uncertainty amid conflicting federal guidance

Related stories

—'We have basically destroyed what capacity we had to respond to a pandemic,' says leading epidemiologist Michael Osterholm

—What are mRNA vaccines, and how do they work?

—'These decisions were completely reckless': Funding cuts to mRNA vaccines will make America more vulnerable to pandemics

At a Sept. 4, 2025, hearing before the Senate Finance Committee, Health and Human Services Secretary Robert F. Kennedy Jr. faced heated questions from numerous senators about his vaccine policies, including his stance on COVID-19 vaccines and mRNA vaccine technology generally.

Although Kennedy agreed that Operation Warp Speed, President Donald Trump's signature initiative to produce COVID-19 vaccines in nine months, was a tremendous achievement, he also maintained that COVID-19 vaccines cause widespread and serious harm, including death, particularly in young people — a claim for which there is no evidence.

Some especially pointed questions came from Republican Sen. Bill Cassidy of Louisiana, a physician who provided the final vote needed for Kennedy's confirmation in February 2025 after Kennedy promised him that he would not change the Centers for Disease Control and Prevention's process for recommending vaccines. Cassidy pointed out that with the limitations and confusion caused by the CDC's new rules around COVID-19 vaccines, "I would say effectively we are denying people vaccines." To which Kennedy replied, "Well, you're wrong."

At the hearing, Kennedy stood by his decision to cut US$500 million in HHS funding for 22 research contracts on mRNA vaccine technology. HHS has said it will instead pour these funds into research on a traditional approach to designing vaccines that was first used more than 200 years ago. With such vaccines, called whole-virus vaccines, a person's immune system is presented with the whole virus, often in weakened or inactivated form. This switcheroo has puzzled many scientists.

A few days before the hearing, on Sept. 1, Trump demanded that pharmaceutical companies prove that COVID-19 mRNA vaccines work, saying that the CDC was "being ripped apart over this question." It was his first public acknowledgment of the chaos roiling the CDC amid the firing of its director, Susan Monarez, and subsequent resignations of four high-level agency officials.

Meanwhile, public health experts and HHS staffers are calling for Kennedy to be fired, and several senators at the hearing echoed that call.

As a vaccinologist who has studied and developed vaccines for over 35 years, I see that the science behind mRNA vaccine technology is being widely misstated. This incorrect information is shaping long-term health policy in the U.S. — which makes it urgent to correct the record.

Are mRNA vaccines less safe than whole-virus vaccines?

HHS defended its cancellation of mRNA vaccine research based, in part, on a nonpeer-reviewed compilation of selected publications called the COVID-19 mRNA "vaccine" harms research collection. This document lists about 750 articles claimed to describe harms caused by mRNA vaccines against COVID-19. However, the vast majority of these articles aren't about vaccines but about the harms of getting infected with SARS-CoV-2, the virus that causes COVID-19. And notably absent from it is the huge body of data showing mRNA vaccines actually prevent these harms.

For example, the document being used to justify RFK Jr.'s claims about mRNA vaccines highlights 375 studies reporting that the virus's spike protein alone, which is produced when the virus replicates, can cause excessive inflammation and tissue damage. This is true. But the document marshals this evidence to support the claim that mRNA vaccines, which are designed to produce spike proteins, cause the same harm — which is not accurate.

While viral replication results in uncontrolled production of a large amounts of the protein, the way it's produced by the mRNA vaccine is very different. The vaccine produces a small, controlled amount of spike protein inside a few cells — just enough to induce an immune response without causing damage. And by blocking the virus's replication, it reduces the amount of spike protein in circulation, actually having the opposite effect.

What about side effects like myocarditis?

Early reports flagged a type of heart swelling called myocarditis as a rare side effect of the mRNA vaccine, particularly for young men ages 18 to 25 after a booster dose. A 2024 review identified about 20 cases out of 1 million people who received the vaccine. However, that same study found that unvaccinated people had an elevenfold higher risk of getting myocarditis after a COVID-19 infection than vaccinated people.

What's more, another 2024 study showed that people who developed myocarditis after vaccination had fewer complications than those who developed the condition after getting infected with COVID-19.

Do mRNA vaccines make the SARS-CoV-2 virus resistant?

Another claim from the compilation of supposed mRNA vaccine harms that was cited as a reason for cutting funding for mRNA technology is that mRNA vaccines cause mutations in the SARS-CoV-2 virus that make them resistant or less susceptible to the vaccine.

When a virus replicates in its host, it produces millions of copies of its genetic material. Mutations are copying errors that occur naturally during the replication process. These acquired mutations produce new variants, which is why both the COVID-19 mRNA and the whole-virus flu vaccine get updated annually — to keep up with natural changes in the virus.

Slowing down viral replication decreases the rate at which a virus can acquire new mutations. Since both mRNA and whole-virus vaccines stop or slow the virus from replicating, both types of vaccines help reduce the emergence of resistant viruses.

Viruses can mutate to escape from antibodies, but the mRNA vaccines are not causing the emergence of more virulent strains, likely for at least two reasons. First, mRNA vaccines induce immune responses that can attack the virus at multiple spots, so it would have to come up with many mutations at once to escape the vaccine's defenses. Second, even if the virus could acquire all these mutations, they would likely weaken it, making it unable to cause or even transmit disease.

mRNA vaccines versus new SARS-CoV-2 variants

Kennedy, in announcing cuts to mRNA vaccine research on Aug. 5, 2025, claimed that mRNA vaccines don't work against respiratory viruses and that HHS was moving toward "safer, broader vaccine platforms that remain effective even as viruses mutate."

Both whole-virus vaccines and mRNA vaccines protected against COVID-19 and prevented hospitalization and death for millions of people worldwide between 2020 and 2024, but there's clear evidence that the mRNA-based vaccines provided significantly better protection than whole-virus vaccines. And for COVID-19, mRNA vaccines are more effective against new variants, which emerge as viruses mutate, than whole-virus vaccines.

The COVID-19 mRNA vaccines started with exceptionally high efficacy, exceeding 94%. When the SARS-CoV-2 delta and omicron variants emerged in the spring and fall of 2021, mRNA vaccines became less effective in preventing infections. However, they remained highly effective in preventing severe illness, whereas in unvaccinated people the rates of severe illness and hospitalization remained high.

This is because mRNA vaccines induce the immune system to make both antibodies and specialized immune cells called T cells. These elements can recognize multiple parts of the virus, including ones that don't change, enabling significant protection against new variants.

What's more, the mRNA vaccines have a superpower that no other type of vaccine can currently match: They can be quickly updated and manufactured within two to three months. To develop a whole-virus vaccine, researchers must first spend months isolating and propagating the virus. Conversely, making an mRNA vaccine requires just sequencing the virus's genetic code — a process that today takes just hours.

If a new pandemic began today, mRNA vaccines are currently the only type of vaccine that could be developed quickly enough to disrupt its spread.

The future of mRNA vaccine technologies

Thirty years ago, when scientists first started developing mRNA vaccine technology, they recognized its potential to overcome major limitations of whole-virus vaccines — namely, slow production time and more limited ability to protect from new viral variants. Today, mRNA vaccines are also being developed to prevent or treat diseases including HIV and cancer, as well as autoimmune and genetic diseases.

Of course, this technology can be further improved. New mRNA vaccine technologies are aimed, among other things, at making mRNA vaccines easier to store to allow for faster distribution and reduce their short-term side effects, eliminate the rare risk of myocarditis and more quickly block a respiratory infection.

The National Institutes of Health is funneling money away from new mRNA technologies toward a single project developing universal vaccines based on traditional whole-virus vaccine technology. Universal vaccines are urgently needed to provide broader protection against ever-changing respiratory viruses, such as influenza, that are major pandemic threats.

A 2022 study in mice and ferrets showed that a universal flu vaccine NIH plans to support has promise. However, multiple studies of potential universal flu vaccines based on mRNA technology show even more potential. Such vaccines could induce broader immunity than whole-virus vaccines by eliciting antibody and T-cell responses that target an even wider range of flu viruses.

It's hard to square those benefits with the fact that HHS and NIH have named the planned new universal vaccine platform "Generation Gold Standard," insisting that it represents a new standard in science and transparency. The effort seems more akin to eliminating all e-bike technology and telling everyone who seeks one to get by with a single brand of a 10-speed bike: Getting to the intended destination may still be possible, but it will be slower and harder.

And in the case of abandoning mRNA vaccine research, it may lead to lives needlessly lost, whether due to potential medicines untapped or to pandemic unpreparedness.

This article was updated to include details from Kennedy's Sept. 4, 2025, hearing.

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

It's August, and parents and caregivers are frantically preparing their kids for a new school year by buying supplies, filling out forms and meeting teachers. This year, many parents also face a question that's more complicated than usual: Should my child get an updated COVID-19 vaccine, and will I even have that choice? For some, that decision may have already been made by chaotic federal policy, just as COVID-19 cases are rising nationwide.

As a pediatrician and researcher who studies vaccine delivery and health policy, I am hearing uncertainty from both parents and health care providers. If that describes you, you are not alone. A poll published Aug. 1, 2025, by the health policy organization KFF found half of parents are unsure whether federal health agencies are recommending COVID-19 vaccines for healthy children this fall.

The process that normally provides clear, consistent recommendations and ensures availability for vaccines before respiratory virus season has been upended, and this year's COVID-19 vaccine guidance for children is a prime example.

How the process typically works

For over two decades, there was a predictable, well-coordinated process to ensure recommended seasonal vaccines, such as the flu shot, were available for anyone who wanted them by early fall. In recent years, COVID-19 vaccines have been incorporated into this same annual cycle.

Beginning in February, the Food and Drug Administration, including its independent committee of experts, reviewed data and approved the optimal formulation. After FDA approval, the Advisory Committee on Immunization Practices, or ACIP, an independent panel of experts that advises the Centers for Disease Control and Prevention, reviewed the evidence in public meetings and issued clear recommendations.

The U.S. has long followed an established set of steps lining up vaccines for any given year.

Manufacturers then scaled up production; insurers confirmed coverage, which is tied to the advisory committee's recommendations; and doses were distributed nationwide so vaccines would be available in clinics and pharmacies before the leaves started turning. This usual series of steps ensured that guidance incorporated input from scientists, epidemiologists, public health experts, clinicians, manufacturers, insurers and consumers. It also fostered trust among health care providers and, in turn, provided parents with clarity and confidence when making decisions.

Related: 'These decisions were completely reckless': Funding cuts to mRNA vaccines will make America more vulnerable to pandemics

What's different this year

Since Robert F. Kennedy Jr. took over as secretary of Health and Human Services in February 2025, that usual, tightly choreographed dance has become a chaotic scramble marked by uncertainty and a lack of transparency. Decisions about vaccine guidance have been made through internal channels without the same level of public discussion, review of the evidence or broad stakeholder input.

In May 2025, Kennedy and FDA leadership bypassed the agency's independent review committee and announced that some COVID-19 vaccines would be approved only for children with high-risk conditions. One formulation has yet to be FDA-approved for children at all. The secretary first announced updated recommendations for children on X, stating COVID-19 vaccines would no longer be recommended for healthy children. Shortly after, the CDC posted guidelines that differed from that announcement and said healthy children "may" receive them. Meanwhile, the Advisory Committee on Immunization Practices was disbanded by Kennedy and replaced with a smaller, hand-picked panel that operates with less transparency and has yet to weigh in on COVID-19 vaccines for children.

Public messaging has added to the confusion. Statements from newly appointed federal health leaders have questioned the safety of COVID-19 vaccines and the long-standing processes for ensuring their safety. Funding for mRNA technology, which supports several COVID-19 vaccines and is being explored for use against other diseases and even some cancers, has been cut. And many of the claims used to justify these actions have been challenged by experts as inaccurate or misleading.

What this means for parents

For parents, the result is uncertainty about whether their children should be vaccinated, when and where the vaccines will be available, whether insurance will cover them, or whether their choice has effectively been made for them by newly appointed health leaders operating outside the guardrails of the normal vetting process. This uncertainty comes at a time when the uptake of COVID-19 vaccines in children is already lower than that of other routine vaccines.

Currently, CDC guidelines say healthy children six months and older "may" receive a COVID-19 vaccine based on shared decision-making with their health care provider. The CDC recommends that children who are moderately or severely immunocompromised receive it. These guidelines differ from FDA approvals and Kennedy's guidelines announced on X, and they have not been reviewed or voted on in an advisory committee on immunization practices meeting.

Parents can start by talking with their child's pediatrician about benefits and potential risks, confirming eligibility and checking on insurance coverage. Pediatricians welcome parents' questions and work tirelessly to provide answers grounded in the best available evidence so families can make truly informed decisions about their child's health.

In some cases, unfortunately, even if parents want the vaccine and their pediatrician agrees, they may not be able to get it due to any number of factors, including local supply shortages, lack of insurance coverage, policies that prevent administration by pharmacists and other health providers without clear federal guidance, or an unwillingness of providers to give it "off-label," meaning in a way that differs from the FDA's official approval. For those parents, their decision has been made for them.

Reducing risks in other ways

Whether or not a child receives an updated COVID-19 vaccine, parents can still take steps to reduce illness, including keeping children home when sick, teaching them cough-and-sneeze hygiene and encouraging frequent hand-washing. The CDC provides national and state data on seasonal respiratory illnesses, including COVID-19, while local public health websites often offer community-level information.

Parents should also remember that the COVID-19 vaccine is not the only thing to consider before school starts. Routine immunizations such as those for measles, mumps and rubella, known as the MMR vaccine; diphtheria, tetanus and pertussis, called DTaP; and influenza are essential for keeping kids healthy and in school. These are widely available for now. This is particularly important, as this year the United States has experienced the highest number of measles cases in decades.

Uncertainty surrounding COVID-19 vaccine recommendations, and potentially other vaccines, may worsen in the coming weeks and months. It is possible parents will continue to see shifting guidance, conflicting statements from federal agencies and reduced access to vaccines in their communities.

In this chaotic environment, parents can look to trusted sources such as their pediatrician or organizations such as the American Academy of Pediatrics, which will continue to provide independent, evidence-based vaccine guidance.

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

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.

The patient: A 60-year-old man in Istanbul

The symptoms: The patient went to a hospital after having hiccups for three days.

What happened next: Doctors in the hospital's neurology department examined the patient and performed an MRI of his head. They found no abnormalities in his brain, and they didn't note any symptoms other than his hiccups, which continued during the MRI exam. He was then moved to the internal medicine department, where specialists conducted further tests and found the man's temperature, oxygen levels, and heart and breathing rates were normal. Blood work showed no signs of influenza or respiratory syncytial virus (RSV) infection.

But when doctors listened to the patient's lungs, they heard "obvious moist crackles," they wrote in a report of the case. A CT scan of the man's chest revealed nodules in both lungs — typically a sign of viral pneumonia. The next day, analysis of a throat-swab sample showed that the patient was infected with SARS-CoV-2, the coronavirus that causes COVID-19.

Related: Weird gadget may cure hiccups, early study suggests

The diagnosis: The patient was admitted to the hospital and diagnosed with moderate pneumonia and COVID-19, and the doctors suspected the infection was behind his hiccups, as well.

Several case studies published in the early 2000s linked persistent hiccups — meaning hiccups lasting two days or longer — to pneumonia. Medical research published in 2020 and 2021 suggested that COVID-19 also could cause persistent hiccups and could make hiccup attacks longer and more severe than usual, doctors wrote in the report.

Hiccups are repeated, involuntary spasms of the diaphragm, the curved muscle between the chest and abdomen that moves during breathing. Many factors can trigger short bouts of hiccups, such as overeating or drinking carbonated beverages. In persistent hiccups or intractable hiccups, which last at least one month, diseases affecting the central nervous system, the gastrointestinal system or the respiratory system can play a part in driving the underlying diaphragm spasms.

The treatment: Doctors gave the man favipiravir, an antiviral medication for flu that was at one point tested as a COVID-19 treatment. He was also given medicines to reduce inflammation and treat bacterial infections. He was not given any antivirals used currently to treat COVID-19, such as Paxlovid.

After two days of treatment, the patient still had hiccups. The doctors then gave him chlorpromazine, an antipsychotic medication known to relax the muscle spasms that cause hiccups. It is the only medical treatment for hiccups approved by the U.S. Food and Drug Administration.

After 12 hours, the man's hiccups finally stopped, and chlorpromazine was administered for two more days after that. The patient tested negative for COVID-19 after 10 days of treatment, and at a follow-up visit two months later, the man reported that his hiccups had not returned.

What makes the case unique: Most cases of hiccups have gastrointestinal origins, in which the stomach, located directly below the diaphragm, becomes distended and irritates the muscle, causing it to contract. Hiccups caused by respiratory ailments, however, are rare.

COVID-19 and pneumonia, whether caused by SARS-CoV-2 or another germ, may cause persistent hiccups by triggering inflammation that irritates the phrenic nerve, which sends motor signals to the diaphragm. Such cases could be more widespread than the literature suggests, the doctors suggested, as many clinicians may not realize that persistent hiccups can result from pneumonia or a COVID-19 infection.

In fact, in the same case report, the man's doctors described a second case of hiccups associated with COVID-19 pneumonia — this time, in a 68-year-old man.

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

Many people first learned about mRNA vaccines during the coronavirus pandemic, when the companies Pfizer-BioNTech and Moderna released their COVID-19 vaccines. The Pfizer-BioNTech shot was the first COVID-19 vaccine to earn emergency authorization in the United States, and later, it would become the first mRNA vaccine of any kind to be fully approved by the U.S. Food and Drug Administration (FDA).

But even though these firsts took place during the pandemic, mRNA vaccines had been in development for many years before COVID-19 emerged as a threat.

Looking forward, they'll likely continue to play a big role in preventing — and even treating — other diseases in the future.

So what, exactly, are mRNA vaccines, and how do they work?

The future of mRNA vaccines

Although mRNA vaccines rose to prominence during the coronavirus pandemic, their applications stretch far beyond infectious diseases.

Today, many cutting-edge research groups are exploring the potential of mRNA technologies to treat conditions such as Celiac disease, lung damage, preeclampsia, brain cancer and pancreatic cancer.

"We are very excited about the application of mRNA vaccines to treat cancer," Balachandran said. "In our work on cancer vaccines, we use mRNA technology because it is amenable to rapid and flexible production, allowing us to customize a vaccine for every patient." Cancer vaccines generally work like a kind of immunotherapy, priming the immune system to go after tumor cells that can otherwise hide from its attacks.

Editor's note: Live Science spoke to Melissa Dibble prior to recent layoffs at the CDC, which the communications department was impacted by. This story was also updated after publication to note the mResvia shot as an additional example of an FDA-approved mRNA vaccine.

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

About 1 in 22 people who survive COVID-19 go on to develop a typically lifelong disease called myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), new research suggests.

Previous research has shown that ME/CFS can be triggered by viral and bacterial infections, such as Epstein-Barr virus, which causes mono, and Coxiella burnetii, which causes Q fever. The new study, published Jan. 13 in the Journal of General Internal Medicine, sought to find out how often people likely develop ME/CFS after a bout of COVID-19.

"By my rough calculations it is possible that over 7 million Americans may have developed ME/CFS following COVID," Beth Pollack, a research scientist at MIT who studies ME/CFS and long COVID, told Live Science in an email.

Pollack, who was not involved in the study, said this estimate is based on the new research, as well as U.S. Census Bureau statistics and the CDC Household Pulse Survey, which was designed to rapidly assess impacts of the coronavirus pandemic across the United States.

Related: 'It took the rug right out from under my life': Milestone ME/CFS study begins to explain disease, but will it lead to treatments?

ME/CFS (formerly called "chronic fatigue syndrome") affects roughly 1 in 100 adults in the U.S. One of its main components is post-exertional malaise, in which people's symptoms suddenly worsen after physical or mental exertion. People with the condition often experience unrefreshing sleep, brain fog and orthostatic intolerance, or sudden blood-pressure dips upon standing. Doctors are still trying to understand the biological causes of this understudied condition, but as of yet, no approved treatments exist.

Notably, ME/CFS has many overlapping symptoms with long COVID, an umbrella term that describes a range of health issues that emerge or worsen after a COVID-19 infection. Scientists are not yet sure if ME/CFS and long COVID are separate illnesses, said Dr. Anthony Komaroff, a professor of medicine at Harvard Medical School and senior physician at Brigham and Women's Hospital who was not involved in the study.

Emerging evidence suggests they might be "two examples of a larger illness that humans and other animals can experience after an infection or a major non-infectious injury," Komaroff told Live Science in an email.

Tracking ME/CFS after COVID

To investigate the relationship between COVID-19 and ME/CFS, the researchers studied 11,785 U.S. adults who had contracted SARS-CoV-2, the virus that causes COVID-19. Most of the participants were vaccinated at the time of the study, and most were enrolled as the omicron variant of the virus was circulating.

The team also studied 1,439 adults who had never caught COVID-19. The status of this group was confirmed through negative results on tests that looked for the virus itself and for antibodies against it. Notably, antibody levels wane over time, so these tests can't completely rule out infections that took place a long time ago.

At three-month intervals, all of the study participants completed questionnaires designed to track possible symptoms of ME/CFS. The researchers then grouped the participants based on symptom severity, monitoring whether they had all the symptoms needed for a diagnosis, only some symptoms or no symptoms at all.

Participants with a formal ME/CFS diagnosis before the study were excluded from the analysis. Typically, being diagnosed with ME/CFS requires meeting specific diagnostic criteria, which include fatigue accompanied by physical impairment, post-exertional malaise, unrefreshing sleep, and either cognitive impairment or orthostatic intolerance.

In the study, only 0.6% of people without a history of COVID-19 developed ME/CFS, compared with 4.5% of adults who developed the condition at least six months after having COVID-19. This suggests that COVID-19 significantly increases the risk of developing ME/CFS.

Pollack noted that 79.5% of people who developed ME/CFS in the study were female, which aligns with previous research showing that both ME/CFS and long COVID disproportionately affect females. "It will be critical to further study why this is, and to examine the roles of sex hormones and sex differences in pathological immune responses to infection," she said.

The study also found that 88.7% of participants with ME/CFS after COVID-19 were also diagnosed with long COVID.

"Long COVID and ME/CFS have not only very similar symptoms, but very similar underlying abnormalities of the brain, immune system, energy metabolism and cardiovascular system," Komaroff said."In my opinion, both Long COVID and ME/CFS are likely to be examples of post-acute infection syndromes," he said.

To strengthen their conclusions, the researchers used a technique called propensity score matching. This means they compared participants in the COVID-19 group with uninfected participants with similar demographics and preexisting conditions, to help minimize baseline differences between the groups.

But the team noted that some participants may have had undiagnosed ME/CFS before having COVID-19, which could be a limitation of the work. The questionnaire-based nature of the study presented another limitation, because participants may have struggled to remember whether their symptoms started before or after they had COVID-19.

Despite these limitations, the findings do suggest that COVID-19 raises the risk of ME/CFS. And currently, neither ME/CFS nor long COVID have approved treatments.

"This study's findings underscore the urgent need for treatments," Pollack said. "ME/CFS can be caused by multiple triggers in addition to SARS-CoV-2, and it has been among the least funded illnesses for research, despite its severity."

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.

Immune cells produced during a severe COVID-19 infection may cause cancerous tumors to shrink, research in mice suggests.

The study, published Friday (Nov. 15) in The Journal of Clinical Investigation, found that genetic information from the virus that causes COVID-19 led the immune system to produce special cells with anti-cancer properties. These immune cells, a type of white blood cell called monocytes, helped shrink several types of cancer in mice.

Normally, cancer spreads when monocytes assemble at a tumor site. The tumor cells then convert these monocytes into cancer-friendly cells, said study lead author Dr. Ankit Bharat, chief of thoracic surgery at Northwestern Medicine. These monocytes then help shield the cancer cells from the immune system, allowing tumors to grow.

"They essentially form like a castle around the cancer cells, protecting them from being invaded by the body's immune system," Bharat told Live Science.

Past research has shown that certain inflammatory conditions, such as COVID-19, can induce changes in monocyte properties. These "induced" monocytes are trained to specifically target the virus to orchestrate a more effective immune response, said Dr. Christopher Ohl, an infectious-disease specialist at Atrium Health Wake Forest Baptist and a professor at Wake Forest University School of Medicine in Winston-Salem, North Carolina, who was not involved in the study.

Bharat and his colleagues had noticed that some patients who had both severe COVID-19 and cancer had their tumors shrink after infection.

So they analyzed blood samples from people who had had a bout of severe COVID-19 and found that monocytes produced after severe infection retained a special receptor that bound well to a specific sequence of COVID-19 RNA.

“If the monocyte was a lock, and the COVID RNA was a key, then COVID RNA is the perfect fit,” Bharat said.

The researchers also looked at mice with different types of Stage 4 cancer tumors — melanoma, lung, breast and colon cancer. The mice were given a drug to induce the monocytes and thus mimic the immune response to COVID-19 infection. The tumors shrank for the four types of cancer studied.

The researchers saw that the transformed monocytes had cancer-fighting properties. These induced monocytes are also not converted by tumors into "cancer-friendly" cells that shield tumors.

Instead, the transformed monocytes migrated to the mice’s tumor sites — something most immune cells cannot do. Once near the tumor, the monocytes activated natural killer cells. The killer cells then attacked the cancer cells, causing the cancer to shrink, Bharat said.

Bharat thinks the mechanism may work in humans and against other types of cancer as well since it disrupts a way most cancers spread throughout the body. "By activating this pathway, we precondition the monocytes to never become the cancer-friendly cells," Bharat said.

The COVID-19 vaccines on the market are unlikely to trigger this mechanism, since they do not use the same RNA sequence that the virus does, Bharat said. But future drugs and vaccines could be developed to spur the development of cancer-fighting monocytes, he added.

Importantly, the mechanism provides a new therapeutic possibility for advanced cancers that don't respond to approaches such as immunotherapy, which rely on the body's immune system to fight cancer.

While immunotherapy works roughly 20% to 40% of the time, it can fail if the body can't produce enough functioning T cells, which destroy cancer cells, said Dr. Yibin Kang, a professor of molecular biology at Princeton University, who was not involved in the study. For instance, a 2021 study in the British Journal of Cancer found that less than 15% of cancer patients saw an "effective anti-cancer immune response" from immunotherapy drugs alone.

"The problem [with current immunotherapy] is the reliance on T cell immunity against cancer," Kang told Live Science.

The current study is promising because it proposes a way to selectively kill tumors that is independent of T cells, Kang said.

Ohl agreed, saying the mechanism is a "detour" that bypasses traditional roadblocks encountered during immunotherapy.

Still, clinical trials are needed to determine whether the mechanism produces the same cancer-fighting effect in humans.

Adults 65 and older and people with weakened immune systems should get two doses of the newly updated COVID-19 vaccine, the Centers for Disease Control and Prevention (CDC) recommends.

People in these groups should seek their second dose at least six months after getting their first dose, the CDC said Wednesday (Oct. 23). This recommendation also opens the door for people with moderate to severe immunosuppression to get three doses, or even more, the agency added. Patients can speak with their medical provider about whether they could benefit from getting three or more doses.

"The recommendation acknowledges the increased risk of severe disease from COVID-19 in older adults and those who are immunocompromised," the CDC stated. It also acknowledges that, unlike the seasonal flu, COVID-19 circulates year-round, so certain patients could benefit from getting a boost in immunity more than once a year.

"Receiving recommended 2024-2025 COVID-19 vaccines can restore and enhance protection against the virus variants currently responsible for most infections and hospitalizations in the United States," the CDC said. "COVID-19 vaccination also reduces the chance of suffering the effects of Long COVID."

Related: Virus that causes COVID-19 uses a secret 'back door' to infect the brain

Everyone 6 months and older is recommended to get at least one dose of a 2024-2025 COVID-19 vaccine. There are three vaccines available, made by Pfizer-BioNTech, Moderna, and Novavax. The first two shots use mRNA, a genetic molecule, as their base, while the Novavax vaccine contains virus proteins and a substance to rev up the immune system.

The CDC doesn't recommend one type of vaccine over another, except to note that Novavax is only approved for people ages 12 and up, while the others can be given to children as young as 6 months. Young kids may be recommended to get one to three doses of the vaccine, depending on which brand they get this year and whether they've been vaccinated for COVID-19 previously. Those details are spelled out on the CDC website.

The 2024-2025 vaccines differ from prior shots in that they've been updated to guard against new versions of the coronavirus that have recently emerged. The Pfizer and Moderna shots target a branch of the omicron family tree called KP.2, which began gaining dominance in June. The Novavax shot was designed to target an earlier variant, called JN.1, which KP.2 overtook.

Since summer, new variants have emerged, with one called KP.3.1.1 gaining traction in August and remaining on top as of mid-October. Although the virus continues to evolve, laboratory tests suggest that all three 2024-2025 vaccines generate antibodies against a wide range of JN.1 descendents, including KP.2, KP.3 and their close relatives.

The CDC hopes that, by recommending additional doses to high-risk groups, people can be better protected from the virus year-round.

You can learn more about where to get a COVID-19 vaccine on the CDC website.

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!

Scientists have discovered the trigger that makes inflammation spiral out of control for some children after a COVID-19 infection.

It turns out, the immune system mistakes a protein made in most parts of the body as foreign because it mimics one that forms part of SARS-CoV-2, the virus that causes COVID-19.

The condition, called multisystem inflammatory syndrome in children (MIS-C), was first identified early in the pandemic in a small percentage of children who recovered from COVID-19.

Many of these children were initially asymptomatic during a bout with the viral infection but, two to six weeks later, had life-threatening, runaway inflammation in the heart, brain, skin, blood or digestive system.

Related: Rare clotting effect of early COVID shots finally explained

MIS-C always comes with a fever, but it can also cause weakness, dizziness, stomach pain or rash.

Until recently, scientists weren't sure exactly how COVID-19 and MIS-C were linked or why the immune system might turn on the body after an infection. To understand what drives inflammation in MIS-C, researchers profiled the immune systems of 199 children with MIS-C and 45 who recovered without developing the condition.

The study, published Aug. 7 in the journal Nature, revealed 30 autoantibodies — antibodies that target a person's own body instead of a foreign invader — that were present in patients with MIS-C but not in those without the condition.

The autoantibodies with the strongest profile targeted a protein called SNX8, which is found in almost every part of the body because of its role in sorting and transporting molecules within cells.

It turned out that part of the coronavirus' "nucleocapsid protein" closely resembles the part of SNX8 that's targeted by these autoantibodies. The nucleocapsid protein is part of the virus' outer shell, which encases its genetic material. This similarity raised the possibility that, in some patients, the immune system was mistaking SNX8 for its SARS-CoV-2 lookalike and, therefore, was attacking tissues that expressed it.

To buttress this theory, the team studied T cells, which recognize and kill virus-infected cells in the body, from patients with and without MIS-C. Only T cells from MIS-C patients reacted to both SARS-CoV-2 and SNX8, supporting the mistaken-identity hypothesis. The discovery may offer new approaches to diagnosing the condition going forward.

However, SNX8 is unlikely to be the whole story behind MIS-C.

"We believe a number of rare factors come together to allow someone to get MIS-C," senior author Joseph DeRisi, a professor of biochemistry and biophysics at the University of California, San Francisco (UCSF), told Live Science. "Antibodies are one part of that but not the only part."

Either way, MIS-C is much less of a problem than it once was.

"The fascinating thing is that MIS-C has largely vanished, except in children who are unvaccinated or whose vaccines have waned," said Dr. Aaron Bodansky, study first author and a pediatric critical care fellow at UCSF. "If you predispose the immune system [to SARS-CoV-2] by vaccinating, it won't have as much time to develop this unusual response."

However, declining vaccination rates with new, updated COVID-19 vaccines may signal trouble ahead. "I think that's a serious concern," DeRisi said. "If that trend goes up, I expect we would see MIS-C increase."

For now, they aim to use their study as a model to understand other autoimmune or inflammatory conditions that may be triggered by viral infections, like diabetes or multiple sclerosis.

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!

An experimental two-in-one vaccine triggered strong immune responses against both the flu and SARS-CoV-2, the virus behind COVID-19, in an advanced clinical trial that included adults ages 50 and older.  

The ongoing clinical trial pits this new combination shot, called mRNA-1083, against several licensed vaccines that protect against either COVID-19 or the flu. Compared with these separate vaccines, the combo shot produced "significantly higher immune responses" to three subtypes of flu and to the coronavirus, the pharmaceutical company Moderna, which developed the vaccine, announced Monday (June 10).

These results haven't yet been reviewed by scientists outside of Moderna. The company plans to present the data at an upcoming medical conference and to publish the results in a scientific journal. 

Moderna representatives told news outlets that the company aspires to have the new shot approved by fall 2025 — so it won't be available by this flu season, but it might be by the next. Pfizer-BioNTech and Novavax are also working on their own COVID-flu vaccines, but Moderna is the first to release late-stage clinical trial data. 

Related: A branch of the flu family tree has died and won't be included in future US vaccines

People currently have to get their annual flu shots and updated COVID-19 vaccines separately. One major benefit of a combination vaccine would be that it would streamline that vaccination process, boosting coverage through convenience, Dr. Francesca Ceddia, Moderna's chief medical affairs officer, wrote in a Moderna blog post. Such a shot could also free up doctors' and pharmacists' time by cutting the number of individual shots they'd have to give, she wrote.

Beyond convenience, though, it's possible that the new vaccine could be more protective than the current vaccines that are given individually, Moderna's early data hint.

"When we think about the combination vaccine, we often only think about the element of convenience, one shot instead of two," Ceddia told CNN. "But what is really, really breakthrough is the fact that you not only offer that advantage, you also offer the proof of clinical benefit."

The combination vaccine includes two components, both made of a genetic molecule called mRNA. Once inside the human body, mRNA instructs human cells to build specific proteins — in this case, proteins found on the surface of SARS-CoV-2 and influenza viruses. The new vaccine builds upon the Nobel Prize-winning technology used to develop the first COVID-19 vaccines. Since those shots were released, mRNA has been used to develop experimental treatments and vaccines for many diseases, including deadly brain cancers and ultra-rare genetic disorders.

The ongoing trial is testing the new vaccine in two groups of roughly 4,000 adults each: one group of people ages 65 and up, and one group of 50- to 64-year-olds. Participants in the older group received either the new shot alone or Moderna's old COVID-19 vaccine, Spikevax, along with a high-dose flu shot that's recommended to older adults. Participants in the younger group got either the new vaccine or Spikevax and a standard-dose flu shot.

In both age groups, the combo vaccine elicited a superior immune response against a variant of SARS-CoV-2 called omicron XBB.1.5; two types of influenza A virus called H1N1 and H3N2; and a type of influenza B virus known as the Victoria lineage. The researchers measured this immune protection in terms of the number of protective antibodies that appeared in people's blood.

(Notably, newer versions of omicron have now overtaken XBB.1.5, so the new vaccine's effectiveness against those variants isn't yet known.)

The most common side effects of the new shot included pain at the injection site, fatigue, muscle aches and headaches. These side effects also show up with existing COVID-19 and flu vaccines. However, Moderna hasn't released the full details of the trial so it's not yet known whether the rate of side effects differs between the old and new vaccines. 

Between October 2023 and June 2024, up to 810,000 people were hospitalized for influenza in the U.S., and up to 71,000 people died from the infection, the CDC estimates based on preliminary data; firmer figures will be released in coming months. In addition, data recently presented to the Food and Drug Administration suggest that more than 500,000 were hospitalized for COVID-19, and 40,000 died from it, during last autumn and winter, CNN reported.  

This past season, the rate of flu vaccination far outpaced that for COVID-19 vaccination among adults, so some experts hope that introducing combination vaccines could help pull that rate up. For now, Moderna is working with regulators to approve the new vaccine for adults but the company hasn't noted when the shot might be tested in younger groups.

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!

Researchers have discovered a new autoimmune syndrome associated with COVID-19 that can cause life-threatening lung disease. 

The syndrome — which scientists have dubbed "MDA5-autoimmunity and interstitial pneumonitis contemporaneous with the COVID-19 pandemic," or MIP-C for short — is a rare, serious condition in which the immune system inadvertently attacks the body. In the worst cases, the lungs end up so scarred and stiff that the only way to save the patient is a full lung transplant. 

However, only a portion of cases involve the lungs. "Two-thirds of our cases did not have lung disease," said Dr. Dennis McGonagle, a rheumatologist at the University of Leeds in the U.K. who first started piecing together the patterns of the new disease. "But we did see that eight cases rapidly progressed and died despite all the high-tech therapies we could throw at them."  

In all, McGonagle and his colleagues have identified 60 cases of the syndrome so far. They published a study of the cases May 8 in the journal eBioMedicine.

Related: COVID-19 linked to 40% increase in autoimmune disease risk in huge study

The disease looks similar to the known condition MDA5 dermatomyositis, which is seen almost entirely in women of Asian descent, McGonagle told Live Science.

In it, patients experience joint aches, muscle inflammation and skin rashes, and in two-thirds of cases, they develop life-threatening lung scarring. MDA5 dermatomyositis happens when the immune system attacks one of its own: a protein called MDA5 that normally helps detect RNA viruses. Such viruses include those that cause influenza, Ebola and COVID-19.  

To better understand autoimmunity against MDA5, hospitals associated with the University of Leeds in Yorkshire began screening people with autoimmune symptoms for antibodies against the protein. Back in 2018, they found three patients who fit the bill. They saw another three cases the following year and eight more in 2020 — but then, in 2021, there were suddenly 35. 

The patients carried anti-MDA5 antibodies, but their disease was different from the previously known dermatomyositis. Most cases didn't involve the lungs; new patients were mostly white rather than of Asian descent; and affected women only slightly outnumbered men. 

McGonagle reached out to Dr. Pradipta Ghosh at the University of California, San Diego to investigate further. Ghosh had been using a computational framework to take medical testing data and find common threads between conditions. Her team previously published work about lung scarring in COVID-19, as well as MIS-C, an inflammatory syndrome that arises in some children after they have COVID-19. 

The team compared medical records from patients with the mystery condition, patients with COVID-induced pneumonia and patients with lung scarring unrelated to viruses. Patients with pneumonia and the autoimmune condition both showed increased activity in the gene IFIH1, which provides the blueprint for MDA5. 

Most patients with the mystery syndrome did not have a recently confirmed case of COVID-19 in their records, but it's probable many were exposed to the coronavirus and had either mild or asymptomatic disease, McGonagle said, given the timing of their cases. More than half of the patients were confirmed vaccinated for COVID-19, although which specific vaccine each person got is unknown. 

Related: Master regulator of inflammation found — and it's in the brain stem

The new study suggests that exposure to the coronavirus's RNA, COVID-19 vaccines or both may sometimes trigger the production of anti-MDA5 antibodies, McGonagle said.

Normally, MDA5 activates when it senses viral RNA in a cell and prompts the body to make antibodies against the virus. But in people with MIP-C, this immune response goes wrong. Either the body mistakes the MDA5 protein as foreign and attacks it, or the RNA kicks off such a strong immune response that the body's own proteins, including MDA5, become targeted for immune attack, McGonagle suggested.

The activation of IFIH1 came with a flood of an inflammatory protein called interleukin-15 (IL-15), the researchers found. IL-15 activates a class of immune cells that normally kill infected cells but can sometimes go rogue and attack the body's own cells.

"Our work should alert doctors to start thinking that if you see there was some exposure to virus or the vaccine or just a contact to somebody who had COVID and they come in with joint pains, rashes, aches … let's look at the lungs," Ghosh told Live Science. 

The researchers are still collecting data, but new cases of MIP-C now appear to be slowing. In 2022, Yorkshire saw 17 cases — about half of 2021's rate. The intense RNA exposure of the widespread COVID waves of 2021 plus mass vaccination may have driven that year's spike, McGonagle theorized. The researchers said they have received reports of possible MIP-C from other regions, as well.

The study also uncovered a particular genetic sequence within the IFIH1 gene that, in people who had that sequence, seemed to prevent the runaway IL-15 inflammatory response. The next step is to understand why others are vulnerable to it, Ghosh said.

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!

Global life expectancy — the average number of years a person can expect to live from their time of birth — dropped by 1.6 years at the peak of the COVID-19 pandemic, new research shows.

Global life expectancy had been on the rise until the pandemic struck, jumping from 49 years in 1950 to more than 73 years in 2019, according to the new study, published Tuesday (March 12) in the journal The Lancet. But between 2019 and 2021, this historical trend was reversed. This time frame captures the first two years of the pandemic, in which death rates peaked.

"For adults worldwide, the COVID-19 pandemic has had a more profound impact than any event seen in half a century, including conflicts and natural disasters," lead author Austin Schumacher, an acting assistant professor of health metric sciences at the University of Washington in Seattle, said in a statement. 

In 2020 and 2021 combined, approximately 16 million people died either directly from COVID-19 or from the knock-on effects of the global outbreak, which included delays in seeking health care. This excess death toll reduced global life expectancy from 73.4 years in 2019 to below 71.8 years in 2021, with stark regional differences not reflected in these global averages.

The study presents updated mortality estimates from the 2021 Global Burden of Disease Study, which quantified global health trends across places and over time. In the work, researchers analyzed data from 204 countries and territories. Of these, only 32 showed an increase in life expectancy between 2019 and 2021. Those countries included Australia, New Zealand, Japan, Iceland, Ireland and Norway, which are all high-income countries.

Related: Rare clotting effect of early COVID shots finally explained — what could that mean for future vaccines?

"Life expectancy declined in 84% of countries and territories during this pandemic, demonstrating the devastating potential impacts of novel pathogens," Schumacher said.

Among countries, Peru and Bolivia had some of the largest drops in life expectancy across all age groups from 2019 to 2021, according to the statement. In addition, Mexico City saw a particularly large drop compared with other subnational locations. 

When the researchers looked at age groups separately instead of lumping them all together, they found that the South African provinces of KwaZulu-Natal and Limpopo had some of the highest excess mortality rates and largest life expectancy declines in the world. These provinces have relatively young populations whose data can skew the overall life expectancy averages, so parsing the data in this way can help reveal the true impact of COVID-19 on older groups, in particular.

Accounting for the age distribution of the population in a given location also revealed high excess mortality rates in Jordan and Nicaragua, where the death toll had previously been concealed by grouping all age categories together, according to the statement. 

New Zealand, Barbados, and Antigua and Barbuda, on the other hand, had some of the lowest age-adjusted excess mortality rates from the pandemic, despite life expectancy declining between 2019 and 2021 in the two Caribbean countries.

According to the study authors' estimates, the pandemic caused global mortality to jump among all people over age 15, with a 22% increase in mortality for males and a 17% increase for females between 2019 and 2021. Child mortality, on the other hand, declined by 7% during the same period, with half a million fewer deaths among children under age 5 in 2021 compared with in 2019.

"Our study suggests that, even after taking stock of the terrible loss of lives the world experienced due to the pandemic, we have made incredible progress over 72 years since 1950, with child mortality continuing to drop globally," co-lead author Hmwe Kyu, an associate professor of health metric sciences at the University of Washington, said in the statement.

Although this global trend stayed on track, stark differences in child mortality rates persisted among regions. The highest rates were recorded in South Asia and sub-Saharan Africa, even after adjusting for mortality linked to the ongoing AIDS epidemic in these regions. 

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! 

At least 200 million people worldwide have struggled with long COVID: a slew of symptoms that can persist for months or even years after an infection with SARS-CoV-2, the virus that causes COVID. But research suggests that that number would likely be much higher if not for vaccines.

A growing consensus is emerging that receiving multiple doses of the COVID vaccine before an initial infection can dramatically reduce the risk of long-term symptoms. Although the studies disagree on the exact amount of protection, they show a clear trend: the more shots in your arm before your first bout with COVID, the less likely you are to get long COVID. One meta-analysis of 24 studies published in October, for example, found that people who'd had three doses of the COVID vaccine were 68.7% less likely to develop long COVID compared with those who were unvaccinated. "This is really impressive," says Alexandre Marra, a medical researcher at the Albert Einstein Israelite Hospital in Brazil and the lead author of the study. "Booster doses make a difference in long COVID."

It is also a welcome departure from earlier studies, which suggested that vaccines provided only a modest defense against long COVID. In 2022 Marra's team published a meta-analysis of six studies that found that a single dose of the COVID vaccine reduced the likelihood of long COVID by 30%. Now, that protection appears to be much greater.

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

A study published in November in the BMJ found that a single COVID vaccine dose reduced the risk of long COVID by 21%, two doses reduced it by 59% and three or more doses reduced it by 73%. Vaccine effectiveness clearly climbed with each successive dose. "I was surprised that we saw such a clear dose response," says Fredrik Nyberg, an epidemiologist at the University of Gothenburg in Sweden and one of the co-authors of the study. "The more doses you had in your body before your first infection, the better." That lines up with the findings of several new studies, which similarly show this ladderlike benefit. Marra's October 2023 meta-analysis found that two doses reduced long COVID likelihood by 36.9% and three doses reduced it by 68.7%. And in a study published last year in the Journal of the American Medical Association, other researchers found that the prevalence of long COVID in health care workers dropped from 41.8% in unvaccinated participants to 30% in those with a single dose, 17.4% with two doses and 16% with three doses.

These studies were conducted in various countries with differing health care systems, demographics, COVID vaccination uptake and COVID prevalence. As such, Marra notes that the COVID vaccines' effectiveness against long COVID will vary and may not be generalizable to other settings. Still, the consistency of the studies' findings is telling — regardless of their settings, many studies agree that boosters provide potent protection against long COVID. Marra's recent meta-analysis, for example, showed that the prevalence of long COVID in the early years of the pandemic was consistently above 20%. Today rates of long COVID have dropped, likely thanks to increased immunity, milder variants and improved treatment. Yet there is still a sharp divide between unvaccinated and vaccinated people. The prevalence of long COVID is currently 11% among those who are unvaccinated and 5% among those who have had two or more doses of the vaccine. "It is a significant difference for those who are unwilling to take the risk," he says.

The question is why. It could be that these vaccines help prevent severe COVID itself, which is a risk factor for long COVID. But that does not appear to be the whole story — in part because the boosters have also been shown to shield people who had only a mild COVID infection. Unfortunately, the precise mechanisms at play are hard to disentangle because the cause of long COVID itself is still cloaked in mystery. One possibility is that the virus lingers in the body, hiding in various organs — such as the gut or brain — and causing chronic inflammation. Another is that long COVID is an autoimmune disease in which the immune response triggered by the initial infection wages an extended war against the body, causing symptoms long after the initial infection has been cleared.

For both scenarios, boosters give people the upper hand, argues Akiko Iwasaki, an immunologist at Yale University who is co-leading a clinical trial on long COVID. That is because boosters enhance antibodies — increasing both their numbers and their ability to bind to the virus — as well as T and B immune cells that help fight the virus. With both components, "people who take the booster shots have an improved ability to fight off infection," Iwasaki says. And that is key, allowing the booster to quash a growing infection before it spirals out of control. "The more you can prevent the replication and spread of the virus within the body, the less chance the virus has to seed a niche — to establish reservoirs or cause excessive inflammation that leads to autoimmunity," she says.

Related: Inflammation is a 'mismatch between our evolutionary history and modern environment,' says immunologist Ruslan Medzhitov

Although it will take time to pinpoint the exact reason behind vaccines' protective effect against long COVID, many medical experts are hopeful that the new studies will help counter the spread of misinformation and disinformation about the COVID immunizations that has contributed to vaccine hesitancy. But experts also note that while vaccines reduce the risk of long COVID, they do not eradicate it, and protection may wane over time. "Breakthrough infections can still occur, and the dynamic of the virus — including the emergence of new variants — add complexity to the situation," Marra says. As such, he notes that it's important to continue to follow public health guidelines to minimize the impact of COVID, including the risk of long-term symptoms.

This article was first published at Scientific American. © ScientificAmerican.com. All rights reserved. Follow on TikTok and Instagram, X and Facebook.

Rare blood clots tied to some early COVID-19 vaccines that are no longer in use may have been the result of two out-of-control immune reactions happening at once.

One of these immune reactions was already known, but the second, reported Oct. 26 in the journal Blood, is a new discovery.

The finding could help to explain how other clotting conditions develop and point to better treatments, as well as suggest ways to make vaccines safer for people who are prone to the side effect.

"Understanding how a drug causes an adverse event allows us to design new approaches to make those treatments safer," said Ishac Nazy, an associate professor of medicine at McMaster University in Canada who studies the vaccine-related clotting disorder but was not involved in the current research.

A rare side effect

The vaccine-related clotting disorder, known as vaccine-induced immune thrombotic thrombocytopenia (VITT), was rare and linked to two shots: the Johnson & Johnson (J&J) and AstraZeneca COVID-19 vaccines. Both shots contained common-cold viruses called adenoviruses that were tweaked so that they couldn't infect cells. Instead, the modified viruses carried DNA instructions for part of SARS-CoV-2, the coronavirus that causes COVID-19, into the body.

VITT was a sobering side effect of what many public health experts had hoped would be a promising technology. Unlike the Moderna and Pfizer-BioNTech COVID-19 shots, which contain RNA, the J&J and AstraZeneca vaccines did not need ultracold storage, making them more accessible where cold-chain storage is unreliable. Adenovirus-based vaccines have been investigated for other diseases, but very few have achieved approval. Exceptions are an adenovirus-based Ebola vaccine approved in China and another approved by the European Union, both used only in at-risk individuals.

Soon after rolling out the J&J and AstraZeneca vaccines, doctors began reporting cases of clotting that looked a lot like a previously known disorder called Heparin-induced thrombocytopenia (HIT). About 20 to 30 years ago, HIT affected 3.5% of patients who had knee or hip replacements, said Dr. Andreas Greinacher, a physician who specializes in clotting disorders at the Greifswald University Hospital in Germany and was not involved in the new research. In these patients, heparin, a blood thinner normally given to prevent blood clots, actually triggered runaway clotting instead.

The adenovirus-based COVID vaccines were triggering the same condition as HIT, though scientists gave it a new acronym to reflect the different origin. Researchers reported that about 1 in 50,000 people under 50 who received the vaccine were affected, as well as about 1 in 100,000 of those 50 and older.

Neither vaccine is currently administered in the U.S. (AstraZeneca's shot was never used in the country, and J&J's vaccine was authorized but then retired due to the clotting issue and availability of better vaccines.) However, learning what triggers VITT could still be useful.

Today, HIT is rare because doctors now understand what causes it and can prescribe different, safer versions of heparin, Greinacher told Live Science. Similarly, he said, studying the mechanisms behind HIT and VITT could make adenovirus vaccines safer.

"Our big aim currently is to find which factor in the vaccines is triggering it," Greinacher said. "If you know the factor, I'm certain there are very smart biotechnologists who can modify the adenovirus vector so this factor is no longer present."

Unraveling VITT

When VITT was first observed in patients getting COVID-19 vaccines in February 2021, scientists soon discovered that it had to do with PF4, a chemical signal released by platelets, the blood cells that form clots.

In rare cases after vaccination with an adenovirus-based vaccine, the body would make antibodies to PF4. These antibodies would latch onto PF4 and form clumps that could then bind to receptors called Fc on other platelets. This would activate the platelets and lead to a runaway clotting response.

The new Blood study found that PF4 alone also activates a second set of receptors that cause platelets to accumulate, likely a second reason why clotting goes haywire in this disorder.

There is still a long way to go, Nazy told Live Science, whose team first reported in 2021 how antibodies against PF4 were causing VITT. The new research suggests that there are actually two different ways that PF4 acts in VITT, he said. These two pathways are not exclusive and may work in tandem.

In the new study, researchers tested blood from healthy individuals and people with VITT to trace the cascade of signals that leads to the overactive clotting. They found that the PF4 activates a receptor called c-Mpl on platelets, which causes them to clump together. This is in addition to the mechanism discovered in 2021, in which complexes of PF4 and PF4 antibodies activate platelets' Fc receptors.

"What we have shown is that as well as that antibody trigger, you've also got PF4 itself binding to platelets and activating them, providing a double whammy," Phillip Nicolson, an associate clinical professor of cardiovascular medicine at the University of Birmingham in the U.K. and the leader of the new study, told Live Science. "That may be why [the clotting] happens to a harmful degree."

Scientists have a few clues as to why adenovirus vaccines can trigger this response. PF4 carries a positive electrical charge on its surface, while adenoviruses are highly negatively charged, Nicolson said, so they may bind together easily. But even that is not confirmed, Nazy said, and has mostly been shown with computer modeling rather than with real molecules.

In rare cases, unusual clotting happens without vaccination or treatment with heparin. A recent paper published in the The New England Journal of Medicine, and co-authored by Nazy, found that in at least two of these unexplained clotting cases, the clotting disorder occurred after typical adenovirus infections. In many cases, the connection between unexplained clotting and a viral infection may be missed. And it's still a mystery why very few people are susceptible to these clotting conditions.

"That's the part we need to understand to prevent the disease from even happening," Nazy said.

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! 

Evidence is continuing to accumulate on the burden and frequency of chronic effects after a COVID infection, which fall under the umbrella term "long COVID."

At least 5% to 10% of people who contract COVID experience long COVID. This can include symptoms (for example, fatigue, brain fog and breathlessness) or conditions (for example, heart conditions, neurological conditions and diabetes) after the initial infection that may be persisting, new or relapsing.

Studies show the symptoms and increased risk of chronic conditions can persist for up to two years after infection. The individual impact of long COVID can range from temporary to severely disabling, and the societal cost — for example due to reduced workforce and increased health-care costs — is enormous.

The lower risk of developing long COVID with up-to-date COVID vaccinations is substantially offset by the high levels of infections and re-infections globally. As a result, the cumulative burden of long COVID has increased, including in lower and middle income countries. A conservative estimate suggests 65 million people may be currently affected globally.

So where are we at with reducing the risk of, and treating, long COVID?

Related: Long COVID: 3 years on, here's what we know so far

Could antivirals reduce the risk of long COVID?

COVID antiviral drugs, taken orally, continue to play an important role in reducing acute severe disease after infection. In Australia, they're available to those at highest risk from COVID.

Observational research has suggested taking antivirals during a COVID infection can reduce the risk of long COVID in people with at least one risk factor for acute severe COVID.

In one study, nirmatrelvir and ritonavir, known as Paxlovid, was associated with a 26% reduced risk of developing long COVID. It was also linked to a 47% reduced risk of death and a 24% reduced risk of hospitalization after the acute infection phase.

A similar 14% reduction in long COVID risk has been reported for molnupiravir (Lagevrio).

Ensitrelvir — a COVID antiviral available in Japan — could also reduce the risk of long COVID, preliminary analyses suggest.

More research is needed, but this data indicates antiviral medications may be a key approach to lessening the risk of long COVID.

The population most at risk of long COVID — often working-age adults — differs from those most at risk of severe disease from a COVID infection, meaning older adults or those with chronic medical conditions. Eligibility criteria to access antivirals do not currently include consideration of long COVID.

Meanwhile, one randomized trial found metformin, a commonly prescribed diabetes medication, could also reduce long COVID risk. The study offered people with symptomatic COVID who were overweight or obese metformin for two weeks, beginning within a week of symptoms starting. This group was 41% less likely to develop long COVID compared with a placebo group that didn't take metformin.

Related: Metformin cuts risk of long COVID by 40% in patients with obesity, trial suggests

The way this works might involve an effect on the powerhouses of our cells, mitochondria, or directly on the virus. Whatever the precise mechanism, further research should be priortized to fast-track this potential.

We're understanding more about long COVID

There are no effective or approved treatments for long COVID at present. Currently about 12 clinical trials are testing potential drugs. A number of candidate treatments exist for certain components of long COVID that may be useful in subgroups of patients.

However, recently we've seen major advances in understanding what's actually driving long COVID in the body. This knowledge opens up approaches for both diagnosis and treatments or interventions.

Research on treatments is lacking

An Australian parliamentary inquiry into long COVID stressed the best way to avoid the condition is to lower the risk of getting infected with COVID in the first place, through protective behaviours such as vaccination, mask wearing and cleaner indoor air.

While these are all important measures, we would benefit from having more tools at our disposal to prevent and treat long COVID. After all, COVID is still evolving rapidly and vast numbers of people are likely to be reinfected in the months and years ahead.

Overall, the quantity and speed of clinical trials into long COVID treatments has been insufficient. And most public health policy approaches are focused on preventing severe disease from a COVID infection, rather than the long-term effects.

That said, Australia recently announced an initial $22 million of funding and a plan for research into long COVID through the Medical Research Future Fund.

In July 2023, the White House established the Office of Long COVID Research and Practice which will coordinate the US government's response to long COVID, as well as two randomized trials of Paxlovid.

What now?

Given what we now know about long COVID, and the additional concern of what we don't know — for example, could organ damage reveal itself many years down the track — we desperately need diagnostic tools, clinical care pathways coupled with health worker training, and treatments to prevent and cure long COVID.

Unaddressed, long COVID may well lead to a new and substantial health and societal burden for many years to come. The response must involve prioritisation of research, such as that which led to the fast development of COVID vaccines and antivirals.

While there are some positive signs in the policy and research space, we need to see stronger recognition of long COVID and a greater sense of urgency around finding solutions.

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

A nerve-block injection may help people with long COVID restore their sense of smell, new research suggests.

The injection, called a stellate ganglion block, is given into a bundle of nerves in the neck. The new study, presented Nov. 20 at the annual meeting of the Radiological Society of North America, along with other preliminary reports, hints that the injection could help long COVID patients with parosmia, or an altered sense of smell. This condition can make pleasant scents seem revolting and can have a major impact on a person's quality of life.

However, other researchers raised concerns about the study's design limitations.

"They lost a third of their patients to follow-up, which is terrible," and means they're working with very limited data, said Dr. Leigh Sowerby, an assistant professor of otolaryngology, or head and neck surgery, at Western University in Ontario, Canada who was not involved with the research.

Related: Brain fog in long COVID may be linked to blood clots

The stellate ganglia are bundles of nerves on either side of the voice box. They contain "sympathetic" nerves that go to the head, neck, arms and upper chest. The sympathetic nervous system controls the body's "fight-or-flight" response and is part of the autonomic nervous system that deals with body functions we don't consciously control, such as heart rate.

Stellate ganglion blocks block the activity of those neck nerves, often to treat chronic pain, headaches or certain vascular diseases.

In the new study, 54 patients received a stellate ganglion block to potentially treat parosmia after COVID-19, but only 37 provided follow-up information. Participants also received a steroid injection to decrease any inflammation in nerves that could impact smell.

Of the 37 patients, 22 reported some improvement one week after treatment and 18 reported notably increased improvement one month afterward. Three months out, the 22 patients reported that their symptoms improved 49%, on average.

Twenty-six participants returned for a second injection at least six weeks after their first. A second injection improved the symptoms of those who responded to the first, but it wasn't helpful for patients who had no effect from the first.

It's not clear why this treatment might be effective for parosmia, said Dr. Adam Zoga, an author of the new research who administered the injections and a radiologist at Jefferson Health in Philadelphia.

Some think the distortion to a person's sense of smell might be due to an overactive sympathetic nervous system, sent into overdrive during the COVID-19 infection, Sowerby said. The theory is that the injection "resets" this part of the nervous system, he said.

There have been previous case reports, as well as survey-based and observational studies, that suggest stellate ganglion blocks might help treat parosmia. But these studies, like the new research, do not include a control group that received a placebo. Without a control group, it's hard to know if the nerve block is truly effective, Sowerby said. Sowerby and a group of other researchers plan to conduct this type of study.

Sowerby said the study's most significant limitation was the number of participants that didn't provide follow-up data. Details of those patients' symptoms or why they didn't follow up could make a substantial difference in the results. Another limitation is that patients reported their symptom improvements, rather than the improvements being objectively measured.

"There are some olfactory [smell] testing tools out there," said Kai Zhao, an associate professor of otolaryngology at the Ohio State University who was not involved in the research. "I'm hoping some future studies can use objective testing."

While more research is needed on stellate ganglion blocks for parosmia, Zoga noted that the procedure is usually fairly low risk and seems to work well for some people, while few other treatments do.

Sowerby agreed — even if the improvements are really a placebo effect, the treatment has the potential to help people. "It's still ultimately about healing your patient," he said.

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 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.

The 2023 Nobel prize in physiology or medicine has been awarded to two scientists who developed the messenger RNA vaccine technology used in the first effective shots against COVID-19.

Katalin Karikó, a professor at the University of Szeged in Hungary), and Dr. Drew Weissman, director of the Penn Institute for RNA Innovations, will share the 11 million Swedish krona ($1.02 million) prize. 

The duo's work led to messenger RNA (mRNA) vaccines that do not generate an unwanted immune response, enabling the shots to enter the body without causing severe inflammation, the Royal Swedish Academy of Sciences in Stockholm said in a statement on Monday (Oct. 2). The COVID-19 vaccines made by Pfizer-BioNTech and Moderna are both built on the mRNA research developed by the scientists. 

"mRNA vaccines, together with other COVID-19 vaccines, have been administered over 13 billion times," Rickard Sandberg, a member of the Nobel committee for physiology or medicine and the Royal Swedish Academy of Sciences, said during the committee's announcement on Monday. "Together [the two prize winners] have saved millions of lives, prevented severe COVID-19, reduced the overall disease burden, and enabled societies to open up again."

Related: 85% of COVID-19 long-haulers have multiple brain-related symptoms 

Vaccines work by prodding the immune system into generating an immune response to a particular germ, such as a virus. Prior to the advent of mRNA vaccines, the first vaccines worked by introducing a killed or severely weakened version of the virus into the body, giving the immune system a chance to acquire immunity before it encounters the full-fledged pathogen. 

Later developed vaccines contained proteins snatched from a virus's surface. Upon exposure to these proteins, immune cells make antibodies that can block them and the viruses they came from. There are also shots, such as Ebola vaccines, that use empty carrier viruses to transport DNA "blueprints" of a pathogen into the body, producing a similar effect, according to the Nobel committee statement. 

However, to manufacture vaccines like these, scientists have to cultivate large batches of cells, infect them with the necessary pathogens and then remove the viral and protein chunks necessary for the vaccine. This process is resource-intensive and slow, which can delay vaccine rollouts during outbreaks and pandemics. 

To get around this, in the 1980s scientists began looking at more efficient ways of getting cells to make the required proteins. One method, called in vitro transcription, worked by generating mRNA (a molecule that transports instructions from DNA to the cell's protein construction factories) directly inside cells in culture. 

But a huge hurdle remained: When animals were injected with lab-made mRNA, they experienced a massive immune response that led to dangerous levels of inflammation, destroying the vaccine and harming the animal. 

The two prize winners refined the injected mRNA's building blocks (or nucleotides) to resemble those found in the body, meaning the immune response was no longer triggered. 

In the early pandemic, this helped scientists to rapidly produce mRNA vaccines that acted against the coronavirus's "spike" protein — a pointy protein on the germ's surface.  

The research has also opened the door for work on potential cancer vaccines and for the rapid development of vaccines in response to possible future viral threats, such as bird flu, the Nobel committee said in its announcement.

"During the biggest public health crisis of our lifetimes, vaccine developers relied upon the discoveries by Dr. Weissman and Dr. Karikó, which saved innumerable lives and paved a path out of the pandemic," Dr. J. Larry Jameson, executive vice president of the University of Pennsylvania for the Health System, said in a statement.

"Now, the same approach is being tested for other diseases and conditions," Jameson said. "More than 15 years after their visionary laboratory partnership, Kati and Drew have made an everlasting imprint on medicine."

In addition to the Nobel Prize, Karikó and Weissman previously won the Breakthrough Prize and Lasker-DeBakey Clinical Medical Research Award for their work on mRNA vaccines.

An antiviral drug used to treat COVID-19 may be driving the virus that causes the disease to evolve, a new study suggests.

But is this concerning, or particularly surprising? Not at this point, and not really, experts told Live Science.   

Scientists analyzed more than 15 million SARS-CoV-2 genomes — genetic material from the virus that causes COVID-19 — and found that molnupiravir induces a "mutational signature" that, if the virus isn't completely obliterated by a course of the drug, can be transmitted to other people. Molnupirivar works by causing mutations in the SARS-CoV-2 genome that prevent the virus from replicating. 

"Previously people had raised the mutagenic effect of molnupiravir on viruses as a theoretical risk," study lead author Theo Sanderson, a researcher at the Francis Crick Institute in London, told Live Science in an email. "Our work makes this more concrete because we have found that molnupiravir can give rise to extensively-mutated viruses that remain transmissible," he said. What's more, some of the mutations that cropped up repeatedly seem to be ones that could help the virus evade the immune system, he added. 

Related: New antiviral pill halves risk of COVID-19 hospitalization, Merck says

The authors of the study, published Monday (Sept. 25) in the journal Nature, found that after molnupiravir's rollout, this mutational signature was common in countries that widely used the drug, such as the U.S. and U.K. However, countries where molnupiravir is not licensed, such as Canada, had fewer examples of these signatures. 

The findings could help regulators to assess the risks and benefits of using the drug, but experts told Live Science that many questions remain unanswered. 

"We should not be concerned with mutations themselves, but rather whether they allow the virus to adapt to infect or transmit better," said Vaughn Cooper, a professor of microbiology and molecular genetics at the University of Pittsburgh who was not involved in the research. "In this case, we see relatively little evidence that molnupiravir is fueling more adaptations to escape prior immunity or alter infectiousness," Cooper told Live Science in an email.

Indeed, Sanderson said from this data alone, it is difficult to quantify how common it is for molnupiravir-derived lineages of SARS-CoV-2 to spread between people. That's because, if a single sample of the virus with this molnupiravir signature shows up in a database but doesn't have any close relatives, scientists can't easily tell if it came from someone treated with the drug or another person infected further down the line.

The study also didn't address the potential risks and benefits of using molnupiravir for individual patients, Sanderson said. This will be important to understand, especially for those with weakened immune systems, he said. These patients have a higher risk of prolonged COVID-19 infections that give the virus more opportunities to pick up lots of mutations. 

Future modeling studies could help predict whether the drug could influence the risk of new variants of concern emerging — another question that the current study didn't explore, Sanderson added. 

"We have yet to see evidence of more fit sequences arising from molnupiravir" — meaning viruses that can more easily spread and multiply — "but this work certainly provides pause for thought and should weigh heavily in considerations around future use of the drug, necessitating at the very least mitigations of the risks of this effect, alongside real world data on the effectiveness of the drug," Aris Katzourakis, a professor of evolution and genomics at the University of Oxford who was not involved in the research, told Live Science in an email. 

Mitigation strategies could include selective prescribing and monitoring chronically infected patients for evidence of viral evolution, but these safeguards would need to be balanced against patients' clinical needs and the availability of alternative treatments, he said. 

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

Like the annual flu shots, COVID-19 vaccines have been getting a yearly update each fall — and we're due for a new batch.

So who should get one this time around? What shots are approved for use, and when will they be available? 

Here's what you need to know about the 2023-2024 COVID-19 vaccines.

Related: When should you get a flu shot? What to know for the 2023-2024 flu season

Adults without health insurance and those whose plans don't cover all costs of vaccines can get COVID-19 shots at no cost through the CDC's Bridge Access Program. These free vaccines are available at state and local health departments, federally supported health centers and participating retail pharmacy chains, including CVS, Walgreens and eTrueNorth. To find local vaccine sites participating in the Bridge Access Program, enter your ZIP code at Vaccine.gov and then check the box that says "Participating in Bridge Access Program."

Children eligible for the Vaccines for Children program, such as those who are uninsured or Medicaid-ineligible, can get no-cost COVID-19 vaccines through providers enrolled in that program.

The brown eyes of a 6-month-old boy turned a deep indigo blue after he was given the antiviral favipiravir to treat COVID-19. 

This case is unusual, but it's not the first time doctors have reported a patient's eyes changing color after they prescribed favipiravir for COVID-19. So what could be causing this bizarre effect?    

First, a bit about favipiravir: The antiviral is used to kill a variety of viruses, including influenza viruses and Ebola viruses, by stopping the germs from replicating their genetic material. It specifically works on viruses that use RNA, a molecular cousin of DNA, as their genetic material; as viruses make copies of their RNA, the drug inserts itself into the still-growing RNA molecules and causes mutations. 

In early 2020, the drug was approved in China to treat COVID-19, as SARS-CoV-2, the coronavirus behind the disease, is RNA-based. Since then, several other countries — including India, Japan and Thailand — have authorized use of the drug to treat mild to severe COVID-19. In Thailand, favipiravir is the main antiviral given to children infected with SARS-CoV-2.

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

Common side effects of favipiravir include diarrhea, a drop in circulating white blood cells and elevated levels of a chemical called uric acid in the blood that, if left untreated, can cause nausea and painful kidney stones to form. But what about the reports of spontaneous blue eyes?

The unusual effect was first reported in December 2021, when the corneas of a 20-year-old man with brown eyes turned blue for a day after he took favipiravir. (The cornea is the transparent tissue that covers the front of the eye. It lays over the iris, the circle of color that surrounds the pupil.)

But in the summer prior to that report, another group of doctors reported having a man come to their hospital with a UV light to show that the surface of his eyes glowed fluorescent after he took favipiravir. And a 2022 case report described flecks of fluorescence that appeared in the whites of three people's eyes, as well as in their nails and some teeth, after they took the drug.      

Most recently, doctors reported the peculiar case of eye discoloration in a 6-month-old boy. According to a report published in April in the journal Frontiers in Pediatrics, the boy was taken to a hospital in Thailand after he developed a fever and cough. After testing positive for COVID-19, he was given favipiravir tablets and also a syrup containing the drug. 

Just 18 hours after the infant took the drug, his mother noticed that his eyes, usually dark brown, shone blue in the sunlight. Upon examining the child, doctors discovered a buildup of blue pigment in both corneas. 

The boy received favipiravir for three days, after which his COVID-19 symptoms improved. His doctor then halted the treatment due to the strange color change in the infant's eyes. Five days after the treatment was stopped, the boy's eyes returned to their usual color.

"Usually the color of the eye is determined by the iris not the cornea and is determined by the amount of pigment that is present in the iris from birth," Dr. Vik Sharma, an eye surgeon at the LondonOC clinic in the U.K. who was not involved in the boy's case, told Live Science in an email.

Instead, the bluish hue caused by favipiravir may result from how the body processes the drug: when the drug is broken down, it may release fluorescent chemicals that then somehow accumulate in the cornea, Sharma said. In support of this idea, researchers previously found that the antiviral can also cause fluorescence in human hair and nails. 

In the new report, the boy's doctors wrote that this fluorescence "may be due to the drug, its metabolites, or additional tablet components such as titanium dioxide and yellow ferric oxide." Favipiravir tablets have been found to be fluorescent under UV light in the lab, they noted, so it may be that the drug's fluorescent components end up accumulating in different tissues.  

When an eye doctor examined the boy's eyes two weeks after he recovered from COVID-19, there were no signs of problems with his vision. However, it remains unclear whether there might be any longer-term effects of the temporary change in his eye color, the doctors wrote in the report. 

"More work is needed to determine the exact cause [of the eye discoloration] and any long-term effects," Sharma said.

Factors such as people's age, treatment duration and drug dosage may influence their odds of developing the rare side effect and how long it takes for the eye discoloration to disappear, the report authors wrote. But again, because this strange effect has only been reported a few times, it's unclear exactly why or how favipiravir discolors some individuals' eyeballs while leaving most people's eyes their original hues.

The debilitating brain fog often experienced by people with long COVID may stem from blood clots, new research suggests.

Long COVID describes myriad symptoms that linger for weeks to years after a COVID-19 infection. Some people with the condition experience problems with blood flow and lung capacity, which have been linked to tiny, abnormal blood clots. Researchers have suggested that blood clots may also drive neurological symptoms of long COVID, like brain fog, which can disrupt people's ability to focus, remember and execute tasks. 

The new study, published Thursday (Aug. 31) in the journal Nature Medicine, backs this idea linking blood clots to brain fog. However, it doesn't fully connect the dots to show how the clots might actually damage nerves or the brain to trigger brain fog.

"I feel optimistic that the science is beginning to give us real insights into what the causes [of long COVID] are and then the potential treatments," study co-author Chris Brightling, a clinical professor in respiratory medicine at the University of Leicester in the U.K., told Politico. 

"What I'm still disappointed in is … there's still a lot of patients that are suffering that haven't yet fully recovered," he said. "And we don't know how long it will take for them to recover."

Related: 85% of COVID-19 long-haulers have multiple brain-related symptoms 

The new research used data from nearly 1,840 adults who were hospitalized with COVID-19 in the U.K. in 2020 and 2021. This narrowed the study's focus to unvaccinated patients who'd developed severe infections, so it's unclear how well the results extend to vaccinated people and those who develop long COVID after mild or asymptomatic infections.  

As part of the post-hospitalization COVID-19 (PHOSP-COVID) study, the participants gave blood samples at the time of hospitalization and then, six months and 12 months later, took cognitive tests and filled out questionnaires, Science reported.

Two proteins involved in blood clotting, called fibrinogen and D-dimer, jumped out as key predictors of people's cognitive problems down the line. Fibrinogen, made by the liver, serves as the major structural component needed to form a blood clot, and D-dimer is a protein fragment released when blood clots break down. 

Compared with those who had less fibrinogen, hospitalized patients with the highest levels of fibrinogen scored worse on memory and attention tests and rated their cognition as worse on surveys. Similarly, people with high D-dimer levels later rated their cognition more poorly on subjective surveys than people with low D-dimer did. The high-D-dimer group was also more likely to report problems with their ability to work six and 12 months out from hospitalization.

The two blood-clotting proteins have previously been linked to severe COVID-19, and separately, fibrinogen alone has been associated with cognitive issues and dementia, Science reported. At this point, it's unknown how the proteins might be driving brain fog in long COVID. 

Lead study author Dr. Maxime Taquet, a clinical psychiatrist at the University of Oxford, told Science that fibrinogen-related blood clots may be derailing blood flow to the brain or perhaps directly interacting with nerve cells. D-dimer may be more linked to clots in the lungs and breathing issues, which were commonly reported in the high-D-dimer group, he said.

"Future research should look at whether treatment targeting blood clotting, for example blood thinners, might help people with these symptoms," Dr. Aravinthan Varatharaj, a clinical lecturer in neurology at the University of Southampton who was not involved in the study, told Politico. This use for blood thinners would have to be rigorously tested in trials. 

A version of the coronavirus called EG.5 — an offshoot of which is nicknamed "Eris" — now accounts for the largest proportion of new COVID-19 cases in the U.S.

Although EG.5, an omicron subvariant that was first detected in February, is dominating by a slim margin, current data suggest that it is very similar to other versions of omicron spreading throughout the country and no more deadly than its counterparts. 

The Centers for Disease Control and Prevention (CDC) estimates that, between July 23 and Aug. 5, EG.5 made up 17.3% of new cases nationwide, up from 11.9% in the previous two-week period. Those percentages were projected using a model, since the hard genetic data drawn from clinical samples in that time haven't been fully processed, the agency notes on its website.

In the most recent projections, EG.5 narrowly outcompeted another omicron spinoff called XBB.1.16, which was estimated to make up 15.6% of cases. Two more omicron subvariants, XBB.2.23 and XBB.1.5, are trailing close behind at 11.2% and 10.3%, respectively. 

All four of these subvariants belong to the broader XBB lineage, which will serve as the target of the new COVID-19 boosters coming this fall.

Related: Long COVID: 3 years on, here's what we know so far 

Just as EG.5 split from existing branches of the omicron family tree, the subvariant has also sprouted its own offshoots. These include a version of the virus called EG.5.1, which was nicknamed "Eris" on Twitter. T. Ryan Gregory, an evolutionary biologist at the University of Guelph in Ontario, posted this moniker, citing a Wikipedia page about the dwarf planet Eris, named for the Greco-Roman goddess of strife and discord.

In his tweet, Gregory emphasized that the nickname serves only as a convenient way to reference the sublineage, not an indication of its danger. "Note that nickname ≠ expected to cause a big wave by itself," he tweeted.

The World Health Organization (WHO) currently lists EG.5 as a "variant under monitoring," meaning the virus's genetics could theoretically boost its transmissibility or virulence but there isn't enough reliable evidence of that yet. 

EG.5 carries a specific mutation in its spike protein — called S:F456L — which likely helps the virus evade some of the body's immune defenses, according to a report from the Neherlab, a computational biology group based at the University of Basel in Switzerland. EG.5.1, or Eris, carries an additional spike change — S:Q52H — that "might also be a slightly beneficial mutation" for the virus.

Even with these changes, EG.5 is only incrementally different from other subvariants, having evolved slightly to "give it a better ability to engage and enter cells a little bit better," Stuart Turville, an associate professor at the University of New South Wales Sydney, told The Washington Post. 

And the virus doesn't seem to be any more lethal than its counterparts — "the impact on the human body is just about the same," Dr. K. Srinath Reddy, a physician at the Public Health Foundation of India, told the Post.

As of mid-July, XBB.1.16 was still more prevalent than EG.5, on a global scale, the WHO reported. Reports from 100 countries suggest that, at that time, the subvariant accounted for 18.4% of sampled SARS-CoV-2 sequences and EG.5 made up only 11.6% of sequences. But that's compared with 6.2% in the prior month, so the subvariant has been on the rise. 

Notably, the WHO's ability to track the emergence of new subvariants has declined recently, following the organization's decision to end the COVID-19 global health emergency.

"If you look at our latest dashboard that we have, looking at the global circulation of COVID-19, this is in the context of declining surveillance and declining reporting, but this virus is circulating in every country and it is circulating pretty much unchecked," Maria Van Kerkhove, the WHO's COVID-19 technical lead, said during a July 26 press conference. 

Although hospitalization and death rates from the virus have dwindled, "the virus will still circulate and it will still infect individuals, and so it is really critical that countries continue to keep up their surveillance," Van Kerkhove said. 

Face mask — check. Goggles — check. Gloves — check. Protective measures like these were all too familiar to health care workers caring for patients during the COVID-19 pandemic. 

But despite all these efforts to reduce the virus' spread, medical providers were still tempted to engage in a likely risky but all-too-common habit: Nose picking. 

In a study of hundreds of hospital health care workers in the Netherlands, scientists found for the first time that nose picking was associated with an increased risk of catching SARS-CoV-2, the virus that causes COVID-19, in the pandemic's early days. 

The findings, published Wednesday (Aug. 2) in the journal PLOS One, may seem somewhat obvious, particularly after health officials urged the public to wash their hands frequently and avoid touching their eyes, mouth or nose to reduce their risk of COVID-19. But the results highlight the importance of these simple behavioral changes that may sometimes be overlooked.

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

"It is important to create awareness in prevention guidelines," lead author Dr. Ayesha Lavell, a physician at the Department of Internal Medicine at Amsterdam University Medical Centers (UMC), told Live Science. When you have "advice to shave your beard" to reduce the risk of catching COVID-19, she said, it should be "advice not to pick your nose, for example."

As COVID-19 hit, health care facilities received guidance on the use of personal protective equipment (PPE) and good hygiene practices, such as using respirators and face masks, wearing gowns and ensuring hands were washed. Despite these precautions, however, hospital health care workers in COVID-19 wards were more likely to be infected with SARS-CoV-2 than those not caring for COVID-19 patients or not working in patient care. 

Some of this risk may come down to imperfect hand washing or PPE use, but the role of habitual behaviors — like nose picking — has been overlooked, the authors wrote. 

In the new study, scientists analyzed rates of SARS-CoV-2 infection among hospital staff working in Amsterdam UMC between March and October 2020. They then asked participants to complete an online survey in 2021, probing whether and how often they picked their nose. The survey also asked whether participants bit their nails, had a beard or wore glasses.

Out of about 220 people who completed the survey, nearly 85% said they picked their nose either daily, weekly or monthly, and these individuals were more likely to be younger and male than those who reported not picking their nose. Importantly, nose picking respondents had a 17.3% chance of being infected with SARS-CoV-2, compared with 5.9% for those who didn't. No association was found between the other behavioral and physical variables studied and catching COVID-19. 

"Hypothetically, if you have the virus on your finger and you introduce it inside your nose, in combination with damaging the mucosa [the tissue that lines the nose], you might facilitate easier entrance [of the virus into the body]," Lavell noted. "But we only looked at associations, so we can't say for sure that if you put your dirty finger in your nose that you'll get COVID-19."

The authors highlighted several limitations of the study — namely, that there was a time lag between the team measuring infections and the participants completing the survey. As such, some participants may have changed their behavior or had skewed memories of their past actions. And relying on self-reporting can also run the risk of people telling fibs, meaning more people may be nose-pickers than admitted to it.

Other grisly details, such as where exactly people picked their noses, how far up people put their fingers and whether they ate their boogers, were also not evaluated. In addition, not being able to examine the influence of newer coronavirus variants like omicron or the effects of widespread vaccination may limit the study's applicability to current practice. 

Nevertheless, Lavell believes the study may raise awareness. "As health care workers we are extra aware of being hygienic, but these findings just show that we are also human," she noted. Given that nose picking is not unique to medical providers, the results may also apply to the overall population, as well as to the spread of other diseases.

"It is possible that the results may be applicable to other viruses that are transmitted in the same way or are comparable to SARS-CoV-2," she added. This is "just one study," though, so more are needed to confirm these results, she concluded. 

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 newly declassified U.S. intelligence report states that there's no evidence linking the start of the COVID-19 pandemic to research or biosafety incidents at the Wuhan Institute of Virology, an institute located near the site of the first reported outbreak of the novel coronavirus.

The new report, publicly released on Friday (June 23) evening, comes from the office of Avril Haines, the Director of National Intelligence. The 10-page document summarizes the U.S. intelligence community's understanding of the research capabilities and actions of the Wuhan Institute of Virology (WIV) leading up to and in the early days of the COVID-19 pandemic. 

"This report does not address the merits of the two most likely pandemic origins hypotheses" — that SARS-CoV-2, the virus that causes COVID-19, spilled over from animals to humans or that the virus "leaked" from a laboratory, the document reads. However, the report does throw water on the notion that actions taken by WIV researchers somehow sparked the coronavirus pandemic.

Prior to the pandemic, WIV researchers did work with coronaviruses but none that could plausibly be precursors to SARS-CoV-2, the report states. The same goes for researchers associated with China's People's Liberation Army, who sometimes use WIV facilities for virology and vaccine-related work and have collaborated with WIV staff on public health initiatives of this nature. 

Related: China must share data on COVID-19's origins 'immediately,' WHO scientist demands 

WIV's research on coronaviruses involved genetic analyses and sampling viruses from animals, such as bats. But again, there's "no indication" that the institute possessed any samples of SARS-CoV-2 or a potential precursor prior to the pandemic. 

"Information available to the IC [intelligence community] indicates that the WIV first possessed SARS-CoV-2 in late December 2019, when WIV researchers isolated and identified the virus from samples from patients diagnosed with pneumonia of unknown causes," the report states.

There is also no "direct evidence" that a research-related incident involving WIV personnel occurred before the pandemic and could have sparked the global outbreak, the report notes. That said, WIV personnel "probably did not use adequate biosafety precautions at least some of the time" prior to the pandemic, and the lab had been working to improve some of its biosafety measures, equipment and training practices prior to the outbreak's start.

As part of their research, WIV staff have genetically engineered coronaviruses using "common laboratory practices," but there's no indication that the institute has done such research with SARS-CoV-2, a closely related precursor, or a "backbone" virus that is closely related enough to SARS-CoV-2 to have been the source of the pandemic.

In addition to probing the research conducted at WIV, the report focused on several cases of mild illness among WIV researchers that occurred in fall 2019. These illnesses involved some symptoms consistent with COVID-19 and some unrelated symptoms. The intelligence community has concluded that the employees' illnesses neither support nor refute either of the pandemic origin hypotheses, in part, because the reported symptoms may have resulted from other conditions, such as allergies or the common cold. 

At this time, U.S. intelligence agencies are split as to whether they favor the spillover or lab leak hypothesis, but five have concluded that the former scenario is the most likely, the report notes. Two agencies — the Department of Energy and the Federal Bureau of Investigation — have supported the lab leak theory, while two more have said they're unable to determine the precise origin of the pandemic. 

Still, "all agencies continue to assess that both a natural and laboratory-associated origin remain plausible hypotheses to explain the first human infection." But crucially, all agencies have concluded that SARS-CoV-2 was not developed as a biological weapon, the report notes.

For potentially millions of people who survive a bout of COVID-19, there are punishing months of chronic symptoms to bear afterward — a syndrome known as long COVID. Now, a study shows that taking the relatively inexpensive drug metformin during a COVID-19 infection can decrease risks of developing long COVID by more than 40%, on average.

The drug may be most effective in the early days of illness. Participants who took metformin within four days of their COVID-19 symptoms starting had a 60% lower chance of long COVID, while those who took the drug after four days saw slightly less benefit. However, this finding should be interpreted with caution, the researchers noted.   

The study, published June 8 in the journal The Lancet Infectious Diseases, investigated the outcomes for COVID-19 patients who were overweight or obese, a demographic with a high risk of severe illness from the coronavirus. The studied drug — metformin — is a relatively accessible treatment across the world and widely used for other conditions. Its safety has been thoroughly researched, even for pregnant and lactating women. 

"I for one was very surprised by the results," Dr. David Boulware, an infectious disease physician-scientist at the University of Minnesota and one of the leaders of the study, told Live Science in an email. 

Related: These 4 risk factors may increase your chance of long COVID, study hints 

Metformin is primarily used to treat type 2 diabetes and gestational diabetes and helps the body lower blood sugar levels. Previous modelling studies had suggested that it could potentially suppress the coronavirus' ability to build new proteins, and thus, make copies of itself. 

This prompted the researchers to design a clinical trial for metformin to see if it could prevent the development of severe illness in COVID-19. However, increasing awareness of long COVID led the authors to add follow-up surveys to investigate metformin's potential preventative action against this outcome, too. 

The study included 1,126 participants who consented to long-term follow-up and completed at least one survey 180 days post-treatment or later. Of these patients, 93 would report being diagnosed with long COVID within the 300 days post-treatment. Roughly half the participants had been prescribed metformin during their COVID-19 infections and the other half a placebo. Two other drugs, ivermectin and fluvoxamine, were also included in the trial but were not found to prevent long COVID. 

The definition of long COVID has been updated frequently and the condition's symptoms can fluctuate, making them difficult to assess, the study authors noted. In the trial, the researchers only counted long COVID cases that had been diagnosed by a medical provider following a participants' initial illness. By this criteria, 6.3% of those who received metformin after contracting COVID-19 developed long COVID, compared to 10.4% of those who received the placebo. 

"While metformin had theoretical reasons why it could have clinical benefits, a lot of concepts don't actually pan out when tested," said Boulware. 

The study was unique in that it included pregnant and lactating women, who are prone to poor outcomes from COVID-19 but excluded from 99% of clinical trials not directly related to childbirth. 

Although the trial was limited to people who are overweight or obese, the team thinks metformin works by acting on the coronavirus itself, and "this effect should be present regardless of BMI," Boulware said. However, he cautions that "at present, we can conclusively say that we don't know for sure."  

Nonetheless, the study points toward an important therapeutic solution for a demographic that is particularly vulnerable to poor outcomes from COVID-19.

The work by Boulware and his colleagues is valuable in that it's focused on "providing answers to the community at extreme risk of poor outcomes — obese patients," said Dr. Valentina Puntmann, a cardiologist and co-author of the American College of Cardiology 2022 Guidelines on Postacute Cardiac Sequelae (PASC) of COVID. 

In an email, Puntmann praised the trial organizers' use of a medication that's readily available, which she said "should be a priority of the public health research." She suggested that metformin may protect against long COVID by reducing vascular damage caused by high blood sugar levels and related immune system changes that "appear to drive the long-covid symptoms."

"Face blindness," or the inability to recognize faces, may be a rare symptom of long COVID, a new case report suggests. 

A case report published in March in the journal Cortex suggests a possible link between long COVID and selective face recognition problems, but, for now, it's unclear if people other than the report's subject have developed the condition after a bout of coronavirus infection.

Annie, the case report subject, fell ill with symptoms consistent with COVID-19 in March 2020. That June, meeting her family for the first time since the onset of her illness, she couldn't recognize her father's face. As a part-time portrait artist, Annie also noticed that she could no longer hold faces in her mind, having to continually depend on reference photos to draw, rather than checking them a few times an hour, as she'd previously done.

Face blindness, or prosopagnosia, is a condition that an estimated 3% of the population are born with, and roughly 1 in 30,000 acquire as a result of damage to regions in the brain specialized for processing faces, such as the fusiform gyrus. In Annie's case, she apparently acquired face blindness after falling ill with COVID-19. Annie also reported difficulties in navigating familiar spaces, such as her local grocery store. Navigational problems like this can often co-occur with face blindness.

Related: Brain shrinkage linked to COVID-19 

It is not the first time that an infectious disease has been associated with acquired face blindness. Cases have been reported following bacterial meningitis, which causes inflammation of the brain and spinal cord, and Whipple disease, another bacterial infection that can affect the nervous system, although such cases appear rare. 

Another case of a person developing face blindness after COVID-19 infection was reported in a 2021 study in the journal Acta Neuropsychologia. That patient, however, had also suffered a right hemisphere stroke, which is commonly associated with acquired prosopagnosia.

"For most people, there is no known cause," said John Towler, a lecturer in psychology at Swansea University in the U.K., who was not involved in Annie's case.

Researchers at Dartmouth College in the U.S. conducted assessments to better understand Annie's problems with face recognition. These included four face identity memory tests gauging Annie's ability to recognize and remember both celebrity's faces and random, new-to-her faces. Compared with a control group of 10 women similar to Annie in age, she performed significantly worse on all four tests.

Annie also showed other symptoms of long COVID, including fatigue and brain fog. However, it is unlikely that her prosopagnosia symptoms arose from a general decline in cognitive function. Her impairment appeared to be highly specific to facial recognition; additional tests showed that her abilities to detect faces, face identity perception (the ability to perceive and cognitively process a face), recognize objects and scenes (such as houses and natural scenes), and retain non-visual memories were spared. 

"It's not necessarily surprising that a disease that has such a profound impact on the brain can lead to impairments. What is really interesting is that it is such a selective and highly specific impairment," said Marie-luise Kieseler, lead author of the study and a doctoral student at Dartmouth.

Even in mild cases, COVID-19 has been linked to structural changes in the brain. However, research so far indicates that the brain structures such as the limbic and olfactory cortical system are those most affected by the coronavirus.

It is unclear exactly how COVID-19 might have contributed to Annie's sudden face blindness. Annie's case raises the question as to whether other people with long COVID may be affected with similar symptoms.

To begin investigating this, the researchers at Dartmouth collected self-reported data from long COVID patients. A majority of this group indicated their overall visual recognition — not specifically related to faces — and navigation capabilities had declined since their illness onset.

Since the pandemic, neither Kieseler nor Towler has noticed an increase in people coming forward with symptoms of face blindness. However, symptoms of face blindness exist on a spectrum, and mild cases, where the inability to recognize faces may not be so severe, may go unreported. "If you only decline mildly, that might not be your main concern, especially if you are dealing with a lot of other things due to COVID," Kieseler said.

In future research projects, including brain imaging studies, the team plans to work with more people who've developed face-processing problems after catching COVID-19 to better understand the link between the infection and face blindness.

Treatment for face blindness is limited, although this may change. Jodie Davies-Thompson, another lecturer of psychology at Swansea, has developed a training program for improving face discrimination in both developmental and acquired face blindness. Towler said that they've seen improvements in specific face perception tasks among people in the program, but further development is needed to ensure these improvements translate to real-world scenarios. 

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."

In rare cases, COVID-19 infections in pregnancy can cross the placenta and cause fetal brain damage via harmful inflammation, two new cases suggest. Evidence presented in the paper also "raises the possibility" that the coronavirus may be able to directly infect the fetal brain.

The new report, published Thursday (April 6) in the journal Pediatrics, described two mothers who both tested positive for SARS-CoV-2, the virus that causes COVID-19, during their second trimesters of pregnancy. They caught the virus in 2020, before vaccines were available. 

Catching COVID-19 in pregnancy is known to raise the risk of other complications, such as preterm birth or preeclampsia (severely high blood pressure in pregnancy), but overall, the outcomes of affected newborns are generally good, according to the medical resource UpToDate. The authors of the new case report stressed that these cases of fetal brain damage appear to be very rare. 

"Many women are affected by COVID-19 during pregnancy, but to see these kinds of problems in their infants at birth was clearly unusual," study senior author Dr. Shahnaz Duara, medical director of the NICU at Holtz Children's Hospital in Miami, said in a statement. "We're trying to understand what made these two pregnancies different so we can direct research toward protecting vulnerable babies." 

Related: Brain shrinkage linked to COVID-19 

One mother described in the report tested positive for SARS-CoV-2 in her second trimester but developed no symptoms. She tested positive again at her time of delivery. Her newborn had seizures soon after birth. The newborn also carried antibodies that bound to the coronavirus. After her initial discharge, the baby girl was readmitted several times for seizures. At 1 year old, she was diagnosed with microcephaly, a condition in which the head is significantly smaller than average, and showed significant neurodevelopmental delay. The baby is currently in hospice care.

The second mother developed pneumonia due to COVID-19 at the end of her second trimester and was treated in the intensive care unit. She gave birth via Cesarean section about five weeks later. She and her newborn tested negative for SARS-CoV-2 at that time, but the baby had a small head, trouble breathing and seizures. The newborn also carried SARS-CoV-2 antibodies, and his brain scans revealed signs of hemorrhage (blood loss from damaged vessels). These signs later resolved, but at that point the brain showed severe atrophy, or tissue degeneration.

After being repeatedly readmitted to the hospital for infections and "failure to thrive," the baby died of cardiac arrest at 13 months old. An autopsy revealed dramatic brain tissue loss and "evidence of virus throughout the brain," the report states. 

"We became suspicious that the virus somehow managed to breach the placental barrier to damage the central nervous system, but this had not been documented before," said Dr. Ali Saad, director of the pediatric and perinatal pathology service at Holtz Children’s Hospital, said in the statement.

The coronavirus also cropped up in both mothers' placentas, along with signs of inflammation and oxygen deprivation. Strikingingly, the placentas contained remarkably little human chorionic gonadotropin, a hormone key for fetal development, including brain development.

"Most women who contract COVID go on to have healthy babies. But there is a sub-population of people who have babies who are sick," Duara said at a news briefing, The Miami Herald reported. "And so this is not to panic the population whose babies may have been exposed to COVID. But we do think that these are the extremes and we do think if you've had COVID during pregnancy, something you should tell your pediatrician, and maybe those babies need a little closer follow-up." 

Scientists in China collected key coronavirus data in 2020 from a market in Wuhan — ground zero of the first reported outbreak of COVID-19 — but didn't share the raw data publicly until March 2023. And experts suspect that China has much more data from the early pandemic that "have yet to be shared" with the global research community.

That's according to a new editorial, published Thursday (April 6) in the journal Science and penned by Maria Van Kerkhove, the COVID-19 technical lead for the World Health Organization (WHO). China likely has data that could shed light on how the pandemic began, Van Kerkhove wrote, and the country's failure to disclose the data makes the whole world more vulnerable to future pandemics.

These undisclosed data likely include details of China's wild- and farmed-animal trades, as well as the operations of labs in Wuhan that work with coronaviruses, according to the editorial. The data also may include details about the earliest potential cases of COVID-19 detected in China and the diagnostic testing that was conducted in humans and animals in the early days of the pandemic. 

"WHO continues to call on China and all countries to share any data on the origins of SARS-CoV-2, immediately," Van Kerkhove wrote. "The world needs to move away from the politics of blame and, instead, exploit all diplomatic and scientific approaches so that the global scientific community can do what it does best — collaborate, focus on this health crisis, and find evidence-based solutions to thwart future pandemics." 

Related: Will we ever find COVID-19's 'Patient Zero?' 

Van Kerkhove's statement was prompted by events that took place last month. In early March, researchers from the Chinese Center for Disease Control and Prevention (China CDC) uploaded never-before-seen coronavirus data to Global Initiative on Sharing Avian Influenza Data (GISAID), an open-access database that includes data on influenza viruses and SARS-CoV-2, the virus that causes COVID-19. The data was later removed from GISAID but not before being downloaded by researchers outside China.

This international team of researchers reported that the data showed that SARS-CoV-2 genetic material and the DNA of common raccoon dogs (Nyctereutes procyonoides) were present in and around the exact same stalls at Wuhan's Huanan Seafood Wholesale Market in January 2020. The data cannot prove that the raccoon dogs, a fox relative, were actively infected with SARS-CoV-2 at the time, but they strongly raise the possibility that infected animals were at the market, potentially spreading the virus to other animals and to humans.

This analysis prompted a meeting of the WHO Scientific Advisory Group for the Origins of Novel Pathogens (SAGO), the China CDC researchers and the international team that analyzed the newly released raccoon dog data. China's failure to share the data back in 2020 is "simply inexcusable," Van Kerkhove wrote in her editorial.

"Still needed are studies that trace and test those animals to their source and serologic studies of the workers in live animal markets in Wuhan or in the source farms," Van Kerkhove wrote. "Without such investigations, we cannot fully understand the factors that led to the start of this pandemic." 

"Every new piece of data could potentially move the world closer to stopping another pandemic — perhaps a worse one — in the future," she wrote.

Scientists found the strongest evidence yet that the coronavirus SARS-CoV-2 leapt from animals to humans at a market in China, fueling the first reported outbreak of COVID-19. The genetic data was uploaded to a public database and then promptly removed at the request of the Chinese team that first shared it. 

An international team of scientists reported that swab samples taken in and around the stalls at Huanan Seafood Wholesale Market in early 2020 contained SARS-CoV-2 genetic sequences commingled with the DNA of common raccoon dogs (Nyctereutes procyonoides). The Atlantic first reported the findings on Friday (March 17). Raccoon dogs, a fox relative with dark blotches around their eyes, are known to be able to carry and transmit the coronavirus, The New York Times reported. 

Given when and how the swab samples were collected, and the fact that the virus can't persist indefinitely in the environment without a host, the analysis suggests that raccoon dogs infected with SARS-CoV-2 may have shedding infectious virus while they were being illegally traded at the market in December 2019, the team concluded. 

The analysis, which is not yet complete and has not yet been published, cannot definitely prove that infected raccoon dogs were present at the market. And if the animals were infected, the research cannot show how they caught the virus or how the virus spread from there.

Related: Will we ever find COVID-19's 'Patient Zero?' 

However, the presence of SARS-CoV-2 and raccoon dog genetic material in the exact same swab samples at least suggests that infected wild animals were at the market, and thus, had the potential to spread the virus, the scientists said. 

"This is a really strong indication that animals at the market were infected," Angela Rasmussen, a  virologist involved in the research, told The Atlantic. "There's really no other explanation that makes any sense."

The newly-analyzed genetic sequences were uploaded earlier this month to GISAID, an open-access genomic database, by researchers affiliated with China's Center for Disease Control and Prevention (CDC), according to The Atlantic. Evolutionary biologist Florence Débarre spotted that the raw sequence data had been shared and alerted other researchers.

Just hours after downloading the data from GISAID, scientists led by Kristian Andersen, Edward Holmes, and Michael Worobey uncovered the raccoon dog DNA commingled with SARS-CoV-2 genetic material. The team presented their findings Tuesday (March 14) to the World Health Organization's (WHO) Scientific Advisory Group for the Origins of Novel Pathogens, The Atlantic reported. 

Back in February 2020, the Chinese CDC researchers had analyzed the same data but published only part of it, making no mention of raccoon dog DNA. In a preprint, they reported finding an "abundance" of Homo sapien DNA associated with SARS-CoV-2, which they said suggested infected humans carried the virus into the market. They couldn't find any evidence pointing to an animal host in that data, they wrote. But graphs in the same preprint contradicted that claim, showing animal DNA had been found mixed up with SARS-CoV-2, Science first reported in 2022.

Shortly after Tuesday's WHO meeting, the Chinese research group's 2020 preprint went into review at a peer-reviewed Nature Research journal, suggesting a new version will soon be published. 

The team that presented their findings to the WHO initially reached out to the Chinese researchers to collaborate on the research, but shortly after they made contact, the genetic sequences were removed from GISAID, The New York Times reported.  

GISAID noted that the sequences were removed at the request of the submitter, Science reported. When asked why the sequences weren't shared sooner, the former head of the China CDC George Gao told Science that the data was "[n]othing new. It had been known there was illegal animal dealing and this is why the market was immediately shut down." When asked why GISAID took down the sequence data, Gao did not reply, but indicated that the data did not resolve the question of SARS-CoV-2's origin, which he said is "still scientific and open."

Critics of the widely-supported spillover hypothesis — that SARS-CoV-2 jumped from animals to humans — may ultimately want more conclusive evidence than research can offer, Joel Wertheim, an evolutionary biologist involved in the analysis, told Science.

"You can't observe the zoonotic transmission of a novel virus from animals to humans," he said. "We're just never going to get that level of data."

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.

The U.S. Food and Drug Administration (FDA) has authorized the first over-the-counter combination test for both influenza and COVID-19, the agency announced on Feb. 24. However, the test's maker recently filed for bankruptcy, so it's unclear whether the company has the resources to ramp up manufacturing and sell the test on a large scale, STAT reported.   

The single-use, at-home test kit, made by the California-headquartered company Lucira Health, can differentiate between the two major types of influenza viruses — influenza A and influenza B — as well as detect SARS-CoV-2, the virus that causes COVID-19. The test uses nasal swab samples and provides results in 30 minutes or less; it's intended for use in individuals who've developed signs and symptoms of a respiratory tract infection. 

"In individuals with symptoms, the Lucira COVID-19 & Flu Home Test correctly identified 99.3% of negative and 90% of positive Influenza A samples, 100% of negative and 88.3% of positive COVID-19 samples and 99.9% of negative Influenza B samples," the FDA statement reads. 

The agency noted that, since influenza B viruses are circulating at extremely low levels compared with influenza A, "there are currently not enough cases of Influenza B circulating to include in a clinical study." Because of this, Lucira confirmed that its test can detect influenza B by using "contrived" viruses, not taken directly from patients but rather grown in a lab setting. The FDA granted an "emergency use authorization" for the test based on this data, but to earn full FDA approval, Lucira will need to collect patient samples to confirm that their test reliably detects influenza B in real-world settings, the FDA said.

Related: Could we ever eradicate the flu? 

All rapid diagnostic tests produce some false positives — where a person tests positive when they're not actually infected — and false negatives — where they test negative despite being infected, the FDA noted. That said, Lucira's test does use "nucleic acid amplification" technology, which magnifies the amount of virus in the swab sample, making it more likely to detect both flu and COVID-19 than a typical rapid test, STAT reported. 

Those who test negative on a Lucira test, especially for COVID-19 or influenza B, should consider confirming their result with a more-sensitive laboratory test, like one that uses PCR, the FDA said. "Individuals who test negative and continue to experience symptoms of fever, cough and/or shortness of breath may still have a respiratory infection and should seek follow up care with their healthcare provider."

Lucira hasn't disclosed the price of its at-home test, according to STAT.

Catching COVID-19 may raise the risk of developing autoimmune disease by 43% in the months following the infection, according to the largest study of its kind. 

"The impact of this study is huge — it's the strongest evidence so far answering this question of COVID-19 and autoimmune disease risk," said Anuradhaa Subramanian, a research fellow in health informatics at the University of Birmingham, who was not involved in the study. The new research, which has yet to be peer reviewed, was posted Jan. 26 in the preprint database medRxiv.

Scientists previously linked COVID-19 to an increased risk of autoimmune disease, in which the immune system mistakenly attacks healthy parts of the body. However, this research was limited to small studies that focused on just a few conditions, such as autoimmune hemolytic anemia, which affects red blood cells, and Guillain-Barre syndrome, which affects nerve cells. 

Now, researchers have analyzed the health records of 640,000 people in Germany who caught COVID-19 in 2020 and 1.5 million people who didn't knowingly catch the coronavirus that year to explore how the infection might affect the risk of developing any of 30 autoimmune conditions.

Related: 'Rogue' antibodies found in brains of teens with delusions and paranoia after COVID-19

They examined the rate at which people were newly diagnosed with autoimmune diseases in the three to 15 months after they tested positive for COVID-19. They compared these rates to those of the people who hadn't caught COVID-19. Roughly 10% of the participants in each group had preexisting autoimmune diseases.

Among the people with no history of autoimmunity, more than 15% of people who'd caught COVID-19 developed an autoimmune disease for the first time during the follow-up period, compared with roughly 11% of the people who hadn't caught COVID-19. In other words, the COVID-19 group had a 43% higher likelihood of autoimmune disease than the control group.

Among those with existing autoimmunity, those who caught COVID-19 had a 23% higher chance of developing an additional autoimmune disease in the follow-up period.

COVID-19 was most strongly linked to an increased risk of vasculitis, which causes inflammation of the blood vessels; the previously infected group had a 63% higher rate of a type of vasculitis called arteritis temporalis than the uninfected group did. Autoimmune-driven problems with the thyroid, a butterfly-shaped organ in the throat that releases hormones, and the skin condition psoriasis were also strongly linked to prior COVID-19 infection, as was rheumatoid arthritis, which causes swelling in the joints.

"These findings just cannot be ignored," Subramanian said. "We need to pursue research into how COVID-19 is potentially triggering autoimmunity because many people are continuing to suffer from the effects of COVID-19." There are several hypotheses as to how COVID-19 might trigger autoimmunity, and it's possible that different mechanisms affect different organ systems, the researchers noted. 

"Understanding how COVID-19 impacts autoimmune disease risk will help in executing the prevention measures and early treatments to prevent associated morbidity and mortality," said Jagadeesh Bayry, a professor of biological sciences and engineering at the Indian Institute of Technology Palakkad who was not involved in the study.

Other viral infections, including influenza, have been linked to autoimmune disease, so more research is needed to establish what effects are specific to COVID-19, Bayry said. Future studies should also examine these links in diverse populations, beyond people living in Germany, Subramanian said.

Although the large sample size makes this a strong study, it is worth noting that it "only shows an association between COVID-19 and autoimmune disease but doesn't prove causality," said Dr. Atsushi Sakuraba, an associate professor of gastroenterology at the University of Chicago who was not involved in the research.

Another limitation is that there may have been people in the study's uninfected group who actually caught COVID-19 but developed little to no symptoms, and thus didn't know they'd been infected. The study also can't show whether different coronavirus variants are linked to a higher or lower risk of autoimmune disease, or how COVID-19 vaccination affects that risk. 

Long COVID is a complex condition that is still not fully understood. According to the Department of Health and Human Services, the working definition of long COVID is "signs, symptoms and conditions that continue or develop after initial COVID-19 or SARS-CoV-2 infection." These can affect many organ systems and last for weeks, months or even years.

Dr. Maureen Baker, the chief medical officer at digital care platform Healthily and the former chair of the Royal College of General Practitioners in the U.K., told Live Science that understanding what causes long COVID is crucial to helping people manage their symptoms. 

"Why do some people develop long COVID while others do not? The answer to this question is not yet clear," she said. "There are likely multiple, potentially overlapping causes of long COVID, so the underlying reasons for the illness are likely to be different for different people."

Experts still don't understand why this condition happens, but thanks to an intense global research effort, they are getting closer to finding answers. Three years on from the start of the COVID-19 pandemic, here's what we know about long COVID so far.

What are the symptoms of long COVID?

Patients with long COVID report a wide range of symptoms and conditions that can have a debilitating impact on both physical and mental health, according to a landmark 2023 review published in the journal Nature Reviews Microbiology. Researchers have identified more than 200 symptoms across multiple organ systems, with the onset and timing of symptoms differing between individuals. 

According to the Center for Disease Control and Prevention (CDC), common symptoms of long COVID include:

• Tiredness or fatigue
• Post-exertional malaise (symptoms that get worse after physical or mental effort)  
• Fever
• Cardiorespiratory problems, such as cough and heart palpitations 
• Neurological symptoms, such as memory loss and sleep problems 
• Digestive symptoms, such as abdominal pain and diarrhea 
• Muscle and joint pain 

Long COVID can also significantly impact a person's mental health. Some individuals may experience trauma and distress from ongoing symptoms, said Catherine Tregoning, a chartered health psychologist and a mental health officer at the U.K.-based Autoimmune and Support Awareness Foundation, a nonprofit aimed at improving awareness and reducing the isolation of those with autoimmune conditions.

"Those who have been affected by long COVID can be understandably concerned about catching COVID again, worry about their long-term health and find it difficult to cope with their symptoms," Tregoning told Live Science in an email. "This can result in low mood, and stress and anxiety behaviours like difficulty sleeping, irritability and easily feeling overwhelmed." 

It may be possible to group long COVID symptoms into four different subphenotypes, or clusters, according to a 2022 study published in the journal Nature Medicine. These clusters are:

• Cardiac and renal (kidney-related) 
• Respiratory, sleep and anxiety 
• Musculoskeletal and nervous system  
• Digestive and respiratory system 

Each cluster was linked with distinct patient demographics, underlying health conditions and SARS-CoV-2 infection severity. For example, Baker said, women were more likely to be affected by respiratory and sleep problems.

The review researchers believe this way of categorizing symptoms could enable more targeted long-COVID treatments. However, more research is needed to understand how this discovery may be applied in clinical practice, particularly in relation to patients who may not neatly fall into one of these subcategories.  

What causes long COVID?

There are likely multiple causes of long COVID, according to the Nature Reviews Microbiology review. 

Immune dysregulation

One of the main features of long COVID is severe dysregulation of the immune system – meaning when the body can't control or sustain an immune response. According to the Nature Reviews Microbiology review, studies have shown that the illness can cause alterations to the number and functioning of white blood cells (responsible for fighting infections and destroying cancerous tissues) and interferons (proteins released by host cells to alert other cells of potential danger). 

Scientists have also suggested that the body's inability to clear itself of the virus could be a driver of long COVID symptoms. Viral proteins have been found in numerous organs, including the brain, muscles, lymph nodes, liver and blood plasma, weeks and even months after the initial infection, the review noted. 

In addition, many researchers point to the similarity between long COVID and chronic fatigue syndrome (CFS), a condition previously linked to immune dysregulation.

"Chronic fatigue is a condition of extreme fatigue in someone present for more than six months, accompanied by post-exertional malaise," said Dr. Deepak Ravindran, co-founder of the Berkshire Long COVID Integrated Service in England. In many patients, it presents after a viral illness, Ravindran told Live Science in an email.

"There are many similarities between long COVID symptoms and chronic fatigue symptoms, including fatigue, brain fog, aches and pains, stomach disturbances, chest pain and irregular heart rates," Ravindran said. "The present understanding is that there is likely to be some underlying mechanisms that are similar to both conditions."

Circulatory system disruption

Patients with long COVID may have impaired blood clotting and problems with circulation, according to a 2021 study published in the journal Frontiers in Cardiovascular Medicine and a 2022 study published in the journal Cardiovascular Diabetology. 

"These clots can form in the small blood vessels in the lungs, leading to scarring, which can impair blood flow and reduce lung capacity," Baker said. 

Researchers also found that long COVID can promote inflammation of the heart muscle and cause dysfunction in the cells that line blood vessels, leading to a narrowing of the arteries that may lead to chest pain and high blood pressure, according to the Nature Reviews Microbiology review.

Neurological and cognitive systems

Scientists are not sure what causes long COVID's neurological symptoms, nor whether they are all caused by the same mechanisms, said Maxime Taquet, a senior research fellow at the University of Oxford in England who is investigating neurological and psychiatric outcomes of long COVID. 

One hypothesis is that SARS-CoV-2 triggers inflammation in many different parts of the body, which can include the brain, Taquet told Live Science over email. Other hypotheses include the formation of blood clots in the brain; the body attacking itself with antibodies; the virus staying hidden in pockets within the body and possibly the brain; and the virus reactivating dormant infections such as Epstein–Barr virus, the pathogen behind "mono," he said. 

Long COVID may also be linked to the loss of nerve fibers in the eyes, according to a 2022 study published in The British Journal of Ophthalmology.  

What are the risk factors for long COVID?

Scientists are still unsure exactly what puts someone at risk of long COVID, Taquet said.

"We can speculate that some of it has to do with the severity of the illness," he said, and a 2021 retrospective study in the journal PLoS Medicine found that people who initially had severe COVID-19 infections were more likely to develop long COVID. 

However, Ravindran said that patients seem to respond differently. "We thought that more severe cases of acute COVID will be left with long COVID, but we are finding that a lot more patients have had mild versions of COVID before going on to have very severe symptoms of long COVID," he said. "This is very new and very different to our usual understanding of infectious diseases." 

Whether the severity of the infection plays a role in long COVID is yet to be determined, according to the Nature Reviews Microbiology. Researchers estimated the incidence of long COVID at 10 % to 30% among non-hospitalized cases and 50% to 70% among hospitalized cases of COVID-19.

• Related: These 4 risk factors may increase your chance of long COVID, study hints 

The SARS-CoV-2 variant someone is infected with may also be a factor, Taquet found in a 2022 study. "The delta variant caused more neurological conditions than omicron," he noted, "And some of it has to do with the patient themselves."

According to the Nature Reviews Microbiology review, medical conditions that may make a person more likely to get long COVID include type 2 diabetes, connective tissue disorders, attention deficit hyperactivity disorder (ADHD) and chronic urticaria (a raised, itchy rash). However, the review authors noted that a third of people with long COVID have no identified pre-existing conditions.

Understanding more about who is at risk of getting long COVID is important for putting the right prevention strategies in place, Ravindran said.

How is long COVID diagnosed?

Dr. Stuart Katz, an investigator at Researching COVID to Enhance Recovery (RECOVER), a National Institutes of Health (NIH) research initiative, told Live Science in an email that diagnostic tools for long COVID are mostly still in development. 

"Right now, there is no universal definition for long COVID, and this is because research is ongoing," he said. "The key to doing this is identifying biomarkers or biological indicators of disease. But before we can identify long COVID biomarkers, we need to collect, analyze, and test our data to help narrow down key disease characteristics." 

According to the Nature Reviews Microbiology review, the current approach to diagnosis is largely symptom-based. Diagnostic tools may include imaging to detect blood clots, corneal microscopy to identify nerve damage in the eye, electrocardiograms to scan for heart damage, and use of hyperpolarized magnetic resonance imaging (MRI) to detect abnormal gas exchange in the lungs.

Can long COVID be prevented?

One of the best ways to protect against developing long COVID is to get vaccinated, Taquet said.

"It protects against COVID-19 in the first place and one of the best ways to avoid long COVID is to avoid COVID," he said. There is some evidence that among those with breakthrough infections — i.e. COVID-19 after being vaccinated — that the risk of long-term symptoms is lower, he added. According to the 2023 review, studies indicate that vaccines may provide partial protection, reducing the risk of having long COVID by 15% to 41%. These mixed results could be explained by differing study methods, time since vaccination and definitions of long COVID, as well as differing variants of the SARS-CoV-2 virus, researchers suggested. 

More research is needed to understand which prevention strategies may be most effective.

Is long COVID treatable?

There are no known curative treatments for long COVID, but there are some ways to manage symptoms, Katz told Live Science. 

According to the review in Nature Reviews Microbiology, pharmacological treatments for long COVID symptoms include:

• Intravenous immunoglobulins: Immunoglobulins, often referred to as antibodies, are proteins released by the immune system to identify and neutralize bacteria and viruses. Patients are given a cocktail of these through a drip into a vein to treat immune dysfunction.
• Low-dosage naltrexone: Medication primarily used for the treatment of alcohol and opioid use disorders and also prescribed off-label to treat some chronic pain and autoimmune conditions. This helps reduce inflammation within the nervous system, according to a 2014 review published in the journal Clinical Rheumatology. 
• Beta-blockers: Medication prescribed for blood pressure and heart rate disruptions.
•  Anticoagulants: Medications that prevent the formation of blood clots.  

Other options include:  

• Antihistamines: Medication used to relieve allergy symptoms such as running nose and congestion. 
• Paxlovid: Antiviral medication used for treating COVID-19. Paxlovid reduces the mortality and hospitalization rates in patients with COVID-19, but it's unclear how effective this drug may be against long COVID symptoms, according to a 2022 meta-analysis published in the journal Annals of Medicine.   
• Sulodexide: Medication used to treat vein and artery disorders. Preliminary study published in the journal Archives of Cardiovascular Diseases has shown that Sulodexide may help improve cardiovascular symptoms of long COVID.

A psychological approach to long COVID focuses on supporting patients to self-manage their physical and mental symptoms, Tregoning said.

"Stress management can reduce fatigue, relaxation techniques can help sleep disturbances and anxiety management can improve brain fog," she said. "Mental health teams provide strategies to help with pacing, pain management, panic attacks resulting from breathing issues and memory problems to name but a few."

Evidence is emerging that patients with long COVID may also benefit from occupational or physical therapy, when patients are prescribed activities designed to improve their balance, coordination, flexibility and strength, according to a 2022 review in the journal Viruses. Preliminary trials showed improvements in strength, respiratory function, physical fitness and quality of life, with no adverse side effects, such as increased fatigue or muscle pain. However, more studies are needed to determine which exercise protocols may be most effective. For example, exercise is currently not recommended for patients with long COVID who have chronic fatigue syndrome or post exertional malaise (the worsening of symptoms following even minor physical or mental exertion), according to Nature Reviews Microbiology.  

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

A one-time shot with an experimental drug halved COVID-19 patients' risk of being hospitalized with the illness compared with a placebo, a late-stage trial shows. However, the treatment may still be early in its journey to approval in the U.S., the drug's maker told Live Science.

The trial participants received an injection of the drug, called pegylated interferon lambda (PEG-lambda), within one week of developing COVID-19 symptoms. Those who received PEG-lambda early, within the first three days of developing symptoms, reaped the most benefit: Overall, these individuals were 65% less likely to be hospitalized in the following month. Among the subset of these individuals who were unvaccinated, the risk of hospitalization fell by about 89%, compared with a placebo.

Pfizer's antiviral pill Paxlovid (generic name nirmatrelvir) also lowers unvaccinated people's risk of hospitalization by about 89%, according to a late-stage trial that helped the drug earn emergency use authorization (EUA) from the Food and Drug Administration (FDA). However, one major difference between PEG-lambda and Paxlovid is that, while the former is a one-and-done injection, the latter requires users to take three tablets twice a day for five days, which totals 30 pills. 

While the Paxlovid regimen may be difficult for patients to stick to, "[PEG-lambda] has 100% compliance, by definition, because it's one dose and you're done," said Dr. Jeffrey Glenn, a professor of medicine and of microbiology and immunology at Stanford University School of Medicine, and the director of ViRx@Stanford, which develops antiviral agents to prepare for potential pandemics. 

And while Paxlovid targets the coronavirus SARS-CoV-2, PEG-lambda theoretically raises the immune system's first line of defense against many pathogens, which reduces the chances that the virus will evolve resistance to it, Glenn said.

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

Glenn is the senior author of a new report, published Wednesday (Feb. 8) in the New England Journal of Medicine, which describes the trial data in detail. Glenn also founded Eiger BioPharmaceuticals, the drug's maker, and he currently sits on the company's board. 

PEG-lambda contains a type of protein known as a type III interferon, which the body naturally produces in response to viral invasion. Once released, these proteins travel to cell surfaces, where they lock into receptors. Latching onto these receptors sets off a chain reaction inside the cell that ultimately raises its guard against viruses, making it more difficult for pathogens to infiltrate cells, replicate and spread.

The interferon within PEG-lambda specifically binds to receptors found in tissues lining the lungs, airways and gut, as well as the liver — all prime targets for SARS-CoV-2. The drug combines this interferon with polyethylene glycol, which slows the rate at which the interferon gets cleared from the body. PEG-lambda hangs around in the body for at least a week after injection, Glenn said.

The late-stage trial of PEG-lambda took place in Brazil and Canada and included more than 1,900 participants between ages 18 and 92. All the participants tested positive for SARS-CoV-2 on a rapid antigen test and were treated at outpatient clinics within seven days of developing COVID-19 symptoms. The majority had at least one characteristic that put them at high risk of severe infection, including a history of diabetes, smoking or lung disease. Around 83% of the participants had received at least one dose of a COVID-19 vaccine, and up to three doses. 

About 930 participants received an under-the-skin injection of PEG-lambda, and of these, 25 were hospitalized or had a lengthy emergency room visit due to COVID-19 in the following month. That's compared with 57 people out of about 1,020 in the placebo group — or a 51% difference in hospitalization risk between the groups. 

The trial took place between June 2021 and February 2022, and genetic analyses suggested the participants were infected by a variety of SARS-CoV-2 variants, including alpha, delta, gamma, zeta and the BA.1 lineage of omicron. PEG-lambda fared equally well against all these variants. And again, because the treatment boosts human cells' defense systems, rather than targeting SARS-CoV-2 directly, future variants aren't likely to develop resistance to the drug, as they might against other antivirals, Glenn said.

Although this positive data has now been published in a peer-reviewed journal, PEG-lambda still faces barriers to approval in the U.S. In October 2022, Eiger announced that it had requested a pre-EUA meeting with the FDA and had been denied. At that time, the FDA cited concerns about the "conduct" of the clinical trial and noted that, "in the current context of the pandemic," it would be unlikely to issue an EUA based on that trial's data.  

The concerns about the trial's conduct were related to the fact that PEG-lambda was tested through the TOGETHER Trial, an international effort launched in the early days of the pandemic to test a slew of potential COVID-19 treatments, Ingrid Choong, Eiger's senior vice president of clinical development, told Live Science. 

Typically, to earn FDA authorization, a company runs its own trial start to finish; collaborates with the FDA to set the protocols ahead of time; and periodically sends experts to each study site to ensure rigorous, industry standards are being followed. The FDA didn't have the same level of oversight over the TOGETHER Trial, and in addition, by the time Eiger was preparing to apply for an EUA, the urgency of the pandemic in the U.S. had somewhat "waned," Choong noted.

"In the context of the pandemic, I think it was really the right thing to do, to provide the drug, to try and generate important data during the crisis," Dr. David Apelian, Eiger's interim chief executive officer, told Live Science. And "I think the data show the utility of the treatment." 

At this point, Eiger may seek the emergency use authorization for PEG-lambda in countries beyond the U.S., and the company is currently evaluating how it might pursue traditional approval in the U.S., as the FDA has suggested. To that end, rather than going after only COVID-19, the company may consider testing the interferon as a "panviral" treatment that can be used against many viruses, Apelian said. 

"It's pretty likely that this could work in a similar fashion for flu and for RSV [respiratory syncytial virus], so I would see that as maybe a more prudent way of developing this through a traditional path," Apelian said. (Separately, Eiger will also continue testing the drug's effectiveness against hepatitis D, he noted; the liver disease was the first condition the company attempted to treat with PEG-lambda.)

Glenn echoed the idea of using PEG-lambda as a broad-spectrum treatment for many respiratory viruses. "I hope we will see a study designed to show how lambda can counter all the viruses in the 'tripledemic'," referencing the flu, RSV and COVID-19, Glenn told Live Science. 

In addition, Glenn said he is interested in trialing the drug as a treatment for long COVID. There's evidence that at least some symptoms of long COVID stem from residual virus lingering in the body, according to a report published Jan. 13 in the journal Nature Reviews Microbiology, and Glenn wonders if PEG-lambda could help clear these reservoirs. 

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]."

Moderna's experimental respiratory syncytial virus (RSV) vaccine was about 84% effective at protecting older adults from lower respiratory tract disease in a late-stage trial, the drugmaker announced Tuesday (Jan. 17). 

Moderna has yet to release the full trial results, but based on the company's analyses, it plans to submit the vaccine for Food and Drug Administration approval "in the first half of 2023," the company announced. Separately, the same vaccine is also being tested in children in an ongoing early-stage trial, the statement notes.

RSV most often causes mild, cold-like illnesses, but it can cause severe disease in infants, young children with certain medical conditions, and adults ages 65 and older, especially those with weakened immune systems or chronic heart or lung disease, according to the Centers for Disease Control and Prevention. There is no approved vaccine to prevent RSV, although several pharmaceutical companies are in the midst of late-stage trials testing vaccines in these high-risk groups.

Like Moderna's COVID-19 vaccines, the company's RSV vaccine contains messenger RNA (mRNA), a genetic molecule that instructs the body's cells to build specific proteins. In this case, the mRNA contains the blueprints for an "F glycoprotein," which RSV uses to break into cells; these proteins are locked into the shape they adopt just before fusing to their cellular victims.

Related: New RSV vaccine given in pregnancy protects newborns from illness, Pfizer says 

Moderna's ongoing late-stage trial includes about 37,000 adults ages 60 and older in 22 countries, including the U.S. The newly released data highlights the 64 cases of lower respiratory tract disease — infections that affect the lungs and airways below the "voicebox" — that have occurred within this cohort so far. 

All of the cases involved at least two symptoms of lower respiratory tract disease, such as cough and fever, and of these, 55 occurred in the placebo group and nine occurred in the vaccinated group. 20 cases involved three or more symptoms; 17 cases were in the placebo group, and three were in the vaccinated group.

Based on these numbers, the vaccine was 83.7% effective against lower respiratory tract disease involving two or more symptoms and 82.4% effective against disease involving three or more symptoms. "The trial is ongoing, and additional efficacy analyses are planned as cases accrue, including for severe RSV," Moderna's statement reads.

No safety concerns arose in the trial; the most common side effects of vaccination were pain at the injection site, fatigue, headache, muscle aches and joint stiffness. "Safety and tolerability will continue to be followed in this ongoing study," the Moderna statement reads.

"Today's results represent an important step forward in preventing lower respiratory disease due to RSV in adults 60 years of age and older," Stéphane Bancel, Moderna's CEO, said in the statement. "We look forward to publishing the full data set and sharing the results at an upcoming infectious disease medical conference." 

Are viruses the new gourmet meal du jour? Maybe for the tiny, single-celled organisms that live in freshwater bodies around the world.

A new study, published Dec. 27 in the journal Proceedings of the National Academy of Sciences, finds that single-celled organisms called Halteria may be munching on viruses like Pac-Man eats pellets — and could possibly change the way scientists think about global carbon cycling. 

The viruses in question belong to the genus Chlorovirus genus and are found in essentially every body of freshwater, but mostly in inland water such as lakes and ponds. Chloroviruses infect algae, stuffing the algae full of viruses until they explode. This explosion releases carbon and other nutrients into the environment that would have otherwise been eaten by the algae's predators; instead, these nutrients are made available to other microorganisms.

This micro-recycling, while a bonus for other microorganisms, may not benefit the food chain overall, study first author John DeLong, an ecologist at the University of Nebraska–Lincoln, said in a statement. Energy generally passes upward through the food chain as predators eat prey that have themselves consumed more simple and basic sources of nutrients, like algae. But when viruses destroy algae, that traps those nutrients at the bottom of the food chain.

"That's really just keeping carbon down in this sort of microbial soup layer, keeping grazers from taking energy up the food chain," DeLong said.

Related: 12 microscopic discoveries that went 'viral' in 2022

With the sheer numbers of viruses and microorganisms teeming in lakes, ponds and other bodies of freshwater, DeLong wondered, is there anything eating viruses and restoring the movement of nutrients up the food chain? In a literature search, he found previous research about virus-eating single-celled organisms called protists, so there was precedent for "virovory," a term that DeLong and his team coined to refer to virus-only diets.

"[Viruses are] made up of really good stuff: nucleic acids, a lot of nitrogen and phosphorus," he said. "Everything should want to eat them. So many things will eat anything they can get a hold of. Surely something would have learned how to eat these really good raw materials."

Luckily, samples for his study weren't hard to find. DeLong drove to a nearby pond and took some pond water back to the lab. He concentrated as many microorganisms as he could into drops of water and added a generous helping of Chlorovirus to some of them.

What he found was, devoid of any other food source, Halteria seemed to be chowing down on viruses. The Halteria in a drop of water with viruses grew 15 times their original size within two days, while the number of chloroviruses plummeted. In the water drop without viruses, Halteria did not grow.

To confirm the viruses were eaten by the microscopic Halteria, DeLong's team tagged the chlorovirus's DNA with fluorescent green dye; soon enough, they spotted the glowing viruses in Halteria's vacuole, a structure equivalent to its stomach.

The team was thrilled, but they have more questions to answer, such as do Halteria eat viruses in nature? Or did they just gobble up whatever snack they could find in their small drop of water? Further, what does this potential diet  mean for freshwater ecosystems around the globe? DeLong suspects that in a small pond, Halteria and other microorganisms could be eating 10 trillion viruses per day.

"If you multiply a crude estimate of how many viruses there are, how many [microorganisms] there are and how much water there is, it comes out to this massive amount of energy movement (up the food chain)," DeLong said. "If this is happening at the scale that we think it could be, it should completely change our view on global carbon cycling."

Editor's note: This page will be updated as new data about XBB.1.5 emerges.

A new flavor of the omicron variant of SARS-CoV-2, the virus that causes COVID-19, was identified in October 2022. In the past several weeks, it has steadily gained prominence in the United States. The subvariant is known as XBB.1.5 but has also been given the unofficial nickname "Kraken," after the mythical sea monster.

Here's what we know so far about XBB.1.5 so far.

Related: Most widely used COVID-19 vaccines and how they work 

How did XBB.1.5 emerge and where is it spreading?

Scientists first identified XBB.1.5 in New York state in October 2022, The New York Times reported. 

The subvariant stems from a broader branch of the omicron family tree known as "XBB," which emerged as a result of two earlier versions of omicron — BA.2.10.1 and BA.2.75 — swapping genes, according to the World Health Organization (WHO). These closely related omicron subvariants had the opportunity to swap genes when they infected the same person at the same time. 

From their two parents, XBB viruses gained mutations that helped them evade protective antibodies gained through prior COVID-19 infections and through vaccinations. But there was a tradeoff: XBB viruses simultaneously lost some of their ability to bind tightly to cells, a key step in infection, the New York Times reported. This may explain why other versions of omicron initially outcompeted XBB viruses.

However, as XBB viruses spread, they picked up new mutations and XBB.1.5, a.k.a. the "Kraken," was born. The Kraken harbors a mutation called F486P, which appears to restore the virus's ability to tightly latch onto cells, researchers reported Jan. 5 in research posted to the preprint database bioRxiv. (This research has not yet been peer-reviewed or published in a scientific journal.)

In a Jan. 4 news conference, WHO Director-General Dr. Tedros Adhanom Ghebreyesus reported that XBB.1.5 is "on the increase in the U.S. and Europe and has now been identified in more than 25 countries." Genomic data submitted to the open access database GISAID shows that U.S., U.K., Austria, Denmark, Canada, Israel and Germany have detected the most XBB.1.5 sequences so far, and that the subvariant remains relatively rare elsewhere. 

How easily does it spread?

Available evidence suggests that XBB.1.5 is the "most transmissible" omicron descendent yet detected, Maria Van Kerkhove, the WHO's COVID-19 technical lead, said at a news conference on Jan. 4, according to The New York Times. In the U.S., XBB.1.5 is beginning to gain dominance over other circulating omicron subvariants. 

In early December, the Kraken made up an estimated 2% of all COVID-19 cases in the U.S., The Washington Post reported. That figure jumped to 40% in the last week of December, STAT reported. 

The Centers for Disease Control and Prevention (CDC) have not yet analyzed all the data from early January 2023, but their current projections suggest that XBB.1.5 accounted for more than 27% of U.S. cases in the first week of the year. In the northeastern U.S., where XBB.1.5 was first detected and remains most common, the subvariant accounts for more than 70% of new cases, according to The Washington Post.

That said, nationwide, other flavors of omicron — namely BQ.1 and BQ.1.1 — were still circulating at comparable levels to XBB.1.5 during the first week of January, the CDC's projections suggest.

Is XBB.1.5 more likely to cause severe disease?

Scientists will need to see many weeks of hospitalization and death data before determining whether XBB.1.5 is more likely to trigger severe disease compared with earlier versions of SARS-CoV-2, the virus that causes COVID-19. 

As the U.S. experiences a nationwide surge in COVID-19 infections, "we're seeing hospitalizations have been notching up overall across the country," Dr. Barbara Mahon, director of CDC's Coronavirus and Other Respiratory Viruses Division, told NBC News. "They don’t appear to be notching up more in the areas that have more XBB.1.5," which hints that the subvariant isn't necessarily more likely to cause severe disease than its predecessors. 

How well do boosters and treatments work against XBB.1.5?

Early data suggests that the so-called bivalent boosters — the two recently updated boosters made by Moderna and Pfizer — offer decent protection against XBB viruses, despite the lineage's ability to evade antibodies, according to a Dec. 21 report in the New England Journal of Medicine. 

"Lab studies suggest that the bivalent vaccine is still effective in protecting against severe disease, though perhaps not as much against infection," Andy Pekosz, a professor of Molecular Microbiology and Immunology at the Johns Hopkins Bloomberg School of Public Health, said in a statement. "XBB.1.5 is derived from the omicron variant BA.2, and while the current bivalent vaccine was developed for the BA.5 variant, it has been shown to generate antibodies that recognize BA.2," he said.

"Things like boosters are always beneficial," Kristian Andersen, a professor in the department of immunology and microbiology who tracks coronavirus variants at the Scripps Research Institute, told The Washington Post. "Even if you get infected, you are expected to have less viral load, and you are expected to be able to transmit the virus less."

(Notably, as of Jan. 4, less than 16% of eligible U.S. residents had received a bivalent booster, the CDC reported.)

Palxovid, an oral antiviral pill used to treat COVID-19, will be effective at treating infections with XBB.1.5, The New York Times reported. The pill may not be prescribed to all COVID-19 patients, as it's not compatible with certain medications, Pakosz noted, "but overall, for the vast majority of people, Paxlovid is still a good drug to be prescribed if you get COVID-19."

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.

Viruses have been a near-constant subject of headline news in recent years, especially since the COVID-19 pandemic began. But of course, the pathogens' influence stretches back to the start of human history and beyond — in fact, viruses have had a hand in shaping the trajectory of all life on Earth. In 2022, these 13 "viral" stories highlighted just a few ways the pathogens affect the human body and the world at large. 

1. 'Zombie' viruses in Siberian permafrost reawakened 

Scientists recently isolated never-before-seen viruses from Siberian permafrost and rivers, as well as preserved mammoth wool and an ancient wolf's intestines. The team thawed out these viruses and determined that some of them could still infect amoeba, despite being up to 48,000 years old. Although the newly described viruses can't infect humans, other viruses lurking in permafrost — and now defrosting due to climate change — theoretically could. 

2. Cold sore virus spread thanks to smooching 

The virus behind cold sores, herpes simplex virus 1 (HSV-1), likely gained prominence about 5,200 years ago, possibly due to the rising popularity of kissing as a custom, some researchers argue. Herpesviruses, in general, have been around since long before the Bronze Age. But around that time, mass migrations of people from Eurasia to Europe — and the make-out sessions that took place along the way — may have helped fuel the rise of the modern version of HSV-1. 

3. Viruses named for Norse gods 

Scientists uncovered the genetic traces of a mysterious group of viruses that can infect Asgard archaea, ancient microbes that existed on Earth prior to the first complex cells. These viruses, named after figures in Norse mythology, may have influenced the rise of complex life on Earth, in part, by supplying a precursor to the nucleus that now carries DNA in complex cells. 

4. 'Mono' virus might trigger autoimmune disease 

The virus behind "mono" may fuel the development of multiple sclerosis (MS), an autoimmune disease that affects the brain and spinal cord, in people susceptible to the disease. Scientists are still learning why the virus, called Epstein-Barr virus, is strongly linked to MS, but they have a few theories as to how it might trigger the disease. 

5. Giant viruses in Arctic lake 

The Milne Fiord epishelf lake lies fewer than 500 miles (800 kilometers) from the North Pole and contains giant viruses that infect its resident algae. Such giant viruses can measure larger than some bacteria and contain comparably complex DNA. Scientists are still discovering new varieties of giant viruses, learning how their genes work and how they infect cells. 

6. Viruses slay superbugs 

Viruses that infect bacteria, or "bacteriophages," can make antibiotics more effective, clearing away drug-resistant superbugs that would otherwise defy treatment. In one fascinating case, doctors cultured viruses in lab dishes alongside a bacterial superbug and then selected the best killer from the bunch. They then unleashed that selected virus into a woman's chronic infection, helping to finally cure it. 

7. Ancient viruses show widespread activity in human body 

Remnants of ancient viruses can be found scattered throughout the human genome. Once considered non-functional "junk DNA," it turns out that these genetic snippets are actually active in tissues throughout the body. What these viruses do in healthy tissue is still a mystery, and the answer is likely different in each tissue type. 

8. Never-before-seen viruses found in the ocean 

A team of scientists scoured the world's oceans for viruses containing RNA, a molecular cousin of DNA. Overall, they identified about 5,500 never-before-seen RNA virus species during their quest. To categorize all the new viruses, the team proposed doubling the number of taxonomic groups used to classify RNA viruses, from the existing five phyla to 10 phyla. 

9. Ocean viruses may affect flow of carbon through the ecosystem 

Thousands of RNA viruses recently discovered in the world's oceans infect a wide variety of hosts, including fungi, algae, amoebas and even some invertebrates. By infecting organisms that pull carbon dioxide out of the atmosphere, these mysterious viruses may influence how carbon flows through the ocean at large, scientists say. 

10. Virus-carrying ticks break record 

A shockingly high number of ticks at the Lawrence Township Recreational Park in Pennsylvania carry a potentially life-threatening virus called deer-tick virus, which can be transmitted to humans through tick bites. Of 25 ticks sampled from the park in a recent survey, 92% tested positive for the virus. By comparison, the highest infection rate among ticks previously measured at a single U.S. site was 25%. 

11. Climate change may push 'Japanese encephalitis' outbreaks south 

"Japanese encephalitis" (JE), a viral disease that can sometimes spark dangerous inflammation in the brain, reached southern Australia in 2022, a region where it hadn't previously spread. The JE virus gets passed to humans through the bites of infected mosquitoes and typically affects people in Asia and parts of the Western Pacific. Its appearance in Victoria, New South Wales, South Australia and Queensland hints that climate change may be expanding the disease's range southward.

12. Was the famous 'Russian flu' a coronavirus? 

A mysterious illness that emerged in Russia in the late 1880s and then spread around the globe may have been caused by a coronavirus, some scientists think. Known as the "Russian flu," the virus caused a pandemic eerily similar to the ongoing COVID-19 pandemic, but researchers are still hunting for hard evidence of the virus' true identity. If they can find this evidence, they plan to investigate whether a descendent of the virus is still circulating today, perhaps causing milder disease than its predecessor. 

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.

An ongoing measles outbreak in central Ohio has sickened 74 children since mid-October, resulting in 26 hospitalizations so far, Columbus Public Health reported. There have been no reported deaths linked to the outbreak. 

Between Jan. 1 and Dec. 8, 2022, the Centers for Disease Control and Prevention (CDC) received reports of 88 measles cases across the nation, meaning most can be attributed to the Ohio outbreak. By comparison, a total of 62 U.S. measles cases were reported to the CDC in 2020 and 2021 combined. 

Of the children sickened in the Ohio outbreak, 69 out of 74 hadn't received any doses of the measles, mumps and rubella (MMR) vaccine, according to Columbus Public Health. Four children had received one dose of the vaccine out of the two recommended doses, although notably, "some cases may not have been eligible yet for the second dose due to age," the health department noted. The remaining child's vaccination status is unknown. 

The CDC recommends that children receive their first MMR dose between 12 months and 15 months old and their second dose between 4 and 6 years old. Alternatively, the MMRV vaccine, which also guards against varicella (chickenpox), may be given following the same vaccination schedule. (If traveling overseas, however, a child may need to get vaccinated at a younger age than usual, the CDC notes.)

Related: This one number shows why measles spreads like wildfire 

One dose of either vaccine is estimated to be 93% protective against measles, and two doses are 97% protective. That means there's a slim chance that vaccinated people can still become infected, but in these cases, they tend to have milder cases of the disease than unvaccinated people do, the CDC states.

In the current outbreak, 51 of the affected children, or 69%, are between 1 and 5 years old. Five of the children are between 6 and 17 years old, and 18 are younger than 1. In general, children younger than 5 face a high risk of complications from measles, according to the CDC. These complications include ear infections, diarrhea and dehydration, as well as more-severe, potentially life-threatening conditions, such as pneumonia and brain swelling (encephalitis), the latter of which can lead to convulsions and changes in hearing ability and cognitive function. 

Measles spreads through an infected person's coughs and sneezes, which release viral particles that can be inhaled or picked up from contaminated surfaces by other people. The incredibly infectious virus infects an estimated 90% of unvaccinated people who spend time near an infected person, and the virus can remain infectious and suspended in the air for up to two hours after the infected person exits the room, according to the CDC. 

In general, measles symptoms begin one to two weeks after exposure; initial symptoms can include cough, runny nose, watery eyes and a fever higher than 104 degrees Fahrenheit (40 degrees Celsius). Then, white dots known as "Koplik spots" appear in the mouth, and a red, splotchy skin rash emerges on the face and then spreads to the neck, trunk, arms, legs and feet.

"There's no way of knowing which children will become so sick they have to be hospitalized," Columbus Public Health spokesperson Kelli Newman told CNN. "The safest way to protect children from measles is to make sure they are vaccinated with MMR." 

Adults without "presumptive evidence of immunity" — meaning a record of MMR vaccination or blood test results showing that they're immune to measles — are also recommended to get at least one dose of the vaccine, the CDC states. Certain adults in this group should get two doses, including students at post-high-school educational institutions, health care personnel, international travelers and those who will be in other settings that pose a high risk for measles transmission.