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  • Why Are We Still Flu-ifying COVID?

    Why Are We Still Flu-ifying COVID?

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    Four years after what was once the “novel coronavirus” was declared a pandemic, COVID remains the most dangerous infectious respiratory illness regularly circulating in the U.S. But a glance at the United States’ most prominent COVID policies can give the impression that the disease is just another seasonal flu. COVID vaccines are now reformulated annually, and recommended in the autumn for everyone over the age of six months, just like flu shots; tests and treatments for the disease are steadily being commercialized, like our armamentarium against flu. And the CDC is reportedly considering more flu-esque isolation guidance for COVID: Stay home ’til you’re feeling better and are, for at least a day, fever-free without meds.

    These changes are a stark departure from the earliest days of the crisis, when public-health experts excoriated public figures—among them, former President Donald Trump—for evoking flu to minimize COVID deaths and dismiss mitigation strategies. COVID might still carry a bigger burden than flu, but COVID policies are getting more flu-ified.

    Read: The flu-ification of COVID policy is almost complete

    In some ways, as the population’s immunity has increased, COVID has become more flu-like, says Roby Bhattacharyya, a microbiologist and an infectious-disease physician at Massachusetts General Hospital. Every winter seems to bring a COVID peak, but the virus is now much less likely to hospitalize or kill us, and somewhat less likely to cause long-term illness. People develop symptoms sooner after infection, and, especially if they’re vaccinated, are less likely to be as sick for as long. COVID patients are no longer overwhelming hospitals; those who do develop severe COVID tend to be those made more vulnerable by age or other health issues.

    Even so, COVID and the flu are nowhere near the same. SARS-CoV-2 still spikes in non-winter seasons and simmers throughout the rest of the year. In 2023, COVID hospitalized more than 900,000 Americans and killed 75,000; the worst flu season of the past decade hospitalized 200,000 fewer people and resulted in 23,000 fewer deaths. A recent CDC survey reported that more than 5 percent of American adults are currently experiencing long COVID, which cannot be fully prevented by vaccination or treatment, and for which there is no cure. Plus, scientists simply understand much less about the coronavirus than flu viruses. Its patterns of spread, its evolution, and the durability of our immunity against it all may continue to change.

    And yet, the CDC and White House continue to fold COVID in with other long-standing seasonal respiratory infections. When the nation’s authorities start to match the precautions taken against COVID with those for flu, RSV, or common colds, it implies “that the risks are the same,” Saskia Popescu, an epidemiologist at the University of Maryland, told me. Some of those decisions are “not completely unreasonable,” says Costi Sifri, the director of hospital epidemiology at UVA Health, especially on a case-by-case basis. But taken together, they show how bent America has been on treating COVID as a run-of-the-mill disease—making it impossible to manage the illness whose devastation has defined the 2020s.

    Each “not completely unreasonable” decision has trade-offs. Piggybacking COVID vaccines onto flu shots, for instance, is convenient: Although COVID-vaccination rates still lag those of flu, they might be even lower if no one could predict when shots might show up. But such convenience may come at the cost of protecting Americans against COVID’s year-round threat. Michael Osterholm, an epidemiologist at the University of Minnesota School of Public Health, told me that a once-a-year vaccine policy is “dead wrong … There is no damn evidence this is a seasonal virus yet.” Safeguards against infection and milder illness start to fade within months, leaving people who dose up in autumn potentially more susceptible to exposures by spring. That said, experts are still torn on the benefits of administering the same vaccine more than once a year—especially to a public that’s largely unwilling to get it. Throughout the pandemic, immunocompromised people have been able to get extra shots. And today, an advisory committee to the CDC voted to recommend that older adults once again get an additional dose of the most recently updated COVID vaccine in the coming months. Neither is a pattern that flu vaccines follow.

    Read: Fall’s vaccine routine didn’t have to be this hard

    Dropping the current COVID-isolation guideline—which has, since the end of 2021, recommended that people cloister for five days—may likewise be dangerous. Many Americans have long abandoned this isolation timeline, but given how new COVID is to both humanity and science, symptoms alone don’t yet seem enough to determine when mingling is safe, Popescu said. (The dangers are even tougher to gauge for infected people who never develop fevers or other symptoms at all.) Researchers don’t currently have a clear picture of how long people can transmit the virus once they get sick, Sifri told me. For most respiratory illnesses, fevers show up relatively early in infection, which is generally when people pose the most transmission risk, says Aubree Gordon, an epidemiologist at the University of Michigan. But although SARS-CoV-2 adheres to this same rough timeline, infected people can shed the virus after their symptoms begin to resolve and are “definitely shedding longer than what you would usually see for flu,” Gordon told me. (Asked about the specifics and precise timing of the update, a CDC spokesperson told me that there were “no updates to COVID guidelines to announce at this time,” and did not respond to questions about how flu precedents had influenced new recommendations.)

    At the very least, Emily Landon, an infectious-disease physician at the University of Chicago, told me, recommendations for all respiratory illnesses should tell freshly de-isolated people to mask for several days when they’re around others indoors; she would support some change to isolation recommendations with this caveat. But if the CDC aligns the policy fully with its flu policy, it might not mention masking at all.

    Read: No one really knows how much COVID is silently spreading … again

    Several experts told me symptom-based isolation might also remove remaining incentives to test for the coronavirus: There’s little point if the guidelines for all respiratory illnesses are essentially the same. To be fair, Americans have already been testing less frequently—in some cases, to avoid COVID-specific requirements to stay away from work or school. And Osterholm and Gordon told me that, at this point in the pandemic, they agree that keeping people at home for five days isn’t sustainable—especially without paid sick leave, and particularly not for health-care workers, who are in short supply during the height of respiratory-virus season.

    But the less people test, the less they’ll be diagnosed—and the less they’ll benefit from antivirals such as Paxlovid, which work best when administered early. Sifri worries that this pattern could yield another parallel to flu, for which many providers hesitate to prescribe Tamiflu, debating its effectiveness. Paxlovid use is already shaky; both antivirals may end up chronically underutilized.

    Flu-ification also threatens to further stigmatize long COVID. Other respiratory infections, including flu, have been documented triggering long-term illness, but potentially at lower rates, and to different degrees than SARS-CoV-2 currently does. Folding this new virus in with the rest could make long COVID seem all the more negligible. What’s more, fewer tests and fewer COVID diagnoses could make it much harder to connect any chronic symptoms to this coronavirus, keeping patients out of long-COVID clinics—or reinforcing a false portrait of the condition’s rarity.

    The U.S. does continue to treat COVID differently from flu in a few ways. Certain COVID products remain more available; some precautions in health-care settings remain stricter. But these differences, too, will likely continue to fade, even as COVID’s burden persists. Tests, vaccines, and treatments are slowly commercializing; as demand for them drops, supply may too. And several experts told me that they wouldn’t be surprised if hospitals, too, soon flu-ify their COVID policies even more, for instance by allowing recently infected employees to return to work once they’re fever-free.

    Early in the pandemic, public-health experts hoped that COVID’s tragedies would prompt a rethinking of all respiratory illnesses. The pandemic showed what mitigations could do: During the first year of the crisis, isolation, masking, distancing, and shutdowns brought flu transmission to a near halt, and may have driven an entire lineage of the virus to extinction—something “that never, in my wildest dreams, did I ever think would be possible,” Landon told me.

    Most of those measures weren’t sustainable. But America’s leaders blew right past a middle ground. The U.S. could have built and maintained systems in which everyone had free access to treatments, tests, and vaccines for a longer list of pathogens; it might have invested in widespread ventilation improvements, or enacted universal sick leave. American homes might have been stocked with tests for a multitude of infectious microbes, and masks to wear when people started to cough. Vaccine requirements in health-care settings and schools might have expanded. Instead, “we seem to be in a more 2019-like place than a future where we’re preventing giving each other colds as much as we could,” Bhattacharyya told me.

    Read: Next winter, what if we test for even more viruses?

    That means a return to a world in which tens of thousands of Americans die each year of flu and RSV, as they did in the 2010s. With COVID here to stay, every winter for the foreseeable future will layer on yet another respiratory virus—and a particularly deadly, disabling, and transmissible one at that. The math is simple: “The risk has overall increased for everyone,” Landon said. That straightforward addition could have inspired us to expand our capacity for preserving health and life. Instead, our tolerance for suffering seems to be the only thing that’s grown.

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    Katherine J. Wu

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  • The Other Group of Viruses That Could Cause the Next Pandemic

    The Other Group of Viruses That Could Cause the Next Pandemic

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    Whether it begins next week, next year, or next decade, another pandemic is on its way. Researchers can’t predict precisely when or how the outbreak might begin. Some 1.6 million viruses are estimated to lurk in the world’s mammalian and avian wildlife, up to half of which could spill into humans; an untold number are attempting exactly that, at this very moment, bumping up against the people hunting, eating, and encroaching on those creatures. (And that’s just viruses: Parasites, fungi, and bacteria represent major infectious dangers too.) The only true certainty in the pandemic forecast is that the next threat will be here sooner than anyone would like.

    But scientists can at least make an educated guess about what might catalyze the next Big One. Three main families of viruses, more than most others, keep scientists up at night: flu viruses, coronaviruses, and paramyxoviruses, in descending order of threat. Together, those groups make up “the trifecta of respiratory death,” Sara Cherry, a virologist at the University of Pennsylvania, told me.

    Flu and coronavirus have a recent track record of trouble: Since 1918, flu viruses have sparked four pandemics, all the while continuing to pester us on a seasonal basis; some scientists worry that another major human outbreak may be brewing now, as multiple H5 flu viruses continue to spread from birds to mammals. The past two decades have also featured three major and deadly coronavirus outbreaks: the original SARS epidemic that began in late 2002; MERS, which spilled into humans—likely from camels—in 2012; and SARS-CoV-2, the pandemic pathogen that’s been plaguing us since the end of 2019. Common-cold-causing coronaviruses, too, remain a fixture of daily living—likely relics of ancient animal-to-human spillovers that we kept transmitting amongst ourselves.

    Read: Bird flu has never done this before

    Paramyxoviruses, meanwhile, have mostly been “simmering in the background,” says Raina Plowright, a disease ecologist at Cornell. Unlike flu viruses and coronaviruses, which have already clearly “proven themselves” as tier-one outbreak risks, paramyxoviruses haven’t yet been caught causing a bona fide pandemic. But they seem poised to do so, and they likely have managed the feat in the past. Like flu viruses and coronaviruses, paramyxoviruses can spread through the air, sometimes very rapidly. That’s certainly been the case with measles, a paramyxovirus that is “literally the most transmissible human virus on the planet,” says Paul Duprex, a virologist at the University of Pittsburgh. And, like flu viruses and coronaviruses, paramyxoviruses are found in a wide range of animals; more are being discovered wherever researchers look. Consider canine distemper virus, which has been found in, yes, canines, but also in raccoons, skunks, ferrets, otters, badgers, tigers, and seals. Paramyxoviruses, like flu viruses and coronaviruses, have also repeatedly shown their potential to hopscotch from those wild creatures into us. Since 1994, Hendra virus has caused multiple highly lethal outbreaks in horses, killing four humans along the way; the closely related Nipah virus has, since 1998, spread repeatedly among both pigs and people, carrying fatality rates that can soar upwards of 50 percent.

    The human versions of those past few outbreaks have petered out. But that may not always be the case—for Nipah, or for another paramyxovirus that’s yet to emerge. It’s entirely possible, Plowright told me, that the world may soon encounter a new paramyxovirus that’s both highly transmissible and ultra deadly—an “absolutely catastrophic” scenario, she said, that could dwarf the death toll of any epidemic in recent memory. (In the past four years, COVID-19, a disease with a fatality rate well below Nipah’s, has killed an estimated 7 million people.)

    All that said, though, paramyxoviruses are a third-place contender for several good reasons. Whereas flu viruses and coronaviruses are speedy shape-shifters—they frequently tweak their own genomes and exchange genetic material with others of their own kind—paramyxoviruses have historically been a bit more reluctant to change. “That takes them down a level,” says Danielle Anderson, a virologist at the Doherty Institute, in Melbourne. For one, these viruses’ sluggishness could make it much tougher for them to acquire transmission-boosting traits or adapt rapidly to spread among new hosts. Nipah virus, for instance, can spread among people via respiratory droplets at close contact. But even though it’s had many chances to do so, “it still hasn’t gotten very good at transmitting among humans,” Patricia Thibault, a biologist at the University of Saskatchewan who studied paramyxoviruses for years, told me.

    The genetic stability of paramyxoviruses can also make them straightforward to vaccinate against. Our flu and coronavirus shots need regular updates—as often as annually—to keep our immune system apace with viral evolution. But we’ve been using essentially the same measles vaccine for more than half a century, Duprex told me, and immunity to the virus seems to last for decades. Strong, durable vaccines are one of the main reasons that several countries have managed to eliminate measles—and why a paramyxovirus called rinderpest, once a major scourge of cattle, is one of the only infectious diseases we’ve ever managed to eradicate. In both cases, it helped that the paramyxovirus at play wasn’t great at infecting a ton of different animals: Measles is almost exclusive to us; rinderpest primarily troubled cows and their close kin. Most flu viruses and SARS-CoV-2, meanwhile, can spread widely across the tree of animal life; “I don’t know how you can eradicate that,” Anderson told me.

    The problem with all of these trends, though, is that they represent only what researchers know of the paramyxoviruses they’ve studied—which is, inevitably, a paltry subset of what exists, says Benhur Lee, a virologist at Mount Sinai’s Icahn School of Medicine. “The devil we don’t know can be just as frightening,” if not more, Lee told me. A pattern-defying paramyxovirus may already be readying itself to jump.

    Researchers are keyed into these looming threats. The World Health Organization highlights Nipah virus and its close cousins as some of its top-priority pathogens; in the U.S., paramyxoviruses recently made a National Institute of Allergy and Infectious Diseases list of pathogens essential to study for pandemic preparedness. Last year, the Bill & Melinda Gates Foundation announced a hefty initiative to fund paramyxovirus antiviral drugs. Several new paramyxovirus vaccines—many of them targeting Nipah viruses and their close relatives—may soon be ready to debut.

    Read: We have a mink problem

    At the same time, though, paramyxoviruses remain neglected—at least relative to the sheer perils they pose, experts told me. “Influenza has been sequenced to death,” Lee said. (That’s now pretty true for SARS-CoV-2 as well.) Paramyxoviruses, meanwhile, aren’t regularly surveilled for; development of their treatments and vaccines also commands less attention, especially outside of Nipah and its kin. And although the family has been plaguing us for countless generations, researchers still don’t know exactly how paramyxoviruses move into new species, or what mutations they would need to become more transmissible among us; they don’t know why some paramyxoviruses spark only minor respiratory infections, whereas others run amok through the body until the host is dead.

    Even the paramyxoviruses that feel somewhat familiar are still surprising us. In recent years, scientists have begun to realize that immunity to the paramyxovirus mumps, once thought to be pretty long-lasting and robust, wanes in the first few decades after vaccination; a version of the virus, once thought to be a problem only for humans and a few other primates, has also been detected in bats. For these and other reasons, rubulaviruses—the paramyxovirus subfamily that includes mumps—are among the potential pandemic agents that most concern Duprex. Emmie de Wit, the chief of the molecular-pathogenesis unit at Rocky Mountain Laboratories, told me that the world could also become more vulnerable to morbilliviruses, the subfamily that includes measles. If measles is ever eradicated, some regulators may push for an end to measles shots. But in the same way that the end of smallpox vaccination left the world vulnerable to mpox, the fall of measles immunity could leave an opening for a close cousin to rise.

    The next pandemic won’t necessarily be a paramyxovirus, or even a flu virus or a coronavirus. But it has an excellent chance of starting as so many other known pandemics have—with a spillover from animals, in parts of the world where we’ve invaded wild habitats. We may not be able to predict which pathogen or creature might be involved in our next big outbreak, but the common denominator will always be us.

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    Katherine J. Wu

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  • This Fall’s COVID Vaccines Are for Everyone

    This Fall’s COVID Vaccines Are for Everyone

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    Paul Offit is not an anti-vaxxer. His résumé alone would tell you that: A pediatrician at Children’s Hospital of Philadelphia, he is the co-inventor of a rotavirus vaccine for infants that has been credited with saving “hundreds of lives every day”; he is the author of roughly a dozen books on immunization that repeatedly debunk anti-vaccine claims. And from the earliest days of COVID-19 vaccines, he’s stressed the importance of getting the shots. At least, up to a certain point.

    Like most of his public-health colleagues, Offit strongly advocates annual COVID shots for those at highest risk. But regularly reimmunizing young and healthy Americans is a waste of resources, he told me, and invites unnecessary exposure to the shots’ rare but nontrivial side effects. If they’ve already received two or three doses of a COVID vaccine, as is the case for most, they can stop—and should be told as much.

    His view cuts directly against the CDC’s new COVID-vaccine guidelines, announced Tuesday following an advisory committee’s 13–1 vote: Every American six months or older should get at least one dose of this autumn’s updated shot. For his less-than-full-throated support for annual vaccination, Offit has become a lightning rod. Peers in medicine and public health have called his opinions “preposterous.” He’s also been made into an unlikely star in anti-vaccine circles. Public figures with prominently shot-skeptical stances have approvingly parroted his quotes. Right-leaning news outlets that have featured vaccine misinformation have called him up for quotes and sound bites—a sign, he told me, that as a public-health expert “you screwed up somehow.”

    Offit stands by his opinion, the core of which is certainly scientifically sound: Some sectors of the population are at much higher risk for COVID than the rest of us. But the crux of the controversy around his view is not about facts alone. At this point in the pandemic, in a country where seasonal vaccine uptake is worryingly low and direly inequitable, where health care is privatized and piecemeal, where anti-vaccine activists will pull at any single loose thread, many experts now argue that policies riddled with ifs, ands, or buts—factually sound though they may be—are not the path toward maximizing uptake. “The nuanced, totally correct way can also be the garbled-message way,” Anthony Fauci, the former director of the National Institute of Allergy and Infectious Diseases, told me.

    For the past two years, the United States’ biggest COVID-vaccine problem hasn’t been that too many young and healthy people are clamoring for shots and crowding out more vulnerable groups. It’s been that no one, really—including those who most need additional doses—is opting for additional injections at all. America’s vaccination pipeline is already so riddled with obstacles that plenty of public-health experts have become deeply hesitant to add more. They’re opting instead for a simple, proactive message—one that is broadly inclusive—in the hope that a concerted push for all will nudge at least some fraction of the public to actually get a shot this year.

    On several key vaccination points, experts do largely agree. The people who bear a disproportionate share of COVID’s risk should receive a disproportionate share of immunization outreach, says Saad Omer, the dean of UT Southwestern’s O’Donnell School of Public Health.

    Choosing which groups to prioritize, however, is tricky. Offit told me he sees four groups as being at highest risk: people who are pregnant, immunocompromised, over the age of 70, or dealing with multiple chronic health conditions. Céline Gounder, an infectious-disease specialist and epidemiologist at NYC Health + Hospitals/Bellevue, who mostly aligns with Offit’s stance, would add other groups based on exposure risk: people living in shelters, jails, or other group settings, for instance, and potentially people who work in health care. (Both Gounder and Offit also emphasize that unvaccinated people, especially infants, should get their shots this year, period.) But there are other vulnerable groups to consider. Risk of severe COVID still stratifies by factors such as socioeconomic status and race, concentrating among groups who are already disproportionately disconnected from health care.

    That’s a potentially lengthy list—and messy messaging has hampered pandemic responses before. As Gretchen Chapman, a vaccine-behavior expert at Carnegie Mellon University, told me last month, a key part of improving uptake is “making it easy, making it convenient, making it the automatic thing.” Fauci agrees. Offit, had he been at the CDC’s helm, would have strongly recommended the vaccine for only his four high-risk groups, and merely allowed everyone else to get it if they wanted to—drawing a stark line between those who should and those who may. Fauci, meanwhile, approves of the CDC’s decision. If it were entirely up to him, “I would recommend it for everyone” for the sheer sake of clarity, he told me.

    Read: Fall’s vaccine routine didn’t have to be this hard

    The benefit-risk ratio for the young and healthy, Fauci told me, is lower than it is for older or sicker people, but “it’s not zero.” Anyone can end up developing a severe case of COVID. That means that shoring up immunity, especially with a shot that targets a recent coronavirus variant, will still bolster protection against the worst outcomes. Secondarily, the doses will lower the likelihood of infection and transmission for at least several weeks. Amid the current rise in cases, that protection could soften short-term symptoms and reduce people’s chances of developing long COVID; it could minimize absences from workplaces and classrooms; it could curb spread within highly immunized communities. For Fauci, those perks are all enough to tip the scales.

    Offit did tell me that he’s frustrated at the way his views have frequently been framed. Some people, for instance, are inaccurately portraying him as actively dissuading people from signing up for shots. “I’m not opposed to offering the vaccine for anyone who wants it,” he told me. In the case of the young and healthy, “I just don’t think they need another dose.” He often uses himself as an example: At 72 years old, Offit didn’t get the bivalent shot last fall, because he says he’s in good health; he also won’t be getting this year’s XBB.1-targeting brew. Three original-recipe shots, plus a bout of COVID, are protection enough for him. He gave similar advice to his two adult children, he told me, and he’d say the same to a healthy thrice-dosed teen: More vaccine is “low risk, low reward.”

    The vax-for-all guideline isn’t incompatible, exactly, with a more targeted approach. Even with a universal recommendation in place, government resources could be funneled toward promoting higher uptake among essential-to-protect groups. But in a country where people, especially adults, are already disinclined to vaccinate, other experts argue that the slight difference between these two tactics could compound into a chasm between public-health outcomes. A strong recommendation for all, followed by targeted implementation, they argue, is more likely to result in higher vaccination rates all around, including in more vulnerable populations. Narrow recommendations, meanwhile, could inadvertently exclude people who really need the shot, while inviting scrutiny over a vaccine’s downsides—cratering uptake in high- and low-risk groups alike. Among Americans, avoiding a strong recommendation for certain populations could be functionally synonymous with explicitly discouraging those people from getting a shot at all.

    Offit pointed out to me that several other countries, including the United Kingdom, have issued recommendations that target COVID vaccines to high-risk groups, as he’d hoped the U.S. would. “What I’ve said is really nothing that other countries haven’t said,” Offit told me. But the situation in the U.S. is arguably different. Our health care is privatized and far more difficult to access and navigate. People who are unable to, or decide not to, access a shot have a weaker, more porous safety net—especially if they lack insurance. (Plus, in the U.K., cost was reportedly a major policy impetus.) A broad recommendation cuts against these forces, especially because it makes it harder for insurance companies to deny coverage.

    Read: The big COVID question for hospitals this fall

    A weaker call for COVID shots would also make that recommendation incongruous with the CDC’s message on flu shots—another universal call for all Americans six months and older to dose up each year. Offit actually does endorse annual shots for the flu: Immunity to flu viruses erodes faster, he argues, and flu vaccines are “safer” than COVID ones.

    It’s true that COVID and the flu aren’t identical—not least because SARS-CoV-2 continues to kill and chronically sicken more people each year. But other experts noted that the cadence of vaccination isn’t just about immunity. Recent studies suggest that, at least for now, the coronavirus is shape-shifting far faster than seasonal flu viruses are—a point in favor of immunizing more regularly, says Vijay Dhanasekaran, a viral-evolution researcher at the University of Hong Kong. The coronavirus is also, for now, simply around for more of the year, which makes infections more likely and frequent—and regular vaccination perhaps more prudent. Besides, scientifically and logistically, “flu is the closest template we have,” Ali Ellebedy, an immunologist at Washington University in St. Louis, told me. Syncing the two shots’ schedules could have its own rewards: The regularity and predictability of flu vaccination, which is typically higher among the elderly, could buoy uptake of COVID shots—especially if manufacturers are able to bundle the immunizations into the same syringe.

    Flu’s touchstone may be especially important this fall. With the newly updated shots arriving late in the season, and COVID deaths still at a relative low, experts are predicting that uptake may be worse than it was last year, when less than 20 percent of people opted in to the bivalent dose. A recommendation from the CDC “is just the beginning” of reversing that trend, Omer, of UT Southwestern, told me. Getting the shots also needs to be straightforward and routine. That could mean actively promoting them in health-care settings, making it easier for providers to check if their patients are up to date, guaranteeing availability for the uninsured, and conducting outreach to the broader community—especially to vulnerable groups.

    Offit hasn’t changed his mind on who most needs these new COVID vaccines. But he is rethinking how he talks about it: “I will stop putting myself in a position where I’m going to be misinterpreted,” he told me. After the past week, he more clearly sees the merits of focusing on who should be signing up rather than who doesn’t need another dose. Better to emphasize the importance of the shot for the people he worries most about and recommend it to them, without reservation, to whatever extent we can.

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    Katherine J. Wu

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  • An Adorable Way to Study How Kids Get Each Other Sick

    An Adorable Way to Study How Kids Get Each Other Sick

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    At the start of 2022, as the Omicron variant of the coronavirus blazed across the United States, Seema Lakdawala was in Pittsburgh, finalizing plans to open a brand-new day care. She had found the perfect facility and signed the stack of paperwork; she had assembled a hodgepodge of plushies, puzzles, and toys. It was the perfect setup, one that “I’ve been dreaming about for years,” Lakdawala, a virologist at Emory University, told me. She couldn’t help but swell with pride, later that spring, when she ushered in her establishments’ first attendees: five young ferrets—including one deliberately infected with the flu.

    Over the next several months, Lakdawala and her colleagues watched several cohorts of ferrets ping-pong flu viruses back and forth as they romped and wrestled and frolicked inside of a shared playpen. The researchers meticulously logged the ferrets’ movements; they took note of the surfaces and other animals that each one touched. Their early findings, now being prepared for publication in a scientific journal, could help researchers figure out how flu viruses most efficiently spread in group settings—not just among ferrets, but among human kids.

    Aerosols, droplets, face-to-face contact, contaminated surfaces—there are plenty of ways for flu viruses to spread. But the nitty-gritty of flu transmission remains “pretty much a black box,” says Aubree Gordon, an epidemiologist at the University of Michigan. Despite decades of research, “we really don’t know the relative importance of each potential route.” Now, though, ferrets in playpens could help researchers to tease out those dynamics—and even, someday, to design flu-blocking measures for bona fide day cares.

    Ferrets have long been the “gold standard for influenza infection and transmission,” says Nicole Rockey, an environmental engineer at Duke University who led the experiments with Lakdawala. The animals’ airway architecture is uncannily similar to ours, and unlike most lab mice, ferrets are vulnerable to catching and passing on flu viruses—even developing the same coughy, sniffly symptoms that so many humans do. But most flu-transmission experiments in ferrets remain limited to artificial circumstances: pairs of animals in tiny cages with dividers between them, where scientists ogle them inhaling each other’s air for days or even weeks. That’s not how animals catch one another’s infections in the wild, and it’s certainly not how human outbreaks unfold. “We don’t interact with each other for 48 hours straight through a perforated wall,” Rockey told me.

    A giant playpen outfitted with toys, air samplers, and video cameras isn’t exactly a natural habitat for a ferret. But the setup does tap into many of the animals’ impish instincts. Domesticated by humans over thousands of years, ferrets “are a very playful species, and they love to be social,” says Alice Dancer, an animal-welfare researcher at the University of London’s Royal Veterinary College. That makes them great models for not just flu transmission, but flu transmission among kids, who are thought to be major drivers of outbreaks. In their day care, the ferrets squabble over toys, clamber up play structures, and canoodle plush snakes; they chase one another around, and nap in big piles when they get tuckered out; they exchange affectionate nuzzles, bonks, and little play bites. Every interaction represents a potential transmission event; so, too, do the surfaces they touch, and the shared pockets of air from which they all breathe.

    Read: The flu may never be the same

    Already, the researchers have collected some results that, Lakdawala told me, are “changing the way I think about transmission a little bit.” In one early experiment, involving an infected animal cavorting with four uninfected ones, they were surprised to find that the ferret with the least direct contact with the flu “donor” was the only “recipient” in the room who got sick. It seemed counterintuitive, Lakdawala told me, until video footage revealed that the newly sickened recipient had been copying everything that the donor did—chewing the toys it chewed, rolling the balls it rolled, swiping the surfaces it swiped. It was as if the first ferret was leaving a trail of infectious breadcrumbs for the second one to snarf. If that finding holds up in other experiments, which the researchers are analyzing now, it could suggest that contaminated surfaces, or fomites, are playing a larger-than-expected role in passing the virus around, Rockey told me.

    Another of the team’s early findings points to a similar notion. When the researchers cranked up the ventilation in their ferret day cares, hoping to clear virus particles out of the air, they found that the same proportion of uninfected ferrets ended up catching the virus. This was disappointing, but not a total shock given how paws-on ferrets—and kids, for that matter—are with one another and their surroundings. It didn’t matter if the air in the room was being exchanged more than once every three minutes. Whenever the ferrets had their run of the room, the researchers would find virus particles smeared on the toys, the snack station, and the playpen walls.

    Ventilation wasn’t totally useless: More air exchanges, the team found, did seem to reduce the concentration of flu genetic material in the air, and the ferrets who got infected under those conditions were slower to start shedding the virus—a hint, Lakdawala thinks, that they might have taken in a lower infectious dose. Among humans, that might translate into less severe cases of disease, Gordon told me, though that would need to be confirmed.

    Whatever upshots Rockey and Lakdawala’s ferret findings might have for human day cares won’t necessarily apply to other venues. In offices, hospitals, and even schools for older kids, people are generally a lot less tactile with one another, and a lot better versed on hygiene. Plus, adult bodies just aren’t built like kids’, says Cécile Viboud, an epidemiologist at the Fogarty International Center at the National Institutes of Health. Their airways are bigger, stronger, and more developed—and some experiments suggest that, for at least some respiratory viruses, the older and larger people are, the more infectious aerosols they might expel. For adults, ventilation may matter all the more.

    Lakdawala and her colleagues are still mulling some other interventions that might work better for ferrets, and eventually kids: humidifiers, air purifiers, targeted cleaning, maybe even keeping individuals from crowding too closely into a portion of the playpen. (They don’t plan to experiment with handwashing or masking; imagine the difficulty of strapping an N95 to a ferret’s face.) Lakdawala is also mulling whether surfaces made of copper—which her team has shown can render flu viruses inactive within minutes—could play a protective role.

    But everything that happens in the ferrets’ playpens will still come with caveats. “It’s still an animal model, at the end of the day,” Viboud told me. For all the similarities between the ferret airway and ours, the way their little noses and snouts are shaped could affect how they cough and sneeze. And the researchers haven’t yet studied spread among ferrets with preexisting immunity to flu, which some day-care attendees will have. Ferrets are also more inclined to bite, wrestle, and defecate wherever they please than the average (potty-trained) kid.

    Still, for the most part, Lakdawala delights in how childlike the ferrets can be. They’re affectionate and mischievous; they seem to bubble with energy and glee. After discovering that the air-sampling robot stationed in the center of their day care was mobile, several of the ferrets began to take it for rides. In watching and sharing the footage at conferences, Lakdawala has received one piece of feedback, over and over again: Oh yeah, parents tell her. My kids do that too.

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    Katherine J. Wu

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  • A Major Breed of Flu Has Gone Missing

    A Major Breed of Flu Has Gone Missing

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    In March 2020, Yamagata’s trail went cold.

    The pathogen, one of the four main groups of flu viruses targeted by seasonal vaccines, had spent the first part of the year flitting across the Northern Hemisphere, as it typically did. As the seasons turned, scientists were preparing, as they typically did, for the virus to make its annual trek across the equator and seed new outbreaks in the globe’s southern half.

    That migration never came to pass. As the new coronavirus spread, pandemic-mitigation measures started to squash flu-transmission rates to record lows. The drop-off was so sharp that several flu lineages may have gone extinct, among them Yamagata, which hasn’t been definitively detected in more than three years despite virologists’ best efforts to root it out.

    Read: The pandemic broke the flu

    Yamagata’s disappearance could still be temporary. “Right now, we’re all just kind of holding our breath,” says Adam Lauring, a virologist at the University of Michigan Medical School. The virus might be biding its time in an isolated population, escaping the notice of tests. But the search has stretched on so fruitlessly that some experts are ready to declare it officially done. “It’s been missing for this long,” says Vijaykrishna Dhanasekaran, a virologist at Hong Kong University. “At this point, I would really think it’s gone.”

    If Yamagata remains AWOL indefinitely, its absence would have at least one relatively straightforward consequence: Researchers might no longer need to account for the lineage in annual vaccines. But its vanishing act could have a more head-spinning implication. Flu viruses, which have been plaguing human populations for centuries, are some of the most well-known and well-studied threats to our health. They have prompted the creation of annual shots, potent antivirals, and internationally funded surveillance programs. And yet, scientists still have some basic questions about why they behave as they do—especially about Yamagata and its closest kin.

    Yamagata, in many ways, has long been an underdog among underdogs. The lineage is one of two in a group called influenza B viruses, and it’s slower to evolve and transmit, and is thus sometimes considered less troublesome, than its close cousin Victoria. As a pair, the B’s are also commonly regarded as the wimpier versions of flu.

    To be fair, the competition is stiff. Flu B’s are constantly being compared with influenza A viruses—the group that contains every flu subtype that has caused a pandemic in our recent past, including the extraordinarily deadly outbreak of 1918. Seasonal flu epidemics, too, tend to be heavily dominated by flu A’s, especially H3N2 and H1N1, two notably tough-to-target strains that feature prominently in each year’s vaccine. Even H5N1, the flavor of avian influenza that’s been devastating North America’s wildlife, is a member of the pathogen’s A team.

    Read: Eagles Are Falling, Bears Are Going Blind

    B viruses, meanwhile, don’t have a particularly daunting résumé. “To our knowledge, there has never been a B pandemic,” says John Paget, an infectious-disease epidemiologist at the Netherlands Institute for Health Services Research. Only once every seven seasons or so does a B virus dominate. And although A and B viruses sometimes tag-team the winter, causing twin outbreaks spaced out by a few weeks, these seasons often open with a major flu A banger and then close out with a more muted B coda.

    The reasons underlying these differences are still pretty murky, though scientists do have some hints. Whereas flu A viruses are known as especially speedy shape-shifters, constantly spawning genetic offshoots that vie to outcompete one another, flu B’s evolve at oddly plodding rates. Their sluggish approach makes it easier for our immune system to recognize the viruses when they reappear, resulting in longer-lasting protection, more effective vaccines, and fewer reinfections than are typical with the A’s. Those molecular differences also seem to drive differences in how and when the viruses spread. The A’s tend to trouble people repeatedly from birth to death, and are great at globe-trotting. But B’s, perhaps because immunity against them is easier to come by, more often concentrate among kids, many of whom have never encountered the viruses before—and who are usually more resilient to respiratory viruses and travel less than adults, keeping outbreaks mostly regional. That might also help explain why B epidemics so frequently lag behind A’s: Slower pathogen evolution facing off with more durable host immunity add up to less rapid B spread, while their A colleagues rush ahead. Our bodies also seem to mount rather fiery defenses against A viruses, steeling them against other infections in the weeks that follow and deepening the disadvantage against any B’s trailing behind. All of that means flu B has a hard time catching humans off guard.

    The virus’s host preferences, too, make flu A viruses more dangerous. Those lineages are great at hopscotching among a whole menagerie of species—most infamously, pigs and wild, water-loving birds—sometimes undergoing rapid bursts of evolution as they go. But flu B’s seem to almost exclusively infect humans, igniting only the rare and fast-resolving outbreak in a limited number of other species—a few seals here, a handful of pigs there. Spillovers from wild creatures into humans are the roots of global outbreaks. And so, with its zoonotic bent, “influenza A will always be the main focus” of concern, says Carolien van de Sandt, a virologist at the Peter Doherty Institute for Infection and Immunity, in Melbourne. Even among some scientists, Yamagata and Victoria register as little more than literal B-list blips.

    Plenty of other experts, though, think flu B’s relative obscurity is misguided—perhaps even a bit dangerous. Flu B’s account for roughly a quarter of annual flu cases, many of which lead to hospitalization and death; they seem hardier than their A cousins against certain antiviral drugs. And scientists simply know a lot less about flu B’s: how, precisely, they interact with the immune system; what factors influence their sluggish evolutionary rate; the nuances of their person-to-person spread; their oddball animal-host range. And that lack of intel on what has for decades been a formidable infectious foe creates a risk all on its own.

    Flu lineages have dipped into relative obscurity before only to come roaring back. After the end of the H2N2 pandemic of the late 1950s, H1N1 appeared to flame out—only to reemerge nearly two decades later to greet a population full of young people whose immune systems hadn’t glimpsed it before. And as recently as the 1990s, the B lineage Victoria underwent a years-long ebb in most parts of the world, before ricocheting back to prominence in the early 2000s.

    As far as researchers can tell, Victoria is alive and well; during the globe’s most recent winter seasons, the lineage appears to have ignited late-arriving outbreaks in several countries, including in South Africa, Malaysia, and various parts of Europe. But based on the viral sequences that researchers have isolated from people sick with flu, Yamagata is still nowhere to be found, says Saverio Caini, a virologist at the cancer research center ISPRO, in Italy.

    The lineage was already teetering on a precipice before the pandemic began, van de Sandt told me. Yamagata and Victoria, which splintered apart in the early 1980s, are still closely related enough that they often compete for the same hosts. And just prior to 2020, Victoria, the more diverse and fleet-footed of the two B lineages, had been reliably edging out its cousin, pushing Yamagata’s prevalence down, down, down. That trend, coupled with several years of use of a well-matched Yamagata strain in the seasonal flu vaccine, meant that Yamagata “had already decreased in incidence and circulation,” van de Sandt said. With the odds so steeply stacked, the addition of pandemic mitigations may have been the final factor that snuffed the lineage out.

    Recently, a few countries—including China, Pakistan, and Belize—have tentatively reported possible Yamagata infections. But there’s been no conclusive genetic proof, several experts told me. Several parts of the world, including the United States, regularly use flu vaccines containing active flu viruses that can trip the same viral tests that the wild, disease-causing pathogens do. “So the reports could be contaminations,” van de Sandt said. Scientists would need to scour the virus’s genetic sequences to distinguish infection from injection; those data, however, haven’t emerged.

    Should the Yamagata dry spell continue, researchers may want to start considering snipping the lineage out of vaccines altogether, perhaps as early as the middle or end of this year. Doing so would punt the world back to the early 2010s, when flu shots were trivalent—designed to protect people against two A viruses, H3N2 and H1N1, plus either Victoria or Yamagata, depending on which lineage researchers forecasted would surge more. (They were often wrong.) Or maybe the space once used for Yamagata could feasibly be filled with another flavor of H3N2, the fastest mutator of the bunch.

    But purging Yamagata from the vaccine would be a gamble. If Yamagata is not gone for good, van de Sandt worries that booting it from the vaccine would leave the world vulnerable to a massive and deadly outbreak. Even Dhanasekaran, who is among the researchers who are fairly confident that we’ve seen the last of Yamagata, told me he doesn’t want to rule out the possibility that the virus is cloistering in an immunocompromised person with a chronic infection, and it’s unclear if it could reemerge from such a hiding place. The only thing scientists can do for now is be patient, says Jayna Raghwani, a computational biologist at the University of Oxford. “If we don’t see it in successive seasons for another two to three years, that will be more convincing,” she told me.

    If Yamagata’s death knell has actually rung, though, it will have reverberating effects. There’s no telling, for instance, how other flu lineages might be affected by their colleague’s supposed retirement. Perhaps Victoria, which can swap genetic material with Yamagata, will evolve more slowly without its partner. At the same time, Victoria may have an easier time infecting people now that it no longer needs to compete as often for hosts.

    If Yamagata has gone to pasture, “there won’t be a ceremony declaring the world Yamagata free,” Lauring told me. And it’s easy, he points out, to forget things we don’t see. But even if Yamagata seems gone for now, the effects of its demise will be significant enough that it can’t be forgotten—not just yet.

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    Katherine J. Wu

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  • COVID Vaccines Are Turning Into Flu Shots

    COVID Vaccines Are Turning Into Flu Shots

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    For all the legwork that public-health experts have done over the past few years to quash comparisons between COVID-19 and the flu, there sure seems to be a lot of effort nowadays to equate the two. In an advisory meeting convened earlier today, the FDA signaled its intention to start doling out COVID vaccines just like flu shots: once a year in autumn, for just about everyone, ad infinitum. Whatever the brand, primary-series shots and boosters (which might no longer be called “boosters”) will guard against the same variants, making them interchangeable. Doses will no longer be counted numerically. “This will be a fundamental transition,” says Jason Schwartz, a vaccine policy expert at Yale—the biggest change to the COVID-vaccination regimen since it debuted.

    Hints of the annual approach have been dropping, not so subtly, for years. Even in the spring of 2021, Pfizer’s CEO was floating the idea of yearly shots; Peter Marks, the director of the FDA’s Center for Biologics Evaluation and Research, teased it throughout 2022. This past September, Joe Biden officially endorsed it as “a new phase in our COVID-19 response,” and Ashish Jha, the White House’s COVID czar, memorably highlighted the convenience of combining a flu shot and a COVID shot into a single appointment: “I really believe this is why God gave us two arms.”

    Still, in today’s meeting, FDA officials were pushier than ever in their advocacy for the flu-ification of COVID vaccines. “We think that simplification of the vaccination regimen would contribute to easier vaccine deployment, better communication, and improved vaccine coverage,” Jerry Weir, the FDA’s director of the division of viral products, said at the meeting. The timing is important: After renewing the U.S.’s pandemic-emergency declaration earlier this month, the Biden administration seems set to allow its expiration this coming April. That makes the present moment awfully convenient for repackaging a chaotic, crisis-caliber vaccination paradigm as a scheduled, seasonal, normal-seeming one. A once-a-year strategy, modeled on a routine recommendation, suggests that “we’re no longer in emergency mode,” says Maria Sundaram, a vaccine researcher at the Marshfield Clinic Research Institute. Or at least, that’s the message that the public is likely to hear.

    But federal regulators may be trying to fit a COVID-shaped peg into a flu-shaped hole. The experts I spoke with largely agreed: Eventually, someday, annual autumn shots for COVID “will probably be sufficient,” says Gregory Poland, a vaccinologist at Mayo Clinic. “Are we ready for that yet? I’m not sure that’s the case at all.”

    Even in the short term, COVID-vaccination tactics need a revamp. “It’s clear above all that the current approach isn’t working,” Schwartz told me. Despite abundant supply, demand for COVID boosters in the U.S. has been abysmal—and interest seems to be declining with each additional dose. Last fall’s bivalent shot has reached the arms of only 15 percent of Americans; even among adults over 65—a majority of whom sign up for flu shots each fall—the vaccination rate hasn’t yet reached 40 percent.

    For most of the time that COVID shots have been around, figuring out when to get them has been a hassle, with different guidelines and requirements that depend on age, sex, risk factors, vaccination history, and more. Pharmacies have had to stock an absurd number of vials and syringes to accommodate the various combinations of brands and dose sizes; record-keeping on flimsy paper cards has been a total joke. “I do this for a living, and I can barely keep track,” Schwartz said. Recommendations on the proper timing and number of doses have also changed so many times that many Americans have simply checked out. After the bivalent recipe debuted, polls found that an alarming proportion of people didn’t even know the shot was available to them.

    Streamlining COVID-vaccine recommendations will remove a lot of that headache, Sundaram told me. Most people would need to keep only one mantra in mind—one dose, each fall—and could top off their flu and COVID immunity at the same time. Burdens on pharmacies and clinics would be lower, and communication would be far easier—a change that could make an especially big difference for those with children, among whom COVID-vaccine uptake has been the lowest. “It’ll be more scheduled, more systematic,” says Charlotte Hobbs, a pediatric infectious-disease specialist at the University of Mississippi Medical Center. COVID shots could simply be offered at annual well-child visits, she told me. “It’s something we already know works well.”

    The advantages of a flu-ified COVID shot aren’t just about convenience. If we have to shoehorn COVID vaccines into an existing paradigm, Sundaram told me, influenza’s is the best candidate. SARS-CoV-2, like the flu, is excellent at altering itself to dodge our defenses; it spreads readily in winter; and our immunity to infection tends to fade rather quickly. All of that adds up to a need for regularly updated shots. Such a system has been in place for decades for the flu: At the end of each winter, a panel of experts convenes to select the strains that should be targeted by the next formulation; manufacturers spend the next several months whipping up big batches in time for an autumn-ish rollout. The pipeline depends on a global surveillance system for flu viruses, as well as regular surveys of antibody levels in the community to suss out which strains people are still protected against. The premise has been so well vetted by now that researchers can skip the chore of running large-scale clinical trials to determine the efficacy and safety of each new, updated recipe.

    But a seasonal strategy works best for a seasonal virus—and SARS-CoV-2 just isn’t there yet, says Hana El Sahly, an infectious-disease physician at Baylor College of Medicine. Though flu viruses tend to hop between the globe’s hemispheres, alternately troubling the north and the south during their respective cold months, this new coronavirus has yet to confine its spread to one part of the calendar. (Marks, of the FDA, tried to address this concern at today’s meeting, asserting that “we’re starting to see some seasonality” and that fall was indeed the very sensible for an annual rollout.) SARS-CoV-2 has also been spitting out concerning variants and subvariants at a faster rate than the flu (and flu shots already have a hard time keeping up with evolution). The FDA’s new proposal suggests picking SARS-CoV-2 variants in June to have a vaccine ready by September, a shorter timeline than is used for flu. That still might not be fast enough: “By the time we detect a variant, it will have ripped through the global population and, in a few more weeks, died down,” El Sahly told me. The world got a preview of this problem with last year’s bivalent shot, which overlapped with the dominance of its target subvariants for only a couple of months. A flu model for COVID would make more sense “if we had stable, predictable dynamics,” says Avnika Amin, a vaccine epidemiologist at Emory University. “I don’t think we’re at that point.”

    Murkiness around vaccine effectiveness makes this transition complicated too. Experts told me that it’s gotten much more difficult to tell how well our COVID vaccines are working, and for how long, fueling debates over how often they should be given and how often their composition should change. Many people have now been infected by the virus multiple times, which can muddy calculations of vaccine effectiveness; better treatments also alter risk profiles. And many researchers told me they’re concerned that the data shortcuts we use for flu—measures of antibodies as a proxy for immune protection—just won’t fly for COVID shots. “We need better clinical data,” El Sahly told me. In their absence, the hasty adoption of a flu framework could lead to our updating and distributing COVID shots too often, or not often enough.

    A flu-ish approach also wouldn’t fix all of the COVID vaccines’ problems. Today’s discussion suggested that, even if a new COVID-shot strategy change goes through, officials will still need to recommend several different dose sizes for several different age groups—a more complex regimen than flu’s—and may advise additional injections for those at highest risk. At the same time, COVID shots would continue to be more of a target for misinformation campaigns than many other vaccines and, at least in the case of mRNA-based injections, more likely to cause annoying side effects. These issues and others have driven down interest—and simply pivoting to the flu paradigm “is not going to solve the uptake problem,” says Angela Shen, a vaccine-policy expert at Children’s Hospital of Philadelphia.

    Perhaps the greatest risk of making COVID vaccines more like flu shots is that it could lead to more complacency. In making the influenza paradigm a model, we also threaten to make it a ceiling. Although flu shots are an essential, lifesaving public-health tool, they are by no means the best-performing vaccines in our roster. Their timeline is slow and inefficient; as a result, the formulations don’t always match circulating strains. Already, with COVID, the world has struggled to chase variants with vaccines that simply cannot keep up. If we move too quickly to the fine-but-flawed framework for flu, experts told me, it could disincentivize research into more durable, more variant-proof, less side-effect-causing COVID shots. Uptake of flu vaccines has never been stellar, either: Just half of Americans sign up for the shots each year—and despite years of valiant efforts, “we still haven’t figured out how to consistently improve that,” Amin told me.

    Whenever the COVID-emergency declaration expires, vaccination will almost certainly have to change. Access to shots may be imperiled for tens of millions of uninsured Americans; local public-health departments may end up with even fewer resources for vaccine outreach. A flu model might offer some improvements over the status quo. But if the downsides outweigh the pluses, Poland told me, that could add to the erosion of public trust. Either way, it might warp attitudes toward this coronavirus in ways that can’t be reversed. At multiple points during today’s meeting, FDA officials emphasized that COVID is not the flu. They’re right: COVID is not the flu and never will be. But vaccines can sometimes become a lens through which we view the dangers they fight. By equating our frontline responses to these viruses, the U.S. risks sending the wrong message—that they carry equal threat.

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    Katherine J. Wu

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  • The Strongest Signal That Americans Should Worry About Flu This Winter

    The Strongest Signal That Americans Should Worry About Flu This Winter

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    Sometime in the spring of 2020, after centuries, perhaps millennia, of tumultuous coexistence with humans, influenza abruptly went dark. Around the globe, documented cases of the viral infection completely cratered as the world tried to counteract SARS-CoV-2. This time last year, American experts began to fret that the flu’s unprecedented sabbatical was too bizarre to last: Perhaps the group of viruses that cause the disease would be poised for an epic comeback, slamming us with “a little more punch” than usual, Richard Webby, an influenza expert at St. Jude Children’s Research Hospital, in Tennessee, told me at the time.

    But those fears did not not come to pass. Flu’s winter 2021 season in the Southern Hemisphere was once again eerily silent; in the north, cases sneaked up in December—only to peter out before a lackluster reprise in the spring.

    Now, as the weather once again chills in this hemisphere and the winter holidays loom, experts are nervously looking ahead. After skipping two seasons in the Southern Hemisphere, flu spent 2022 hopping across the planet’s lower half with more fervor than it’s had since the COVID crisis began. And of the three years of the pandemic that have played out so far, this one is previewing the strongest signs yet of a rough flu season ahead.

    It’s still very possible that the flu will fizzle into mildness for the third year in a row, making experts’ gloomier suspicions welcomingly wrong. Then again, this year is, virologically, nothing like the last. Australia recently wrapped an unusually early and “very significant” season with flu viruses, says Kanta Subbarao, the director of the WHO Collaborating Centre for Reference and Research on Influenza at the Doherty Institute. By sheer confirmed case counts, this season was one of the country’s worst in several years. In South Africa, “it’s been a very typical flu season” by pre-pandemic standards, which is still enough to be of note, according to Cheryl Cohen, a co-head of the country’s Centre for Respiratory Disease and Meningitis at the National Institute for Communicable Diseases. After a long, long hiatus, Subbarao told me, flu in the Southern Hemisphere “is certainly back.”

    Read: The pandemic broke the flu

    That does not bode terribly well for those of us up north. The same viruses that seed outbreaks in the south tend to be the ones that sprout epidemics here as the seasons do their annual flip. “I take the south as an indicator,” says Seema Lakdawala, a flu-transmission expert at Emory University. And should flu return here, too, with a vengeance, it will collide with a population that hasn’t seen its likes in years, and is already trying to marshal responses to several dangerous pathogens at once.

    The worst-case scenario won’t necessarily pan out. What goes on below the equator is never a perfect predictor for what will occur above it: Even during peacetime, “we’re pretty bad in terms of predicting what a flu season is going to look like,” Webby, of St. Jude, told me. COVID, and the world’s responses to it, have put experts’ few forecasting tools further on the fritz. But the south’s experiences can still be telling. In South Africa and Australia, for instance, many COVID-mitigation measures, such as universal masking recommendations and post-travel quarantines, lifted as winter arrived, allowing a glut of respiratory viruses to percolate through the population. The flu flood also began after two essentially flu-less years—which is a good thing at face value, but also represents many months of missed opportunities to refresh people’s anti-flu defenses, leaving them more vulnerable at the season’s start.

    Some of the same factors are working against those of us north of the equator, perhaps to an even greater degree. Here, too, the population is starting at a lower defensive baseline against flu—especially young children, many of whom have never tussled with the viruses. It’s “very, very likely” that kids may end up disproportionately hit, Webby said, as they appear to have been in Australia—though Subbarao notes that this trend may have been driven by more cautious behaviors among older populations, skewing illness younger.

    Interest in inoculations has also dropped during the pandemic: After more than a year of calls for booster after booster, “people have a lot of fatigue,” says Helen Chu, a physician and flu expert at the University of Washington, and that exhaustion may be driving already low interest in flu shots even further down. (During good years, flu-shot uptake in the U.S. peaks around 50 percent.) And the few protections against viruses that were still in place last winter have now almost entirely vanished. In particular, schools—a fixture of flu transmission—have loosened up enormously since last year. There’s also just “much more flu around,” all over the global map, Webby said. With international travel back in full swing, the viruses will get that many more chances to hopscotch across borders and ignite an outbreak. And should such an epidemic emerge, with its health infrastructure already under strain from simultaneous outbreaks of COVID, monkeypox, and polio, America may not handle another addition well. “Overall,” Chu told me, “we are not well prepared.”

    Read: The most important vaccine I’ll get this fall

    At the same time, though, countries around the world have taken such different approaches to COVID mitigation that the pandemic may have further uncoupled their flu-season fate. Australia’s experience with the flu, for instance, started, peaked, and ended early this year; the new arrival of more relaxed travel policies likely played a role in the outbreak’s beginning, before a mid-year BA.5 surge potentially hastened the sudden drop. It’s also very unclear whether the U.S. may be better or worse off because its last flu season was wimpy, weirdly shaped, and unusually late. South Africa saw an atypical summer bump in flu activity as well; those infections may have left behind a fresh dusting of immunity and blunted the severity of the following season, Cohen told me. But it’s always hard to tell. “I was quite strong in saying that I really believed that South Africa was going to have a severe season,” she said. “And it seems that I was wrong.” The long summer tail of the Northern Hemisphere’s most recent flu season could also exacerbate the intensity of the coming winter season, says John McCauley, the director of the Worldwide Influenza Centre at the Francis Crick Institute, in London. Kept going in their off-season, the viruses may have an easier vantage point from which to reemerge this winter.

    COVID’s crush has shifted flu dynamics on the whole as well. The pandemic “squeezed out” a lot of diversity from the influenza-virus population, Webby told me; some lineages may have even entirely blipped out. But others could also still be stewing and mutating, potentially in animals or unmonitored pockets of the world. That these strains—which harbor especially large pandemic potential—could emerge into the general population is “my bigger concern,” Lakdawala, of Emory, told me. And although the particular strains of flu that are circulating most avidly seem reasonably well matched to this year’s vaccines, the dominant strains that attack the north could yet shift, says Florian Krammer, a flu virologist at Mount Sinai’s Icahn School of Medicine. Viruses also tend to wobble and hop when they return from long vacations; it may take a season or two before the flu finds its usual rhythm.

    Another epic SARS-CoV-2 variant could also quash a would-be influenza peak. Flu cases rose at the end of 2021, and the dreaded “twindemic” loomed. But then, Omicron hit—and flu “basically disappeared for one and a half months,” Krammer told me, only tiptoeing back onto the scene after COVID cases dropped. Some experts suspect that the immune system may have played a role in this tag-team act: Although co-infections or sequential infections of SARS-CoV-2 and flu viruses are possible, the aggressive spread of a new coronavirus variant may have set people’s defenses on high alert, making it that much harder for another pathogen to gain a foothold.

    Read: Don’t worry, it’s not the flu

    No matter the odds we enter flu season with, human behavior can still alter winter’s course. One of the main reasons that flu viruses have been so absent the past few years is because mitigation measures have kept them at bay. “People understand transmission more than they ever did before,” Lakdawala told me. Subbarao thinks COVID wisdom is what helped keep Australian flu deaths down, despite the gargantuan swell in cases: Older people took note of the actions that thwarted the coronavirus and applied those same lessons to flu. Perhaps populations across the Northern Hemisphere will act in similar ways. “I would hope that we’ve actually learned how to deal with infectious disease more seriously,” McCauley told me.

    But Webby isn’t sure that he’s optimistic. “People have had enough hearing about viruses in general,” he told me. Flu, unfortunately, does not feel similarly about us.

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    Katherine J. Wu

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