For some ant queens, the secret to long life might be a self-produced insulin blocker.

Ant queens are famously long-lived, even though they shouldn’t be. Generally, animals that put lots of energy into reproduction sacrifice some time off their life. But ant queens produce millions of eggs and live an extraordinarily long time compared with worker ants that don’t reproduce.

Now, researchers have shown how one ant species pulls off this anti-aging feat. When queens and wannabe queens of the species Harpegnathos saltator gear up to reproduce, a part of what’s called the insulin signaling pathway gets blocked, slowing aging, the researchers report in the Sept. 2 Science. That molecular pathway has long been implicated in aging in mammals, including humans.
“There’s been a need to understand why queens, or reproductives, in social insects can live for so amazingly long,” says Marc Tatar, a biologist at Brown University in Providence, R.I., who was not involved with the study. Some ant species have queens that survive 30 times as long as their workers. Other social insects such as bees and termites also have long-lived queens.

In a rare behavior for ants, when a queen H. saltator dies, some female workers begin competing in duels for the chance to replace her (SN: 1/17/14). These hopeful royals develop ovaries, start laying eggs and transition into queenlike forms called gamergates. When a worker transitions to a gamergate, her life span becomes five times as long as it was. But if she doesn’t end up becoming queen and reverts back to a worker, her life span shortens again.

The researchers exploited this behavior to investigate the molecular underpinnings of anti-aging in these ants. H. saltator gamergates, it turns out, extend their life spans by taking advantage of a split in the insulin signaling pathway, the chain of chemical reactions that drive insulin’s effects on the body. One branch of this pathway is involved with reproduction, while the other is implicated in aging.

“Insulin comes with our life — [after] we eat, we have high insulin,” says Hua Yan, a biologist at the University of Florida in Gainesville. “But a constant high level of insulin is bad for longevity.”

Examining patterns of gene activity, Yan and colleagues found that gamergates have more active insulin genes than regular worker ants and, as a result, have increased metabolic activity and ovary development. But the secret sauce protecting the ants from the insulin’s aging effects appears to be a molecule called Imp-L2, which blocks the branch of the insulin pathway linked to aging, experiments showed. The branch involved in reproduction, however, remains active.

“What we don’t understand is how Imp-L2 can act on one aspect of the pathway and not on the other,” says study coauthor Claude Desplan, a developmental biologist at New York University.

These results represent a leap forward in our understanding of extreme social insect longevity, the researchers say, while also showcasing an anti-aging evolutionary adaptation that hasn’t been seen in the wild before.

For some ant queens, the secret to long life might be a self-produced insulin blocker.

Ant queens are famously long-lived, even though they shouldn’t be. Generally, animals that put lots of energy into reproduction sacrifice some time off their life. But ant queens produce millions of eggs and live an extraordinarily long time compared with worker ants that don’t reproduce.

Now, researchers have shown how one ant species pulls off this anti-aging feat. When queens and wannabe queens of the species Harpegnathos saltator gear up to reproduce, a part of what’s called the insulin signaling pathway gets blocked, slowing aging, the researchers report in the Sept. 2 Science. That molecular pathway has long been implicated in aging in mammals, including humans.
“There’s been a need to understand why queens, or reproductives, in social insects can live for so amazingly long,” says Marc Tatar, a biologist at Brown University in Providence, R.I., who was not involved with the study. Some ant species have queens that survive 30 times as long as their workers. Other social insects such as bees and termites also have long-lived queens.

In a rare behavior for ants, when a queen H. saltator dies, some female workers begin competing in duels for the chance to replace her (SN: 1/17/14). These hopeful royals develop ovaries, start laying eggs and transition into queenlike forms called gamergates. When a worker transitions to a gamergate, her life span becomes five times as long as it was. But if she doesn’t end up becoming queen and reverts back to a worker, her life span shortens again.

The researchers exploited this behavior to investigate the molecular underpinnings of anti-aging in these ants. H. saltator gamergates, it turns out, extend their life spans by taking advantage of a split in the insulin signaling pathway, the chain of chemical reactions that drive insulin’s effects on the body. One branch of this pathway is involved with reproduction, while the other is implicated in aging.

“Insulin comes with our life — [after] we eat, we have high insulin,” says Hua Yan, a biologist at the University of Florida in Gainesville. “But a constant high level of insulin is bad for longevity.”

Examining patterns of gene activity, Yan and colleagues found that gamergates have more active insulin genes than regular worker ants and, as a result, have increased metabolic activity and ovary development. But the secret sauce protecting the ants from the insulin’s aging effects appears to be a molecule called Imp-L2, which blocks the branch of the insulin pathway linked to aging, experiments showed. The branch involved in reproduction, however, remains active.

“What we don’t understand is how Imp-L2 can act on one aspect of the pathway and not on the other,” says study coauthor Claude Desplan, a developmental biologist at New York University.

These results represent a leap forward in our understanding of extreme social insect longevity, the researchers say, while also showcasing an anti-aging evolutionary adaptation that hasn’t been seen in the wild before.

Meet the Milky Way in its own words.

The Milky Way: An Autobiography of Our Galaxy takes a tour of our home in the cosmos from an unexpected perspective. Astrophysicist and folklorist Moiya McTier presents herself not as the author, but as the lucky human vessel through which the Milky Way has chosen to tell its story. Then she lets the galaxy take it away, with humor, heart and a huge dose of snark.

The book alternates chapters between science and mythology, reflecting McTier’s dual specialties (her bio says she was the first student in Harvard University’s history to study both). “Many of you don’t realize this, but myths were some of your species’ first attempt at scientific inquiry,” the Milky Way tells us.

The Milky Way is telling its story now because it’s sick of being ignored. Once upon a time, humans looked to the glittering smudge of stars in the sky for insight into when to plant crops or avoid floods. We told stories about the Milky Way’s importance in the origin and fate of the world.

Our galaxy ate it up: For an entity that spends most of its time ripping up smaller galaxies and watching its own stars die, “your stories made me feel loved and needed and, perhaps for the first time in my long existence, more helpful than I was ruinous.” But in the last few centuries, technology and light pollution have pulled humankind away. “At first, I thought it was just a phase,” the Milky Way says. “Then I remembered … that several hundred years is actually a long time for humans.”
So the Milky Way decided to remind us why it’s so important. Its autobiography covers big-picture scientific questions about galaxies, like where they come from (“When a gas cloud loves itself very much,” the Milky Way explains, “it hugs itself extra tight, and after a few hundred million years, a baby galaxy is born. Leave the storks out of it, please.”). It also gets into what galaxies are made of, how they interact with other galaxies, and how they live and die. The book then zooms out to cover the origins and possible ends of the universe, mysteries like dark matter and dark energy, and even humankind’s search for other intelligent life (SN: 8/4/20).

The author takes pains to explain scientific jargon and the technical tools that astronomers use to study the sky. A lot of popular astronomy writing glosses over how astronomers think about cosmic distance or exactly what a spectrum is, but not this book. If you’ve ever been curious about these insider details, The Milky Way has you covered.

McTier’s version of our home galaxy is heavily anthropomorphized. The Milky Way is brash, vain and arrogant in a way that may hide a secret insecurity. Its central black hole is characterized as the physical embodiment of the galaxy’s shame and regrets, a source of deep existential angst. And its relationship with the Andromeda galaxy is like a long-term, long-distance romance, with each galaxy sending stars back and forth as love notes until the two can eventually merge (SN: 3/05/21).

This could have felt gimmicky. But McTier’s efforts to make the metaphors work while keeping the science accurate and up-to-date made the premise endearing and entertaining.

I laughed twice on Page 1. I learned a new word on Page 2. I dog-eared the endnotes early on because it became instantly clear I would want to read every one. I read this book while traveling in rural upstate New York, where the sky is much clearer than at my home outside of Boston. The Milky Way reminded me to look up and appreciate my home in the universe, just like its narrator wanted.

For millions of people, COVID-19 doesn’t end with a negative test. Weeks or months after traces of the virus disappear from noses and throats, symptoms can persist or come back. New ones might pop up and stick around for months. People suffering from long COVID are unwillingly in it for the long haul — and it’s still unclear who’s at the highest risk for the condition.

Researchers don’t yet have an official definition for long COVID, and its symptoms are wide-ranging (SN: 7/29/22). Some people struggle with extreme fatigue that interferes with their daily lives. Others can’t concentrate or struggle with memory amid thick brain fog. Still others have organ damage or a persistent cough and difficulty breathing.
“There are a variety of different kinds of ways that people can have long COVID. It’s not just the one thing,” says Leora Horwitz, an internal medicine physician at New York University Langone Health. “That’s what makes it so hard to study.”

This spectrum of symptoms makes pinning down who’s at high risk for long-term health problems from the disease especially hard. Some post-COVID conditions may stem from virus-induced damage or from the stress of being hospitalized with severe disease. In other cases, the body’s own immune response to the virus could drive the damage. Or the virus may be hiding somewhere in the body, possibly the gut, helping symptoms to persist (SN: 11/24/20). Different causes may have different risk groups, says Hannah Davis, cofounder of the Patient-Led Research Collaborative, a research and advocacy group studying long COVID.

There are some broad hints about who’s at risk. Studies suggest that women are more likely than men to have lingering symptoms. COVID-19 patients with more than five symptoms in the first week of infection or preexisting health conditions such as asthma may be more likely to develop long COVID. Age also appears to be a risk factor, though results are mixed regarding whether the burden falls on older people or middle-aged people. Populations that were disproportionally hit by COVID-19 overall — including Black and Hispanic people — may similarly face disparities for long COVID. And while vaccination seems to protect people from developing long COVID, Horwitz says, it’s still unclear by how much.

Age is a risk factor for severe COVID-19, and the U.S. Centers for Disease Control and Prevention lists more than 30 health problems, including cancer and lung disease, that also raise the risk. “So many researchers assume that those [risk factors] will be the same for long COVID and there’s no scientific basis for that,” Davis says. There are many more that researchers could be missing when it comes to long COVID.

Using health records and exams, and knowledge of ailments with symptoms similar to long COVID, experts are on the hunt for those risk factors.

Examining health
When it comes to getting a better handle on who’s at risk for long COVID — which also goes by the wonky alias Post-Acute Sequelae of SARS-CoV-2 infection — electronic health records may hold important clues.

Horwitz is part of the U.S. National Institutes of Health’s RECOVER initiative that aims to understand the long-term impacts of COVID-19. One arm of the study involves mining millions of electronic health records to find potential patterns.

Studying millions of these records should pinpoint potential risk factors that are rare in the population overall but perhaps more common for people with long COVID, Horwitz says. “That’s hard even in a cohort study of thousands.”

But health records aren’t perfect: They depend on physicians logging that patients are having trouble sleeping or focusing, or that they’re exhausted. “The things people are complaining about, we’re really bad at writing down those diagnoses on the record,” Horwitz says. “So we miss that.”
To account for health records’ deficiencies, Horwitz and colleagues are also directly studying thousands of people. Participants answer a questionnaire every three months so that the team can identify what kinds of symptoms people have and whether they’re getting better or worse.

Then blood, urine, stool and saliva samples can reveal what’s happening in the body. Tests on those samples can uncover if the coronavirus is still around and causing trouble, or if the immune system has learned to attack the body itself. Participants with abnormal test results will undergo additional, targeted testing.

“Unlike electronic health records where it’s hit or miss, like somebody might have had a CAT scan or might not, here we say, ‘OK, you have trouble breathing. We will take a look at your lungs,’” Horwitz says.

The study includes a range of participants: adults and kids, pregnant people, those currently with COVID-19 and people who died after having the disease.

Some of the potential risk factors that the team is looking for include autoimmune diseases and other viral infections. The list may grow as more people join the study. “We’re trying to balance the fishing versus making sure that we’re at least fishing for things that could be in the water,” Horwitz says.

Among short supply, though, are people who never caught the virus — important “controls” to highlight what’s different about people who got COVID-19.

So far, more than 7,000 people have signed up, and the group plans to recruit around 10,000 more. It’s a lot of data, but early results may soon start coming in.

“We’ll probably try to do an interim peek at those data this fall,” Horwitz says. “It’s tricky because we deliberately wanted to enroll 18,000 people so we would have enough power to really look at the things we care about. I don’t want to cheat and look too early, but we also know that there’s a lot of interest.”

Striking similarities
Some long COVID symptoms — brain fog, fatigue and trouble sleeping — mirror another illness: myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS. Other long COVID symptoms, such as rapid heartbeat and dizziness, fall in the category of nervous system disorders called dysautonomia. Similar symptoms could belie similar risk factors.

Yet potential risk factors for those conditions are largely missing from long COVID research, says Davis, who has had long COVID since March 2020. Among the possibilities that scientists are considering are things like Epstein-Barr virus, migraines and some autoimmune diseases.

Epstein-Barr virus could be a big one, Davis says. Infections last a lifetime because the virus can go into hiding in the body and possibly reemerge. That virus has been linked to ME/CFS for decades, though its role in the disease remains unclear, Davis says.
Some early hints of a link between Epstein-Barr virus and long COVID already exist. Multiple studies have found evidence in blood samples from some long COVID patients that the immune system recently battled with Epstein-Barr virus, which can cause infectious mononucleosis, a disease characterized by extreme fatigue. Other studies have found signs of the virus itself. And in 2021, Davis and colleagues found that 40 out of 580 people with symptoms of long COVID who responded to an online survey reported having a current or recent Epstein-Barr virus infection.

With ME/CFS, it’s possible that another illness caused by a different virus triggers the Epstein-Barr virus, which then causes the fatigue syndrome. Given the parallels between that condition and long COVID, some scientists are wondering if the two are actually the same disease, with the coronavirus now known as one trigger.

Examining health conditions that raise the chances of long COVID could provide answers for both diseases, says Nancy Klimas, an immunologist at Nova Southeastern University in Fort Lauderdale, Fla. That’s in part because researchers can more easily identify people who developed lingering symptoms after a bout of COVID-19 compared with unknown infections that may precede ME/CFS.

Also, “there’s a huge difference in these two fields and it’s money,” Klimas says. She now has funding from the CDC to compare long COVID patients with people who have ME/CFS. The team hopes that physical exams and specialized tests will reveal whether the two diseases are indeed the same and be a step toward understanding the mechanisms behind the lingering symptoms.

Still, since long COVID as a whole encompasses such a wide range of symptoms, it will take time to uncover who is at risk of what.

If COVID-19 were just one disease impacting the lungs, heart or brain, the research might be easier, Horwitz says. “But we have to test everything.”

Monkeypox is not yet a global public health emergency, the World Health Organization said June 25.

The decision comes as the outbreak of the disease related to smallpox continues to spread, affecting at least 4,100 people in 46 countries as of June 24. That includes at least 201 cases in the United States. Those cases have been found in 25 states and the District of Columbia, according to the U.S. Centers for Disease Control and Prevention.
“Controlling the further spread of outbreak requires intense response efforts,” and the situation should be reevaluated in a few weeks, the WHO committee evaluating the outbreak said in an announcement.

The declaration of a public health emergency would have potentially made it easier to get treatments and vaccines to people infected with or exposed to the virus. Some medications and vaccines that could help fend off monkeypox are approved for use against smallpox, and can be used against monkeypox only with special authorization.

The virus that causes monkeypox, named for its discovery in monkeys in 1958 though it is probably a virus that mainly infects rodents, is not a new threat. Countries in central Africa, where monkeypox is endemic, have had sporadic outbreaks since researchers found the first human case in 1970. Places in western Africa had few cases until 2017. But most cases outside the continent were travel-related, with limited spread to others (SN: 5/26/22).

“Monkeypox has been circulating in a number of African countries for decades and has been neglected in terms of research, attention and funding,” WHO director-general Tedros Ghebreyesus said in a statement announcing the decision. “This must change not just for monkeypox but for other neglected diseases in low-income countries as the world is reminded yet again that health is an interconnected proposition.”

Monkeypox typically kills fewer than 10 percent of people who contract it. At least one person has died in the global outbreak.

As case numbers climb, researchers are working to decipher the genetic blueprint of the virus, in hopes of uncovering whether some viral mutations might explain why the virus has quickly gained a foothold in new places.

Tracing the mutations
The closest known relative of the versions of the virus behind the global outbreak comes from Nigeria, hinting that the outbreak may have got its start there.

In the newest surge in cases, scientists have uncovered more viral changes than anticipated — a sign that the virus may have been circulating undetected among people for a while, perhaps since Nigeria’s 2017–2018 monkeypox outbreak, new research suggests. What’s more, a group of enzymes known for their virus-fighting abilities in the body may be to blame for many of those mutations.

A genetic analysis of monkeypox viruses involved in the global outbreak from 15 people across seven countries shows that these viruses have an average of 50 more genetic tweaks than versions circulating in 2018 and 2019, researchers report June 24 in Nature Medicine. That’s roughly six to 12 times as many mutations as scientists would have expected the virus to develop over that time. Unlike some other types of viruses, poxviruses, which include smallpox and monkeypox viruses, typically mutate fairly slowly.

The changes have a pattern that is a hallmark of an enzyme family called APOBEC3, the researchers say. These enzymes edit DNA’s building blocks — represented by the letters G, C, A and T — in a specific way: Gs change to As and Cs to Ts. The analysis found that particular pattern in the viral sequences, suggesting that APOBEC3s are responsible for the mutations.

Ideally, so many DNA building blocks are swapped for another that a virus is effectively destroyed and can’t infect more cells. But, sometimes, APOBEC3 enzymes don’t make enough changes to knock out the virus. Such mutated, though still functional, viruses can go on to infect additional cells, and possibly another person.

A big question, though, is whether the genetic tweaks seen in the monkeypox virus are helpful, harmful or have no effect at all on the virus.

While it’s still unknown whether the enzymes are directly responsible for the changes in the monkeypox virus, similar mutations are still popping up, the team found. So, APOBEC3s may still be helping the virus change as it continues to spread. One member of the enzyme family is found in skin cells, where people with monkeypox can develop infectious pox lesions.
Different symptoms
Symptoms reported in the global outbreak have been generally milder than those reported in previous outbreaks, perhaps allowing the disease to spread before a person knows they’re infected.

It is not clear whether those differences in symptoms are related to changes in the virus, Inger Damon, director of the CDC’s Division of High-Consequence Pathogens and Pathology, said June 21 in a news briefing hosted by SciLine, a service for journalists and scientists sponsored by the American Association for the Advancement of Science.

Typically, in previous outbreaks, people would develop flu-like symptoms, including fever, headaches, muscle aches and exhaustion about a week or two after exposure to the virus. Then, one to three days after those symptoms start, a rash including large pus-filled lesions pops up generally starting on the face and limbs, particularly the hands, and spreads over the body. Though generally milder, those symptoms are similar to smallpox, but people with monkeypox also tend to develop swollen lymph nodes.

All patients in the U.S. outbreak have gotten rashes, Damon said, “but the lesions have been scattered or localized to a specific body site, rather than diffuse, and have not generally involved the face or the … palms of the hand or the soles of the feet.” Instead, rashes may start in the genital or anal area where they can be mistaken for sexually transmitted diseases, such as syphilis or herpes, she said.

In many cases, the rashes have not spread to other parts of the body. And the classical early symptoms such as fever have been “mild and sometimes nonexistent before a rash appears,” Damon said.

Monkeypox is transmitted from person to person through close skin-to-skin contact or by contact with contaminated towels, clothes or bedding. It may also be spread by droplets of saliva exchanged during kissing or other intimate contact. The CDC is investigating whether the virus might be spread by semen as well as skin-to-skin contact during sex, Agam Rao, a captain in the U.S. Public Health Service, said June 23 at a meeting of the CDC’s Advisory Committee on Immunization Practices.

“We don’t have any reason to suspect it is spread any other way,” such as through the air, Rao said.

In Nigeria, more monkeypox cases have been recorded among women, while the global outbreak has affected mainly men, particularly men who have sex with men. Experts warn that anyone can be infected with monkeypox, and some people face an increased risk of severe disease. Those at increased risk include children, people who are immunocompromised, pregnant people and people with eczema.

The risk of catching monkeypox through casual contact is still low in the United States, Rao said. But data she presented show that while people in the country have contracted monkeypox while traveling abroad, cases have also spread locally.

For all the coronavirus variants that have thrown pandemic curve balls — including alpha, beta, gamma and delta — COVID-19 vaccines have stayed the same. That could change this fall.

On June 28, an advisory committee to the U.S. Food and Drug Administration met to discuss whether vaccine developers should update their jabs to include a portion of the omicron variant — the version of the coronavirus that currently dominates the globe. The verdict: The omicron variant is different enough that it’s time to change the vaccines. Those shots should be a dual mix that includes both a piece of the nearly identical omicron subvariants BA.4/BA.5 and the virus from the original vaccines, the FDA announced June 30.

“This doesn’t mean that we are saying that there will be boosters recommended for everyone in the fall,” Amanda Cohn, chief medical officer for vaccine policy at the U.S Centers for Disease Control and Prevention said at the meeting. “But my belief is that this gives us the right vaccine for preparation for boosters in the fall.”
The decision to update COVID-19 vaccines didn’t come out of nowhere. In the two-plus years that the coronavirus has been spreading around the world, it has had a few “updates” of its own — mutating some of its proteins that allow the virus to more effectively infect our cells or hide from our immune systems.

Vaccine developers had previously crafted vaccines to tackle the beta variant that was first identified in South Africa in late 2020. Those were scrapped after studies showed that current vaccines remained effective.

The current vaccines gave our immune systems the tools to recognize variants such as beta and alpha, which each had a handful of changes from the original SARS-CoV-2 virus that sparked the pandemic. But the omicron variant is a slipperier foe. Lots more viral mutations combined with our own waning immunity mean that once omicron can gain a foothold in the body, vaccine protection isn’t as good as it once was at fending off COVID-19 symptoms (SN: 6/27/22).

The shots still largely protect people from developing severe symptoms, but there has been an uptick in hospitalizations, especially among older people, Heather Scobie, deputy team lead of the CDC’s Surveillance and Analytics Epidemiology Task Force said at the meeting. Deaths among older age groups are also beginning to increase. And while it’s impossible to predict the future, we could be in for another tough fall and winter, epidemiologist Justin Lessler of the University of North Carolina at Chapel Hill said at the meeting. From March 2022 to March 2023, simulations project that deaths from COVID-19 in the United States might number in the tens to hundreds of thousands.

A switch to omicron-containing jabs may give people an extra layer of protection for the upcoming winter. Pfizer-BioNTech presented data at the meeting showing that updated versions of its mRNA shot gave clinical trial participants a boost of antibodies that recognize omicron. One version included omicron alone, while the other is a twofer, or bivalent, jab that mixes the original formulation with omicron. Moderna’s bivalent shot boosted antibodies too. Novavax, which developed a protein-based vaccine that the FDA is still mulling whether to authorize for emergency use, doesn’t have an omicron-based vaccine yet, though the company said its original shot gives people broad protection, generating antibodies that probably will recognize omicron.

Pfizer and Moderna both updated their vaccines using a version of omicron called BA.1, which was the dominant variant in the United States in December and January. But BA.1 has siblings and has already been outcompeted by some of them.
Since omicron first appeared late last year, “we’ve seen a relatively troubling, rapid evolution of SARS-CoV-2,” Peter Marks, director of the FDA’s Center for Biologics Evaluation and Research, said at the advisory meeting.

Now, omicron subvariants BA.2, BA.2.12.1, BA.4 and BA.5 are the dominant versions in the United States and other countries. The CDC estimates that roughly half of new U.S. infections the week ending June 25 were caused by either BA.4 or BA.5. By the time the fall rolls around, yet another new version of omicron — or a different variant entirely — may join their ranks. The big question is which of these subvariants to include in the vaccines to give people the best protection possible.

BA.1, the version already in the updated vaccines, may be the right choice, virologist Kanta Subbarao said at the FDA advisory meeting. An advisory committee to the World Health Organization, which Subbarao chairs, recommended on June 17 that vaccines may need to be tweaked to include omicron, likely BA.1. “We’re not trying to match [what variants] may circulate,” Subbarao said. Instead, the goal is to make sure that the immune system is as prepared as possible to recognize a wide variety of variants, not just specific ones. The hope is that the broader the immune response, the better our bodies will be at fighting the virus off even as it evolves.

The variant that is farthest removed from the original virus is probably the best candidate to accomplish that goal, said Subbarao, who is director of the WHO’s Collaborating Center for Reference and Research on Influenza at the Doherty Institute in Melbourne, Australia. Computational analyses of how antibodies recognize different versions of the coronavirus suggest that BA.1 is probably the original coronavirus variant’s most distant sibling, she said.

Some members of the FDA advisory committee disagreed with choosing BA.1, instead saying that they’d prefer vaccines that include a portion of BA.4 or BA.5. With BA.1 largely gone, it may be better to follow the proverbial hockey puck where it’s going rather than where it’s been, said Bruce Gellin, chief of Global Public Health Strategy with the Rockefeller Foundation in Washington, D.C. Plus, BA.4 and BA.5 are also vastly different from the original variant. Both have identical spike proteins, which the virus uses to break into cells and the vaccines use to teach our bodies to recognize an infection. So when it comes to making vaccines, the two are somewhat interchangeable.
There are some real-world data suggesting that current vaccines offer the least amount of protection from BA.4 and BA.5 compared with other omicron subvariants, Marks said. Pfizer also presented data showing results from a test in mice of a bivalent jab with the original coronavirus strain plus BA.4/BA.5. The shot sparked a broad immune response that boosted antibodies against four omicron subvariants. It’s unclear what that means for people.

Not everyone on the FDA advisory committee agreed that an update now is necessary — two members voted against it. Pediatrician Henry Bernstein of Zucker School of Medicine at Hofstra/Northwell in Uniondale, N.Y., noted that the current vaccines are still effective against severe disease and that there aren’t enough data to show that any changes would boost vaccine effectiveness. Pediatric infectious disease specialist Paul Offit of Children’s Hospital of Philadelphia said that he agrees that vaccines should help people broaden their immune responses, but he’s not yet convinced omicron is the right variant for it.

Plenty of other open questions remain too. The FDA could have authorized either a vaccine that contains omicron alone or a bivalent shot. Some data presented at the meeting hinted that a bivalent dose might spark immunity that could be more durable, but that’s still unknown. Pfizer and Moderna tested their updated shots in adults. It’s unclear what the results mean for kids. Also unknown is whether people who have never been vaccinated against COVID-19 could eventually start with such an omicron-based vaccine instead of the original two doses.

Maybe researchers will get some answers before boosters start in the fall. But health agencies needed to make decisions now, so vaccine developers have a chance to make the shots in the first place. Unfortunately, we’re always lagging behind the virus, said pediatrician Hayley Gans of Stanford University. “We can’t always wait for the data to catch up.”