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Tag: earliest days

  • Sick Season Will Be Worse From Now On

    Sick Season Will Be Worse From Now On

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    Last fall, when RSV and flu came roaring back from a prolonged and erratic hiatus, and COVID was still killing thousands of Americans each week, many of the United States’ leading infectious-disease experts offered the nation a glimmer of hope. The overwhelm, they predicted, was probably temporary—viruses making up ground they’d lost during the worst of the pandemic. Next year would be better.

    And so far, this year has been better. Some of the most prominent and best-tracked viruses, at least, are behaving less aberrantly than they did the previous autumn. Although neither RSV nor flu is shaping up to be particularly mild this year, says Caitlin Rivers, an epidemiologist at the Johns Hopkins Center for Health Security, both appear to be behaving more within their normal bounds.

    But infections are still nowhere near back to their pre-pandemic norm. They never will be again. Adding another disease—COVID—to winter’s repertoire has meant exactly that: adding another disease, and a pretty horrific one at that, to winter’s repertoire. “The probability that someone gets sick over the course of the winter is now increased,” Rivers told me, “because there is yet another germ to encounter.” The math is simple, even mind-numbingly obvious—a pathogenic n+1 that epidemiologists have seen coming since the pandemic’s earliest days. Now we’re living that reality, and its consequences. “What I’ve told family or friends is, ‘Odds are, people are going to get sick this year,’” Saskia Popescu, an epidemiologist at the University of Maryland School of Medicine, told me.

    Even before the pandemic, winter was a dreaded slog—“the most challenging time for a hospital” in any given year, Popescu said. In typical years, flu hospitalizes an estimated 140,000 to 710,000 people in the United States alone; some years, RSV can add on some 200,000 more. “Our baseline has never been great,” Yvonne Maldonado, a pediatrician at Stanford, told me. “Tens of thousands of people die every year.” In “light” seasons, too, the pileup exacts a tax: In addition to weathering the influx of patients, health-care workers themselves fall sick, straining capacity as demand for care rises. And this time of year, on top of RSV, flu, and COVID, we also have to contend with a maelstrom of other airway viruses—among them, rhinoviruses, parainfluenza viruses, human metapneumovirus, and common-cold coronaviruses. (A small handful of bacteria can cause nasty respiratory illnesses too.) Illnesses not severe enough to land someone in the hospital could still leave them stuck at home for days or weeks on end, recovering or caring for sick kids—or shuffling back to work, still sick and probably contagious, because they can’t afford to take time off.

    To toss any additional respiratory virus into that mess is burdensome; for that virus to be SARS-CoV-2 ups the ante all the more. “This is a more serious pathogen that is also more infectious,” Ajay Sethi, an epidemiologist at the University of Wisconsin at Madison, told me. This year, COVID-19 has so far killed some 80,000 Americans—a lighter toll than in the three years prior, but one that still dwarfs that of the worst flu seasons in the past decade. Globally, the only infectious killer that rivals it in annual-death count is tuberculosis. And last year, a CDC survey found that more than 3 percent of American adults were suffering from long COVID—millions of people in the United States alone.

    Read: Is COVID a common cold yet?

    With only a few years of data to go on, and COVID-data tracking now spotty at best, it’s hard to quantify just how much worse winters might be from now on. But experts told me they’re keeping an eye on some potentially concerning trends. We’re still rather early in the typical sickness season, but influenza-like illnesses, a catchall tracked by the CDC, have already been on an upward push for weeks. Rivers also pointed to CDC data that track trends in deaths caused by pneumonia, flu, and COVID-19. Even when SARS-CoV-2 has been at its most muted, Rivers said, more people have been dying—especially during the cooler months—than they were at the pre-pandemic baseline. The math of exposure is, again, simple: The more pathogens you encounter, the more likely you are to get sick.

    A larger roster of microbes might also extend the portion of the year when people can expect to fall ill, Rivers told me. Before the pandemic, RSV and flu would usually start to bump up sometime in the fall, before peaking in the winter; if the past few years are any indication, COVID could now surge in the summer, shading into RSV’s autumn rise, before adding to flu’s winter burden, potentially dragging the misery out into spring. “Based on what I know right now, I am considering the season to be longer,” Rivers said.

    With COVID still quite new, the exact specifics of respiratory-virus season will probably continue to change for a good while yet. The population, after all, is still racking up initial encounters with this new coronavirus, and with regularly administered vaccines. Bill Hanage, an epidemiologist at Harvard’s T. H. Chan School of Public Health, told me he suspects that, barring further gargantuan leaps in viral evolution, the disease will continue to slowly mellow out in severity as our collective defenses build; the virus may also pose less of a transmission risk as the period during which people are infectious contracts. But even if the dangers of COVID-19 are lilting toward an asymptote, experts still can’t say for sure where that asymptote might be relative to other diseases such as the flu—or how long it might take for the population to get there. And no matter how much this disease softens, it seems extraordinarily unlikely to ever disappear. For the foreseeable future, “pretty much all years going forward are going to be worse than what we’ve been used to before,” Hanage told me.

    Read: The next stage of COVID is starting now

    In one sense, this was always where we were going to end up. SARS-CoV-2 spread too quickly and too far to be quashed; it’s now here to stay. If the arithmetic of more pathogens is straightforward, our reaction to that addition could have been too: More disease risk means ratcheting up concern and response. But although a core contingent of Americans might still be more cautious than they were before the pandemic’s start—masking in public, testing before gathering, minding indoor air quality, avoiding others whenever they’re feeling sick—much of the country has readily returned to the pre-COVID mindset.

    When I asked Hanage what precautions worthy of a respiratory disease with a death count roughly twice that of flu’s would look like, he rattled off a familiar list: better access to and uptake of vaccines and antivirals, with the vulnerable prioritized; improved surveillance systems to offer  people at high risk a better sense of local-transmission trends; improved access to tests and paid sick leave. Without those changes, excess disease and death will continue, and “we’re saying we’re going to absorb that into our daily lives,” he said.

    And that is what is happening. This year, for the first time, millions of Americans have access to three lifesaving respiratory-virus vaccines, against flu, COVID, and RSV. Uptake for all three remains sleepy and halting; even the flu shot, the most established, is not performing above its pre-pandemic baseline. “We get used to people getting sick every year,” Maldonado told me. “We get used to things we could probably fix.” The years since COVID arrived set a horrific precedent of death and disease; after that, this season of n+1 sickness might feel like a reprieve. But compare it with a pre-COVID world, and it looks objectively worse. We’re heading toward a new baseline, but it will still have quite a bit in common with the old one: We’re likely to accept it, and all of its horrors, as a matter of course.

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    Katherine J. Wu

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  • One More COVID Summer?

    One More COVID Summer?

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    Since the pandemic’s earliest days, epidemiologists have been waiting for the coronavirus to finally snap out of its pan-season spree. No more spring waves like the first to hit the United States in 2020, no more mid-year surges like the one that turned Hot Vax Summer on its head. Eventually, or so the hope went, SARS-CoV-2 would adhere to the same calendar that many other airway pathogens stick to, at least in temperate parts of the globe: a heavy winter peak, then a summer on sabbatical.

    But three and a half years into the outbreak, the coronavirus is still stubbornly refusing to take the warmest months off. Some public-health experts are now worried that, after a relatively quiet stretch, the virus is kick-starting yet another summer wave. In the southern and northeastern United States, concentrations of the coronavirus in wastewater have been slowly ticking up for several weeks, with the Midwest and West now following suit; test-positivity rates, emergency-department diagnoses of COVID-19, and COVID hospitalizations are also on the rise. The absolute numbers are still small, and they may stay that way. But these are the clear and early signs of a brewing mid-year wave, says Caitlin Rivers, an epidemiologist at Johns Hopkins University—which would make this the fourth summer in a row with a distinct coronavirus bump.

    Even this far into the pandemic, though, no one can say for certain whether summer waves are a permanent COVID fixture—or if the virus exhibits a predictable seasonal pattern at all. No law of nature dictates that winters must come with respiratory illness, or that summers will not. “We just don’t know very much about what drives the cyclical patterns of respiratory infections,” says Sam Scarpino, an infectious-disease modeler at Northeastern University. Which means there’s still no part of the year when this virus is guaranteed to cut us any slack.

    That many pathogens do wax and wane with the seasons is indisputable. In temperate parts of the world, airborne bugs get a boost in winter, only to be stifled in the heat; polio and other feces-borne pathogens, meanwhile, often rise in summer, along with gonorrhea and some other STIs. But noticing these trends is one thing; truly understanding the triggers is another.

    Read: COVID sure looks seasonal now

    Some diseases lend themselves a bit more easily to explanation: Near the equator, waves of mosquito-borne illness, such as Zika and Chikungunya, tend to be tied to the weather-dependent life cycles of the insects that carry them; in temperate parts of the world, rates of Lyme disease track with the summertime activity of ticks. Flu, too, has pretty strong data to back its preference for wintry months. The virus—which is sheathed in a fragile, fatty layer called an envelope and travels airborne via moist drops—spreads best when it’s cool and dry, conditions that may help keep infectious particles intact and spittle aloft.

    The coronavirus has enough similarities to flu that most experts expect that it will continue to spread in winter too. Both viruses are housed in a sensitive skin; both prefer to move by aerosol. Both are also relatively speedy evolvers that don’t tend to generate long-lasting immunity against infection—factors conducive to repeat waves that hit populations at a fairly stable clip. For those reasons, Anice Lowen, a virologist at Emory University, anticipates that SARS-CoV-2 will continue to show “a clear wintertime seasonality in temperate regions of the world.” Winter is also a time when our bodies can be more susceptible to respiratory bugs: Cold, dry air can interfere with the movement of mucus that shuttles microbes out of the nose and throat; aridity can also make the cells that line those passageways shrivel and die; certain immune defenses might get a bit sleepier, with vitamin D in shorter supply.

    None of that precludes SARS-CoV-2 spread in the heat, even if experts aren’t sure why the virus so easily drives summer waves. Plenty of other microbes manage it: enteroviruses, polio, and more. Even rhinoviruses and adenoviruses, two of the most frequent causes of colds, tend to spread year-round, sometimes showing up in force during the year’s hottest months. (Many scientists presume that has something to do with these viruses’ relatively hardy outer layer, but the reason is undoubtedly more complex than that.) An oft-touted explanation for COVID’s summer waves is that people in certain parts of the country retreat indoors to beat the heat. But that argument alone “is weak,” Lowen told me. In industrialized nations, people spend more than 90 percent of their time indoors.

    That said, an accumulation of many small influences can together create a seasonal tipping point. Summer is a particularly popular time for travel, often to big gatherings. Many months out from winter and its numerous infections and vaccinations, population immunity might also be at a relative low at this time of year, Rivers said. Plus, for all its similarities to the flu, SARS-CoV-2 is its own beast: It has so far affected people more chronically and more severely, and has generated population-sweeping variants at a far faster pace. Those dynamics can all affect when waves manifest.

    And although certain bodily defenses do dip in the cold, data don’t support the idea that immunity is unilaterally stronger in the summer. Micaela Martinez, the director of environmental health at WE ACT for Environmental Justice, in New York, told me the situation is far more complicated than that. For years, she and other researchers have been gathering evidence that suggests that our bodies have distinctly seasonal immunological profiles—with some defensive molecules spiking in the summer and another set in winter. The consequences of those shifts aren’t yet apparent. But some of them could help explain when the coronavirus spreads. By the same token, winter is not a time of disease-ridden doom. Xaquin Castro Dopico, an immunologist at the Karolinska Institute, in Sweden, has found that immune systems in the Northern Hemisphere might be more inflammation-prone in the winter—which, yes, could make certain bouts of illness more severe but could also improve responses to certain vaccinations.

    All of those explanations could apply to COVID’s summer swings—or perhaps none does. “Everybody always wants to have a very simple seasonal answer,” Martinez told me. But one may simply not exist. Even the reasons for the seasonality of polio, a staunch summertime disease prior to its elimination in the U.S., have been “an open question” for many decades, Martinez told me.

    Rivers is hopeful that the coronavirus’s permanent patterns may already be starting to peek through: a wintry heyday, and a smaller maybe-summer hump. “We’re in year four, and we’re seeing the same thing year over year,” she told me. But some experts worry that discussions of COVID-19 seasonality are premature. SARS-CoV-2 is still so fresh to the human population that its patterns could be far from their final form. At an extreme, the patterns researchers observed during the first few years of the pandemic may not prelude the future much at all, because they encapsulate so much change: the initial lack and rapid acquisition of immunity, the virus’s evolution, the ebb and flow of masks, and more. Amid that mishmash of countervailing influences, says Brandon Ogbunu, an infectious-disease modeler at Yale, “you’re going to get some counterintuitive dynamics” that won’t necessarily last long term.

    Read: The next stage of COVID is starting now

    With so much of the world now infected, vaccinated, or both, and COVID mitigations almost entirely gone, the global situation is less in flux now. The virus itself, although still clearly changing at a blistering pace, has not pulled off an Omicron-caliber jump in evolution for more than a year and a half. But no one can yet promise predictability. The cadence of vaccination isn’t yet settled; Scarpino, of Northeastern University, also isn’t ready to dismiss the idea of a viral evolution surprise. Maybe summer waves, to the extent that they’re happening, are a sign that SARS-CoV-2 will remain a microbe for all seasons. Or maybe they’re part of the pandemic’s death rattle—noise in a system that hasn’t yet quieted down.

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    Katherine J. Wu

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  • The Coronavirus-Naming Free-for-All

    The Coronavirus-Naming Free-for-All

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    These days, it’s a real headache to keep tabs on the coronavirus’s ever-shifting subvariants. BA.2, BA.4, and BA.5, three Omicron permutations that rose to prominence last year, were confusing enough. Now, in addition to those, we have to deal with BQ.1.1, BF.7, B.5.2.6, and XBB.1.5, the version of Omicron currently featuring in concerned headlines. Recently, things have also gotten considerably stranger. Alongside the strings of letters and numbers, several nicknames for these subvariants have started to gain traction online. Where once we had Alpha and Delta and Omicron, we now have Basilisk, Minotaur, and Hippogryph. Some people have been referring to XBB.1.5 simply as “the Kraken.” A list compiled on Twitter reads less like an inventory of variants than like the directory of a mythological zoo.

    The nicknames are not official. They were coined not by the World Health Organization but by an informal group of scientists on Twitter who believe Omicron’s many rotating varieties deserve more widespread conversation. The names have, to an extent, caught on: Kraken has already made its way from Twitter to a number of major news sites, including Bloomberg and The New York Times. Unofficial epithets have come and gone throughout the pandemic—remember “stealth Omicron” and the “Frankenstein variant”?—but these new ones are on another level of weirdness. And not everyone’s a fan.

    The names associated with the coronavirus have been a fraught conversation since the pandemic’s earliest days, as scientists and public-health figures have tried to use terms that are comprehensible and hold people’s attention but that also avoid pitfalls of inaccuracy, fear-mongering, or xenophobia and racism (see: Donald Trump referring to the coronavirus as “the Chinese virus” and “kung flu”). The official names for variants and subvariants—names such as SARS-CoV-2 B.1.1.7—come from the Pango naming system, which was fashioned by evolutionary biologists in the early months of the pandemic to standardize variant-naming practices. As baffling as they can seem, they follow a clear logic: Under the system, B refers to a particular COVID lineage, B.1 refers to the sublineage of B lineage, B.1.1 refers to the first sublineage of the B.1 sublineage, and so on. When the names get too long, a letter replaces a string of numbers—B.1.1.529.1, for example, becomes BA.1.

    These official names do not exactly roll off the tongue or stick in the memory, which became a problem when new variants of concern started to arise and the world began groping for ways to talk about them. In May 2021, the WHO instituted its now-familiar Greek-letter naming system to stamp out the geographic associations that were gaining prominence at the time. B.1.1.7, B.1.351, and B.1.617—which were being referred to respectively as the U.K. variant, the South African variant, and the Indian variant—became Alpha, Beta, and Delta. But then, alas, came Omicron. Rather than giving way to yet another new Greek-letter variant, Omicron has spent more than a year branching into sublineages, and sublineages of sublineages. As a result, the nomenclature has devolved back into alphanumeric incomprehensibility. Seven different Omicron sublineages now account for at least 2 percent of all infections, and none accounts for more than about 40 percent (though XBB.1.5 is threatening to overwhelm its competitors).

    It’s great news that the ways in which the coronavirus has been mutating recently haven’t been significant enough to produce a whole new, widespread, and possibly far more worrisome version of itself that the world has to contend with. But it also makes talking about the virus much more annoying. Enter T. Ryan Gregory, an evolutionary biologist at Canada’s University of Guelph who is one of the leaders of a small, informal group of scientists that have taken it upon themselves to name the many subvariants that the WHO does not deem worthy of a new Greek letter. The names—Hydra, Cerberus, Centaurus—originated on Twitter, where Gregory compiled them into a list.

    Their value, Gregory told me, is that they fill the space in between the Greek and Pango systems, allowing people to discuss the many current Omicron variants that do not justify a new Greek letter but are still, perhaps, of interest. You can think of it in the same way we do animal taxonomy, he said. Calling a variant Omicron, like calling an animal a mammal, is not particularly descriptive. Calling a variant by its Pango name, like calling an animal by its Latinate species designation, is highly descriptive but a bit unwieldy in common parlance. When we speak of farm animals that moo and produce milk, we speak not of mammals or of Bos taurus but of cows. And so BA.2.3.20 became Basilisk.

    To decide whether a new lineage deserves its own name, Gregory told me, he and his colleagues consider both evolutionary factors (how different is this lineage from its predecessors, and how concerning are its mutations?) and epidemiological factors (how much havoc is this lineage wreaking in the population?). They’re trying to make the process more formal, but Gregory would prefer that the WHO take over and standardize the process.

    That, however, is unlikely to happen. When I asked about this, Tarik Jasarevic, a WHO spokesperson, told me that the organization is aware of the unofficial names but that, for the moment, they’re not necessary. “Virologists and other scientists are monitoring these variants, but the public doesn’t need to distinguish between these Omicron subvariants in order to better understand their risk or the measures they need to take to protect themselves,” he said. The WHO’s position, in other words, is that the differences between one Omicron subvariant and another simply haven’t mattered much in any practical sense, because they shouldn’t have any effect on our behavior. No matter the sublineage, vaccines and boosters still offer the best protection available. Masks still work. Guidance on testing and isolation, too, is the same across the board. “If there is a new variant that requires public communication and discourse,” Jasarevic told me, “it would be designated a new variant of concern and assigned a new label.”

    The WHO isn’t alone in objecting. For Stephen Goldstein, an evolutionary virologist at the University of Utah, the new names are not just unnecessary but potentially harmful. “It’s absolutely crazy that we’re having random people on Twitter name variants,” he told me. For Goldstein, dressing up each new subvariant with an ominous monster name overplays the differences between the mutations and feeds into the panic that comes every time the coronavirus shifts form. In this view, distinguishing one Omicron sublineage from another is less like distinguishing a wolf from a cow and more like distinguishing a white-footed mouse from a deer mouse: important to a rodentologist but not really to anyone else. To go as far as naming lineages after terrifying mythical beasts, he said, “seems obviously intended to scare the shit out of people … It’s hard to understand what broader goal there is here other than this very self-serving clout chasing.”

    Gregory told me that fear and attention are not his group’s aim. He also said, though, that his group is thinking of switching from mythological creatures to something more neutral, such as constellations, in part to address concerns of whipping up unnecessary panic. When it comes to XBB.1.5, some of that panic certainly already exists, whipped up by less-than-nuanced headlines and Twitter personalities who feast on moments like these. Whether or not the name Kraken has contributed, the fear is that XBB.1.5 might be a variant so immune-evasive that it infects everyone all over again or so virulent that it amps up the risk of any given infection. So far, that does not seem to be the case.

    As my colleague Katherine Wu reported in November, we are likely (though by no means definitely) stuck for the foreseeable future in this Omicron purgatory, with its more gradual, more piecemeal pattern of viral evolution. This is certainly preferable to the sudden and unexpected emergence of a dangerous, drastically different variant. But it does mean that we’re likely going to be arguing about whether and how and with what names to discuss Omicron subvariants for some time to come.

    Whichever side you come down on, the state of variant-naming pretty well encapsulates the state of the pandemic as a whole. Hardly anything about the pandemic has been a matter of universal agreement, but the present nomenclatural free-for-all seems to have taken us somewhere even more splintered, even more anarchic. We’re not just arguing about the pandemic; we’re arguing about how to argue about the pandemic. And there’s no end in sight.

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    Jacob Stern

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  • Pandemic Babies’ Microbiomes Are Bound to Be Different

    Pandemic Babies’ Microbiomes Are Bound to Be Different

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    In the spring of 2021, Brett Finlay, a microbiologist at the University of British Columbia, offered the world a bold and worrying prediction. “My guess is that five years from now we are going to see a bolus of kids with asthma and obesity,” he told Wired. Those children, he said, would be “the COVID kids”: those born just before or during the height of the crisis, when the coronavirus was everywhere, and we cleaned everything because we didn’t want it to be.

    Finlay’s forecast isn’t unfounded. As James Hamblin wrote in The Atlantic last year, our health relies on a constant discourse with trillions of microbes that live on or inside our bodies. The members of the so-called microbiome are crucial for digesting our food, training the immune system, even greasing the wheels of cognitive function; there does not seem to be a bodily system that these tiny tenants do not in some way affect. These microbe-human dialogues begin in infancy, and the first three or so years of life are absolutely pivotal: Bacteria must colonize babies, then the two parties need to get into physiological sync. Major disruptions during this time “can throw the system out of whack,” says Katherine Amato, a biological anthropologist at Northwestern University, and raise a kid’s risk of developing allergies, asthma, obesity, and other chronic conditions later in life.

    The earlier, more intense, and more prolonged the interruptions, the worse. Infants who receive heavy courses of antibiotics—which can nuke microbial diversity—are at greater risk of developing such problems; the same is roughly true for babies who are born by C-section, who formula feed, or who grow up in nature-poor environments. If pandemic-era mitigations re-create even an echo of those effects, that could spell trouble for a whole lot of little kids who may have lost out on beneficial microbes in the ongoing effort to keep nasty ones at bay.

    More than a year and a half after Finlay’s original prediction, children are back in day care and school. People no longer keep their distance or avoid big crowds. Even hygiene theater is (mostly) on the wane. And if the wave of respiratory viral illness now slamming much of the Northern Hemisphere is any indication, microbes are once again swirling between tiny hands and mouths. But for the circa-COVID kids, the specter of 2026 and Finlay’s anticipated chronic-illness “bump” still looms—and it’ll be a good while yet before researchers have clarity on just how much of a difference those months of relative microbial emptiness truly made.

    Read: A year without germs

    For now, “we are in the realm of speculation,” says Maria Gloria Dominguez Bello, a microbiologist at Rutgers. Scientists don’t understand how, or even which, behaviors may affect the composition of our inner flora throughout our life span. Chronic illnesses such as obesity and asthma also take time to manifest. There’s not yet evidence that they’re on the rise among children, and even if they were, researchers wouldn’t expect to see the signal for at least a couple of years, perhaps more.

    Finlay, for one, stands by his original prediction that the pandemic will bring a net microbiome negative. “We underwent a massive societal shift,” he told me. “I am sure we will see an effect.” And he is not the only one who thinks so. “I think it’s almost inevitable that there has been an impact,” says Graham Rook, a medical microbiologist at University College London. If the middle of this decade passes without incident, Rook told me, “I would be very surprised.” Other researchers, though, aren’t so sure. “I don’t think we have doomed a generation of kids,” says Melissa Manus, an anthropologist and microbiome researcher at the University of Manitoba. A few scientists are even pondering whether the pandemic’s ripple effects may have buoyed the microbiomes of the COVID kids. Martin Blaser, a microbiologist at Rutgers University, told me that, “with any luck,” rates of asthma and obesity might even dip in the next few years.

    When it comes to the pandemic’s potential fallout, researchers agree on just one thing: COVID babies undoubtedly had an unusual infancy; on average, their microbiomes are bound to look quite different. Different, though, isn’t necessarily bad. “It’s not like there is one golden microbiome,” says Efrem Lim, a microbiologist at Arizona State University. Take Liz Johnson’s sons, born in March 2018, August 2020, and March 2022. All three were born vaginally, in the same hospital, with the assistance of the same midwife; all of them then breastfed; and none of them has undergone an early, concerning antibiotic course. And still, “they all started off with different microbiomes,” she told me. (As a microbiome researcher at Cornell focused on infant nutrition, Johnson can check.)

    That’s probably totally fine. Across the human population, microbiomes are known to vary wildly: People can carry hundreds of bacterial species on and inside their bodies, with potentially zero overlap from one individual to the next. Bacterial communities aren’t unlike recipes—if you don’t have one ingredient on hand, another can usually take its place.

    Johnson’s middle son, Lucas, had a starkly different birth experience from that of his older brother—even, in many ways, from that of his younger brother. Lucas was born into a delivery room full of masked faces. In the days after his arrival, no family members came to visit him in the hospital. And although his brothers spent several of their early months jet-setting all around the world with their mother for work trips, Lucas stayed put. “Hardly anybody even knew he was born,” Johnson told me. But throughout his first two years, Lucas still breastfed and had plenty of contact with his family at home, as well as with other kids at day care; he romped in green spaces galore. Yet Johnson and others can’t say, precisely, whether all of that outweighs the sanitariness and the uncrowdedness of Lucas’s earliest days. There would have been a cost to both overcaution and under-caution, “so we just tried to balance everything,” Johnson said. When it comes down to it, scientists just don’t know how much microbial exposure constitutes enough.

    Read: Pregnant? Breastfeeding? The vaccine might protect you and your baby

    Among COVID babies, microbiome mileage will probably vary, depending on what decisions their parents made at the height of the pandemic—which itself hinges on the sorts of financial and social resources they had. Amato worries most about the families that may have packaged a bunch of sanitizing behaviors together with more established cullers of microbiome diversity: C-sections, formula-feeding, and antibiotic use. Meghan Azad, an infant-health researcher at the University of Manitoba, told me that some new parents might have found it far tougher to breastfeed during the pandemic’s worst—a time when in-person counseling resources were harder to access, and employment was in flux. Chronically poor diets and stress, which many people experienced these past few years, can also chip away at microbiome health.

    Part of the problem is that many of these risk factors, Rook told me, will disproportionately coalesce among people of lower socioeconomic status, who already tend to have less diverse microbiomes. “I worry this will further increase the health disparity between the rich and the poor,” he said. Even SARS-CoV-2 infections themselves, which have continued to concentrate among essential workers and in crowded living settings, appear to alter the microbiome—a shift that may be temporary in adults, but potentially less so in infants, whose microbiomes haven’t yet matured into a stable state.

    Many families exist in a gray zone. Maybe they bleached their households often, but found it easier to breastfeed and cook healthful meals while working from home. Maybe their kids weren’t mingling with tons of other toddlers at day care, but they spent much more time rolling around in the backyard, coated in their pandemic puppy’s drool. If all of those factors feed into an equation that sums up to healthy or not, scientists can’t yet do the math. They’re still figuring out how to appropriately weigh each component, and how to identify others they’ve missed.

    Even in the absence of extra outdoorsiness or dog slobber, Lim isn’t very concerned about the behavioral mitigations people picked up. We’re all “exposed to thousands of microbes all the time,” Lim, who has a 1-and-a-half-year-old daughter, told me. Some extra hand-washing, masking, and time at home is nothing compared with, say, an antibiotic blitzkrieg. Even kids who stayed pretty cloistered “were not living in a bubble.” Some of the social sacrifices kids made may even have strange silver linings. Children no longer attending day care or preschool might have skirted a whole slew of other viral infections that would otherwise have gotten them inappropriate and microbiome-damaging antibiotics prescriptions. Antibiotic use in outpatient settings dropped substantially in 2020, compared with the prior year. Stacked up against the relatively minor toll of pandemic mitigations, Blaser told me, the plus of avoiding antibiotics might just win out. When antibiotic use declines, for example, so do asthma rates.

    Finlay and others are still keeping an eye out for signals that might start to appear in the next few years. Perhaps most at risk are kids whose families went into “hyper-hygiene mode” in the first couple months of their life, when microbes are crucial for properly calibrating the immune system’s anti-pathogen alarms. Miss out on those opportunities, and our body’s defensive cells might end up mistaking enemies for allies, or vice versa, sparking particularly severe infections or autoimmune disease. Once wired into a developing child, Finlay said, such changes might be difficult to reverse, especially for the youngest of the COVID cohort. But other experts are hopeful that certain microbial losses can still be recouped through some combination of diet, outdoor play, and socialization (with people who aren’t sick)—restorative interventions that, ideally, happen as early as possible. “The sooner we fix it, the better,” Blaser said.

    Read: The pandemic broke the flu … again

    No one can choose precisely which microbes to be exposed to: Tactics that halt the transmission of known pathogens have a way of halting the transmission of benign bugs too. But context matters. It’s possible for microbe-inviting behaviors, such as outdoor play, to coexist alongside microbe-shunning tactics, such as ventilating indoor spaces when there’s a massive respiratory outbreak. The fact that we can influence microbial colonization at all is powerful. During the pandemic, mitigations that kept COVID at bay also cratered rates of flu and RSV. Now that those viruses are back, experts are pointing out that we already know how they can once again be stopped. And the choices that people made, and continue to make, to protect their families from pathogens shouldn’t be viewed as some harmful mistake, says Ariangela Kozik, a microbiologist at the University of Michigan.

    Pandemic kids can get on board with that concept too. Kozik’s now-7-year-old son was a toddler when the pandemic began; even amid society’s hygiene craze, he learned the joys of tumbling around in the dirt and playing with the family’s two dogs. “We talk about how not all germs are the same,” Kozik told me. Her son also picked up and maintained an infection-quashing habit that makes his mom proud: Every day, when he comes home from school, he makes a beeline for the sink to wash his hands. “It’s the first thing he does,” Kozik told me, “even without being asked.”

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    Katherine J. Wu

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