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Tag: people’s bodies

  • What Should Go Into This Year’s COVID Vaccine?

    What Should Go Into This Year’s COVID Vaccine?

    This fall, millions of Americans might be lining up for yet another kind of COVID vaccine:  their first-ever dose that lacks the strain that ignited the pandemic more than three and a half years ago. Unlike the current, bivalent vaccine, which guards against two variants at once, the next one could, like the first version of the shot, have only one main ingredient—the spike protein of the XBB.1 lineage of the Omicron variant, the globe’s current dominant clade.

    That plan isn’t yet set. The FDA still has to convene a panel of experts, then is expected to make a final call on autumn’s recipe next month. But several experts told me they hope the agency follows the recent recommendation of a World Health Organization advisory group and focuses the next vaccine only on the strains now circulating.

    The switch in strategy—from two variants to one, from original SARS-CoV-2 plus Omicron to XBB.1 alone—would be momentous but wise, experts told me, reflecting the world’s updated understanding of the virus’s evolution and the immune system’s quirks. “It just makes a lot of sense,” said Melanie Ott, the director of the Gladstone Institute of Virology, in San Francisco. XBB.1 is the main coronavirus group circulating today; neither the original variant nor BA.5, the two coronavirus flavors in the bivalent shot, is meaningfully around anymore. And an XBB.1-focused vaccine may give the global population a particularly good shot at broadening immunity.

    At the same time, COVID vaccines are still in a sort of beta-testing stage. In the past three-plus years, the virus has spawned countless iterations, many of which have been extremely good at outsmarting us; we humans, meanwhile, are only on our third-ish attempt at designing a vaccine that can keep pace with the pathogen’s evolutionary sprints. And we’re very much still learning about the coronavirus’s capacity for flexibility and change, says Rafi Ahmed, an immunologist at Emory University. By now, it’s long been clear that vaccines are essential for preventing severe disease and death, and that some cadence of boosting is probably necessary to keep the shots’ effectiveness high. But when the virus alters its evolutionary tactics, our vaccination strategy must follow—and experts are still puzzling out how to account for those changes as they select the shots for each year.

    In the spring and summer of 2022, the last time the U.S. was mulling on a new vaccine formula, Omicron was still relatively new, and the coronavirus’s evolution seemed very much in flux. The pathogen had spent more than two years erratically slingshotting out Greek-letter variants without an obvious succession plan. Instead of accumulating genetic changes within a single lineage—a more iterative form of evolution, roughly akin to what flu strains do—the coronavirus produced a bunch of distantly related variants that jockeyed for control. Delta was not a direct descendant of Alpha; Omicron was not a Delta offshoot; no one could say with any certainty what would arise next, or when. “We didn’t understand the trajectory,” says Kanta Subbarao, the head of the WHO advisory group convened to make recommendations on COVID vaccines.

    And so the experts played it safe. Including an Omicron variant in the shot felt essential, because of how much the virus had changed. But going all in on Omicron seemed too risky—some experts worried that “the virus would flip back,” Subbarao told me, to a variant more similar to Alpha or Delta or something else. As a compromise, several countries, including the United States, went with a combination: half original, half Omicron, in an attempt to reinvigorate OG immunity while laying down new defenses against the circulating strains du jour.

    And those shots did bolster preexisting immunity, as boosters should. But they didn’t rouse a fresh set of responses against Omicron to the degree that some experts had hoped they would, Ott told me. Already trained on the ancestral version of the virus, people’s bodies seemed to have gotten a bit myopic—repeatedly reawakening defenses against past variants, at the expense of new ones that might have more potently attacked Omicron. The outcome was never thought to be damaging, Subbarao told me: The bivalent, for instance, still broadened people’s immune responses against SARS-CoV-2 compared with, say, another dose of the original-recipe shot, and was effective at tamping down hospitalization rates. But Ahmed told me that, in retrospect, he thinks an Omicron-only boost might have further revved that already powerful effect.

    Going full bore on XBB.1 now could keep the world from falling into that same trap twice. People who get an updated shot with that strain alone would receive only the new, unfamiliar ingredient, allowing the immune system to focus on the fresh material and potentially break out of an ancestral-strain rut. XBB.1’s spike protein also would not be diluted with one from an older variant—a concern Ahmed has with the current bivalent shot. When researchers added Omicron to their vaccine recipes, they didn’t double the total amount of spike protein; they subbed out half of what was there before. That left vaccine recipients with just half the Omicron-focused mRNA they might have gotten had the shot been monovalent, and probably a more lackluster antibody response.

    Recent work from the lab of Vineet Menachery, a virologist at the University of Texas Medical Branch, suggests another reason the Omicron half of the shot didn’t pack enough of an immunizing punch. Subvariants from this lineage, including BA.5 and XBB.1, carry at least one mutation that makes their spike protein unstable—to the point where it seems less likely than other versions of the spike protein to stick around for long enough to sufficiently school immune cells. In a bivalent vaccine, in particular, the immune response could end up biased toward non-Omicron ingredients, exacerbating the tendencies of already immunized people to focus their energy on the ancestral strain. For the same reason, a monovalent XBB.1, too, might not deliver the anticipated immunizing dose, Menachery told me. But if people take it (still a big if), and hospitalizations remain low among those up-to-date on their shots, a once-a-year total-strain switch-out might be the choice for next year’s vaccine too.

    Dropping the ancestral strain from the vaccine isn’t without risk. The virus could still produce a variant totally different from XBB.1, though that does, at this point, seem unlikely. For a year and a half now, Omicron has endured, and it now has the longest tenure of a single Greek-letter variant since the pandemic’s start. Even the subvariants within the Omicron family seem to be sprouting off each other more predictably; after a long stint of inconsistency, the virus’s shape-shifting now seems “less jumpy,” says Leo Poon, a virologist at the University of Hong Kong. It may be a sign that humans and the virus have reached a détente now that the population is blanketed in a relatively stable layer of immunity. Plus, even if a stray Alpha or Delta descendant were to rise up, the world wouldn’t be caught entirely off guard: So many people have banked protection against those and other past variants that they’d probably still be well buffered against COVID’s worst acute outcomes. (That reassurance doesn’t hold, though, for people who still need primary-series shots, including the kids being born into the world every day. An XBB.1 boost might be a great option for people with preexisting immunity. But a bivalent that can offer more breadth might still be the more risk-averse choice for someone whose immunological slate is blank.)

    More vaccination-strategy shifts will undoubtedly come. SARS-CoV-2 is still new to us; so are our shots. But the virus’s evolution, as of late, has been getting a shade more flu-like, and its transmission patterns a touch more seasonal. Regulators in the U.S. have already announced that COVID vaccines will probably be offered each year in the fall—as annual flu shots are. The viruses aren’t at all the same. But as the years progress, the comparison between COVID and flu shots could get more apt still—if, say, the coronavirus also starts to produce multiple, genetically distinct strains that simultaneously circulate. In that case, vaccinating against multiple versions of the virus at once might be the most effective defense.

    Flu shots could be a useful template in another way: Although those shots have followed roughly the same guidelines for many years, with experts meeting twice a year to decide whether and how to update each autumn’s vaccine ingredients, they, too, have needed some flexibility. Until 2012, the vaccines were trivalent, containing ingredients that would immunize people against three separate strains at once; now many, including all of the U.S.’s, are quadrivalent—and soon, based on new evidence, researchers may push for those to return to a three-strain recipe. At the same time, flu and COVID vaccines share a major drawback. Our shots’ ingredients are still selected months ahead of when the injections actually reach us—leaving immune systems lagging behind a virus that has, in the interim, sprinted ahead. Until the world has something more universal, our vaccination strategies will have to be reactive, scrambling to play catch-up with these pathogens’ evolutionary whims.

    Katherine J. Wu

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  • No One Really Knows How Much COVID Is Silently Spreading … Again

    No One Really Knows How Much COVID Is Silently Spreading … Again

    In the early days of the pandemic, one of the scariest and most surprising features of SARS-CoV-2 was its stealth. Initially assumed to transmit only from people who were actively sick—as its predecessor SARS-CoV did—the new coronavirus turned out to be a silent spreader, also spewing from the airways of people who were feeling just fine. After months of insisting that only the symptomatic had to mask, test, and isolate, officials scrambled to retool their guidance; singing, talking, laughing, even breathing in tight quarters were abruptly categorized as threats.

    Three years later, the coronavirus is still silently spreading—but the fear of its covertness again seems gone. Enthusiasm for masking and testing has plummeted; isolation recommendations have been pared down, and may soon entirely disappear. “We’re just not communicating about asymptomatic transmission anymore,” says Saskia Popescu, an infectious-disease epidemiologist and infection-prevention expert at George Mason University. “People think, What’s the point? I feel fine.”

    Although the concern over asymptomatic spread has dissipated, the threat itself has not. And even as our worries over the virus continue to shrink and be shunted aside, the virus—and the way it moves between us—is continuing to change. Which means that our best ideas for stopping its spread aren’t just getting forgotten; they’re going obsolete.

    Read: A negative COVID test has never been so meaningless

    When SARS-CoV-2 was new to the world and hardly anyone had immunity, symptomless spread probably accounted for most of the virus’s spread—at least 50 percent or so, says Meagan Fitzpatrick, an infectious-disease transmission modeler at the University of Maryland’s School of Medicine. People wouldn’t start feeling sick until four, five, or six days, on average, after being infected. In the interim, the virus would be xeroxing itself at high speed in their airway, reaching potentially infectious levels a day or two before symptoms started. Silently infected people weren’t sneezing and coughing—symptoms that propel the virus more forcefully outward, increasing transmission efficiency. But at a time when tests were still scarce and slow to deliver results, not knowing they had the virus made them dangerous all the same. Precautionary tests were still scarce, or very slow to deliver results. So symptomless transmission became a norm, as did epic superspreading events.

    Now, though, tests are more abundant, presymptomatic spread is a better-known danger, and repeated rounds of vaccination and infection have left behind layers of immunity. That protection, in particular, has slashed the severity and duration of acute symptoms, lowering the risk that people will end up in hospitals or morgues; it may even be chipping away at long COVID. At the same time, though, the addition of immunity has made the dynamics of symptomless transmission much more complex.

    On an individual basis, at least, silent spread could be happening less often than it did before. One possible reason is that symptoms are now igniting sooner in people’s bodies, just three or so days, on average, after infection—a shift that roughly coincided with the rise of the first Omicron variant and could be a quirk of the virus itself. But Aubree Gordon, an infectious-disease epidemiologist at the University of Michigan, told me that faster-arriving sicknesses are probably being driven in part by speedier immune responses, primed by past exposures. That means that illness might now coincide with or even precede the peak of contagiousness, shortening the average period in which people spread the virus before they feel sick. In that one very specific sense, COVID could now be a touch more flulike. Presymptomatic transmission of the flu does seem to happen on occasion, says Seema Lakdawala, a virologist at Emory University. But in general, “people tend not to hit their highest viral levels until after they develop symptoms,” Gordon told me.

    Coupled with more population-level immunity, this arrangement could be working in our favor. People might be less likely to pass the virus unwittingly to others. And thanks to the defenses we’ve collectively built up, the pathogen itself is also having more trouble exiting infected bodies and infiltrating new ones. That’s almost certainly part of the reason that this winter hasn’t been quite as bad as past ones have, COVID-wise, says Maia Majumder, an infectious-disease modeler at Harvard Medical School and Boston Children’s Hospital.

    That said, a lot of people are still undoubtedly catching the coronavirus from people who aren’t feeling sick. Infection per infection, the risk of superspreading events might now be lower, but at the same time people have gotten chiller about socializing without masks and testing before gathering in groups—a behavioral change that’s bound to counteract at least some of the forward shift in symptoms. Presymptomatic spread might be less likely nowadays, but it’s nowhere near gone. Multiply a small amount of presymptomatic spread by a large number of cases, and that can still seed … another large number of cases.

    Read: You probably have an asymptomatic infection right now

    There could be some newcomers to the pool of silent spreaders, too—those who are now transmitting the virus without ever developing symptoms at all. With people’s defenses higher than they were even a year and a half ago, infections that might have once been severe are now moderate or mild; ones that might have once been mild are now unnoticeable, says Seyed Moghadas, a computational epidemiologist at York University. At the same time, though, immunity has probably transformed some symptomless-yet-contagious infections into non-transmissible cases, or kept some people from getting infected at all. Milder cases are of course welcome, Fitzpatrick told me, but no one knows exactly what these changes add up to: Depending on the rate and degree of each of those shifts, totally asymptomatic transmission might now be more common, less common, or sort of a wash.

    Better studies on transmission patterns would help cut through the muck; they’re just not really happening anymore. “To get this data, you need to have pretty good testing for surveillance purposes, and that basically has stopped,” says Yonatan Grad, an infectious-disease epidemiologist at Harvard’s School of Public Health.

    Meanwhile, people are just straight-up testing less, and rarely reporting any of the results they get at home. For many months now, even some people who are testing have been seeing strings of negative results days into bona-fide cases of COVID—sometimes a week or more past when their symptoms start. That’s troubling on two counts: First, some legit COVID cases are probably getting missed, and keeping people from accessing test-dependent treatments such as Paxlovid. Second, the disparity muddles the start and end of isolation. Per CDC guidelines, people who don’t test positive until a few days into their illness should still count their first day of symptoms as Day 0 of isolation. But if symptoms might sometimes outpace contagiousness, “I think those positive tests should restart the isolation clock,” Popescu told me, or risk releasing people back into society too soon.

    Read: People are fed up with rapid tests

    American testing guidelines, however, haven’t undergone a major overhaul in more than a year—right after Omicron blew across the nation, says Jessica Malaty Rivera, an infectious-disease epidemiologist at Boston Children’s Hospital. And even if the rules were to undergo a revamp, they wouldn’t necessarily guarantee more or better testing, which requires access and will. Testing programs have been winding down for many months; free diagnostics are once again growing scarce.

    Through all of this, scientists and nonscientists alike are still wrestling with how to define silent infection in the first place. What counts as symptomless depends not just on biology, but behavior—and our vigilance. As worries over transmission continue to falter and fade, even mild infections may be mistaken for quiet ones, Grad told me, brushed off as allergies or stress. Biologically, the virus and the disease may not need to become that much more muted to spread with ease: Forgetting about silent spread may grease the wheels all on its own.

    Katherine J. Wu

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  • Is COVID a Common Cold Yet?

    Is COVID a Common Cold Yet?

    At the start of the coronavirus pandemic, one of the worst things about SARS-CoV-2 was that it was so new: The world lacked immunity, treatments, and vaccines. Tests were hard to come by too, making diagnosis a pain—except when it wasn’t. Sometimes, the symptoms of COVID got so odd, so off-book, that telling SARS-CoV-2 from other viruses became “kind of a slam dunk,” says Summer Chavez, an emergency physician at the University of Houston. Patients would turn up with the standard-issue signs of respiratory illness—fever, coughing, and the like—but also less expected ones, such as rashes, diarrhea, shortness of breath, and loss of taste or smell. A strange new virus was colliding with people’s bodies in such unusual ways that it couldn’t help but stand out.

    Now, nearly three years into the crisis, the virus is more familiar, and its symptoms are too. Put three sick people in the same room this winter—one with COVID, another with a common cold, and the third with the flu—and “it’s way harder to tell the difference,” Chavez told me. Today’s most common COVID symptoms are mundane: sore throat, runny nose, congestion, sneezing, coughing, headache. And several of the wonkier ones that once hogged headlines have become rare. More people are weathering their infections with their taste and smell intact; many can no longer remember when they last considered the scourge of “COVID toes.” Even fever, a former COVID classic, no longer cracks the top-20 list from the ZOE Health Study, a long-standing symptom-tracking project based in the United Kingdom, according to Tim Spector, an epidemiologist at King’s College London who heads the project. Longer, weirder, more serious illness still manifests, but for most people, SARS-CoV-2’s symptoms are getting “pretty close to other viruses’, and I think that’s reassuring,” Spector told me. “We are moving toward a cold-like illness.”

    That trajectory has been forecast by many experts since the pandemic’s early days. Growing immunity against the coronavirus, repeatedly reinforced by vaccines and infections, could eventually tame COVID into a sickness as trifling as the common cold or, at worst, one on par with the seasonal flu. The severity of COVID will continue to be tempered by widespread immunity, or so this thinking goes, like a curve bending toward an asymptote of mildness. A glance at the landscape of American immunity suggests that such a plateau could be near: Hundreds of millions of people in the U.S. have been vaccinated multiple times, some even quite recently with a bivalent shot; many have now logged second, third, and fourth infections with the virus. Maybe, just maybe, we’re nearing the level of cumulative exposure at which COVID gets permanently more chill. Then again? Maybe not—and maybe never.

    Read: What does it mean to care about COVID anymore?

    The recent trajectory of COVID, at least, has been peppered with positive signs. On average, symptoms have migrated higher up the airway, sparing several vulnerable organs below; disease has gotten shorter and milder, and rates of long COVID seem to be falling a bit. Many of these changes roughly coincided with the arrival of Omicron in the fall of 2021, and part of the shift is likely attributable to the virus itself: On the whole, Omicron and its offshoots seem to prefer infecting cells in the nose and throat over those in the lungs. But experts told me the accumulation of immune defenses that preceded and then accompanied that variant’s spread are almost certainly doing more of the work. Vaccination and prior infection can both lay down protections that help corral the virus near the nose and mouth, preventing it from spreading to tissues elsewhere. “Disease is really going to differ based on the compartment that’s primarily infected,” says Stacey Schultz-Cherry, a virologist at St. Jude Children’s Research Hospital. As SARS-CoV-2 has found a tighter anatomical niche, our bodies have become better at cornering it.

    With the virus largely getting relegated to smaller portions of the body, the pathogen is also purged from the airway faster and may be less likely to be passed to someone else. On the individual level, a sickness that might have once unfurled into pneumonia now gets subdued into barely perceptible sniffles and presents less risk to others; on the population scale, rates of infection, hospitalization, and death go down.

    This is how things usually go with respiratory viruses. Repeat tussles with RSV tend to get progressively milder; post-vaccination flu is usually less severe. The few people who catch measles after getting their shots are less likely to transmit the virus, and they tend to experience such a trivial course of sickness that their disease is referred to by a different name, “modified” measles, says Diane Griffin, a virologist and an immunologist at Johns Hopkins University.

    It’s good news that the median case of COVID diminished in severity and duration around the turn of 2022, but it’s a bit more sobering to consider that there hasn’t been a comparably major softening of symptoms in the months since. The full range of disease outcomes—from silent infection all the way to long-term disability, serious disease, and death—remains in play as well, for now and the foreseeable future, Schultz-Cherry told me. Vaccination history and immunocompromising conditions can influence where someone falls on that spectrum. So too can age as well as other factors such as sex, genetics, underlying medical conditions, and even the dose of incoming virus, says Patricia García, a global-health expert at the University of Washington.

    New antibody-dodging viral variants could still show up to cause more severe disease even among the young and healthy, as occasionally happens with the flu. The BA.2 subvariant of Omicron, which is more immune-evasive than its predecessor BA.1, seemed to accumulate more quickly in the airway, and it sparked more numerous and somewhat gnarlier symptoms. Data on more recent Omicron subvariants are still being gathered, but Shruti Mehta, an epidemiologist at Johns Hopkins, says she’s seen some hints that certain gastrointestinal symptoms, such as vomiting, might be making a small comeback.

    Read: Will we get Omicron’d again?

    All of this leaves the road ahead rather muddy. If COVID will be tamed one day into a common cold, that future definitely hasn’t been realized yet, says Yonatan Grad, an epidemiologist at Harvard’s School of Public Health. SARS-CoV-2 still seems to spread more efficiently and more quickly than a cold, and it’s more likely to trigger severe disease or long-term illness. Still, previous pandemics could contain clues about what happens next. Each of the past century’s flu pandemics led to a surge in mortality that wobbled back to baseline after about two to seven years, Aubree Gordon, an epidemiologist at the University of Michigan, told me. But SARS-CoV-2 isn’t a flu virus; it won’t necessarily play by the same epidemiological rules or hew to a comparable timeline. Even with flu, there’s no magic number of shots or past infections that’s known to mollify disease—“and I think we know even less about how you build up immunity to coronaviruses,” Gordon said.

    The timing of when and how those defenses manifest could matter too. Almost everyone has been infected by the flu or at least gotten a flu shot by the time they reach grade school; SARS-CoV-2 and COVID vaccines, meanwhile, arrived so recently that most of the world’s population met them in adulthood, when the immune system might be less malleable. These later-in-life encounters could make it tougher for the global population to reach its severity asymptote. If that’s the case, we’ll be in COVID limbo for another generation or two, until most living humans are those who grew up with this coronavirus in their midst.

    COVID may yet stabilize at something worse than a nuisance. “I had really thought previously it would be closer to common-cold coronaviruses,” Gordon told me. But severity hasn’t declined quite as dramatically as she’d initially hoped. In Nicaragua, where Gordon has been running studies for years, vaccinated cohorts of people have endured second and third infections with SARS-CoV-2 that have been, to her disappointment, “still more severe than influenza,” she told me. Even if that eventually flips, should the coronavirus continue to transmit this aggressively year-round, it could still end up taking more lives than the flu does—as is the case now.

    Wherever, whenever a severity plateau is reached, Gordon told me that our arrival to it can be confirmed only in hindsight, “once we look back and say, ‘Oh, yeah, it’s been about the same for the last five years.’” But the data necessary to make that call are getting harder to collect as public interest in the virus craters and research efforts to monitor COVID’s shifting symptoms hit roadblocks. The ZOE Health Study lost its government funding earlier this year, and its COVID-symptom app, which engaged some 2.4 million regular users at its peak, now has just 400,000—some of whom may have signed up to take advantage of newer features for tracking diet, sleep, exercise, and mood. “I think people just said, ‘I need to move on,’” Spector told me.

    Mehta, the Johns Hopkins epidemiologist, has encountered similar hurdles in her COVID research. At the height of the Omicron wave, when Mehta and her colleagues were trying to find people for their community studies, their rosters would immediately fill up past capacity. “Now we’re out there for weeks” and still not hitting the mark, she told me. Even weekly enrollment for their long-COVID study has declined. Sign-ups do increase when cases rise—but they drop off especially quickly as waves ebb. Perhaps, in the view of some potential study volunteers, COVID has, ironically, become like a common cold, and is thus no longer worth their time.

    For now, researchers don’t know whether we’re nearing the COVID-severity plateau, and they’re worried it will get only more difficult to tell. Maybe it’s for the best if the mildness asymptote is a ways off. In the U.S. and elsewhere, subvariants are still swirling, bivalent-shot uptake is still stalling, and hospitalizations are once more creeping upward as SARS-CoV-2 plays human musical chairs with RSV and flu. Abroad, inequities in vaccine access and quality—and a zero-COVID policy in China that stuck around too long—have left gaping immunity gaps. To settle into symptom stasis with this many daily deaths, this many off-season waves, this much long COVID, and this pace of viral evolution would be grim. “I don’t think we’re quite there yet,” Gordon told me. “I hope we’re not there yet.”

    Katherine J. Wu

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  • Will Flu and RSV Always Be This Bad?

    Will Flu and RSV Always Be This Bad?

    In the Northern Hemisphere, this year’s winter hasn’t yet begun. But Melissa J. Sacco, a pediatric-intensive-care specialist at UVA Health, is already dreading the arrival of the one that could follow.

    For months, the ICU where Sacco works has been overflowing with children amid an early-arriving surge of respiratory infections. Across the country, viruses such as RSV and flu, once brought to near-record lows by pandemic mitigations, have now returned in force, all while COVID-19 continues to churn and the health-care workforce remains threadbare. Most nights since September, Sacco told me, her ICU has been so packed that she’s had to turn kids away “or come up with creative ways to manage patients in emergency rooms or emergency departments,” where her colleagues are already overwhelmed and children more easily slip through the cracks. The team has no choice: There’s nowhere else for critically ill kids to go.

    Similar stories have been pouring in from around the nation for weeks. I recently spoke with a physician in Connecticut who called this “by far the worst spike in illness I’ve seen in 20 years”; another in Maryland told me, “There have been days when there is not an ICU bed to be found anywhere in the mid-Atlantic.” About three-quarters of the country’s pediatric hospital beds are full; to accommodate overflow, some hospitals have set up tents outside their emergency department or contemplated calling in the National Guard. Last week, the Children’s Hospital Association and the American Academy of Pediatrics asked the Biden administration to declare a national emergency. And experts say there’s no end to the crisis in sight. When Sacco imagines a similar wave slamming her team again next fall, “I get that burning tear feeling in the back of my eyes,” she told me. “This is not sustainable.”

    Read: The worst pediatric-care crisis in decades

    The experts I spoke with are mostly optimistic that these cataclysmic infection rates won’t become an autumn norm. But they also don’t yet fully understand the factors that have been driving this year’s surge, making it tough to know with certainty whether we’re due for an encore.

    One way or another, COVID has certainly thrown the typical end-of-year schedule out of whack. Respiratory viruses typically pick up speed in late fall, peak in mid-to-late winter, and then bow out by the spring; they often run in relay, with one microbe surging a bit before another. This year, though, nearly every pathogen arrived early, cresting in overlapping waves. “Everything is happening at once,” says Kathryn Edwards, a pediatrician and vaccinologist at Vanderbilt University. November isn’t yet through, and RSV has already sent infant hospitalizations soaring past pre-pandemic norms. Flu-hospitalization rates are also at their worst in more than a decade; about 30 states, plus D.C. and Puerto Rico, are reporting high or very high levels of the virus weeks before it usually begins its countrywide climb. And the country’s late-summer surge in rhinovirus and enterovirus has yet to fully abate. “We just haven’t had a break,” says Asuncion Mejias, a pediatrician at Nationwide Children’s Hospital.

    Previous pandemics have had similar knock-on effects. The H1N1-flu pandemic of 2009, for example, seems to have pushed back the start of the two RSV seasons that followed; seasonal flu also took a couple of years to settle back into its usual rhythms, Mejias told me. But that wonky timetable wasn’t permanent. If the viral calendar is even a little more regular next year, Mejias said, “that will make our lives easier.”

    This year, flu and RSV have also exploited Americans’ higher-than-average vulnerability. Initial encounters with RSV in particular can be rough, especially in infants, whose airways are still tiny; the sickness tempers with age as the body develops and immunity builds, leaving most children well protected by toddlerhood. But this fall, the pool of undefended kids is larger than usual. Children born just before the pandemic, or during the phases of the crisis when mitigations aplenty were still in place, may be meeting influenza or RSV for the first time. And many of them were born to mothers who had themselves experienced fewer infections and thus passed fewer antibodies to their baby while pregnant or breastfeeding. Some of the consequences may already have unfurled elsewhere in the world: Australia’s most recent flu season hit kids hard and early, and Nicaragua’s wave at the start of 2022 infected children at rates “higher than what we saw during the 2009 pandemic,” says Aubree Gordon, an epidemiologist at the University of Michigan.

    Read: What a ‘tripledemic’ means for your body

    In the U.S., many hospitals are now admitting far more toddlers and older children for respiratory illnesses than they normally do, says Mari Nakamura, a pediatric-infectious-disease specialist at Boston Children’s Hospital. The problem is worsened by the fact that many adults and school-age kids avoided their usual brushes with flu and RSV while those viruses were in exile, making it easier for the pathogens to spread once crowds flocked back together. “I wouldn’t be surprised,” Gordon told me, “if we see 50 to 60 percent of kids get infected with flu this year”—double the estimated typical rate of 20 to 30 percent. Caregivers too are falling sick; when I called Edwards, I could hear her husband and grandson coughing in the background.

    By next year, more people’s bodies should be clued back in to the season’s circulating strains, says Helen Chu, a physician and an epidemiologist at the University of Washington. Experts are also hopeful that the toolkit for fighting RSV will soon be much improved. Right now, there are no vaccines for the virus, and only one preventive drug is available in the U.S.: a tough-to-administer monoclonal antibody that’s available only to high-risk kids. But at least one RSV vaccine and another, less cumbersome antibody therapy (already being used in Europe) are expected to have the FDA’s green light by next fall.

    Even with the addition of better tech, though, falls and winters may be grueling for many years to come. SARS-CoV-2 is here to stay, and it will likely compound the respiratory burden by infecting people on its own or raising the risk of co-infections that can worsen and prolong disease. Even nonoverlapping illnesses might cause issues if they manifest in rapid sequence: Very serious bouts of COVID, for instance, can batter the respiratory tract, making it easier for other microbes to colonize.

    A few experts have begun to wonder if even milder tussles with SARS-CoV-2 might leave people more susceptible to other infections in the short or long term. Given the coronavirus’s widespread effects on the body, “we can’t be cavalier” about that possibility, says Flor Muñoz Rivas, a pediatrician at Baylor College of Medicine. Mejias and Octavio Ramilo, also at Nationwide, recently found that among a small group of infants, those with recent SARS-CoV-2 infections seemed to have a rougher go with a subsequent bout of RSV. The trend needs more study, though; it’s not clear which kids might be at higher risk, and Mejias doubts that the effect would last more than a few months.

    Gordon points out that some people may actually benefit from the opposite scenario: A recent brush with SARS-CoV-2 could bolster the body’s immune defenses against a second respiratory invader for a few days or weeks. This phenomenon, called viral interference, wouldn’t halt an outbreak by itself, but it’s thought to be part of the reason waves of respiratory disease don’t usually spike simultaneously: The presence of one microbe can sometimes crowd others out. Some experts think last year’s record-breaking Omicron spike helped punt a would-be winter flu epidemic to the spring.

    Even if all of these variables were better understood, the vagaries of viral evolution could introduce a plot twist. A new variant of SARS-CoV-2 may yet emerge; a novel strain of flu could cause a pandemic of its own. RSV, for its part, is not thought to be as quick to shape-shift, but the virus’s genetics are not well studied. Mejias and Ramilo’s data suggest that the arrival of a gnarly RSV strain in 2019 may have pushed local hospitalizations past their usual highs.

    Read: Will we get Omicron’d again?

    Behavioral and infrastructural factors could cloud the forecast as well. Health-care workers vacated their posts in droves during the pandemic, and many hospitals’ pediatric-bed capacity has shrunk, leaving supply grossly inadequate to address current demand. COVID-vaccination rates in little kids also remain abysmal, and many pediatricians are worried that anti-vaccine sentiment could stymie the delivery of other routine immunizations, including those against flu. Even temporary delays in vaccination can have an effect: Muñoz Rivas points out that the flu’s early arrival this year, ahead of when many people signed up for their shot, may now be aiding the virus’s spread. The new treatments and vaccines for RSV “could really, really help,” Nakamura told me, but “only if we use them.”

    Next fall comes with few guarantees: The seasonal schedule may not rectify itself; viruses may not give us an evolutionary pass. Our immune system will likely be better-prepared to fend off flu, RSV, rhinovirus, enterovirus, and more—but that may not be enough on its own. What we can control, though, is how we choose to arm ourselves. The past few years proved that the world does know how to drive down rates of respiratory disease. “We had so little contagion during the time we were trying to keep COVID at bay,” Edwards told me. “Is there something to be learned?”

    Katherine J. Wu

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