Tag: Northern Hemisphere

Ig Nobel Awards Honor Studies On Pigeon-Guided Missiles, Swimming Abilities Of Dead Fish

BOSTON (AP) — A study that explores the feasibility of using pigeons to guide missiles and one that looks at the swimming abilities of dead fish were among the winners Thursday of this year’s Ig Nobels, the prize for comical scientific achievement.

Held less than a month before the actual Nobel Prizes are announced, the 34th annual Ig Nobel prize ceremony at the Massachusetts Institute of Technology was organized by the Annals of Improbable Research magazine’s website to make people laugh and think. Along with handing out the awards, the audience makes and tosses paper airplanes.

“While some politicians were trying to make sensible things sound crazy, scientists discovered some crazy-sounding things that make a lot of sense,” Marc Abrahams, master of ceremonies and editor of the magazine, said in an e-mail interview.

The winners, honored in 10 categories, also included scientists who showed a vine from Chile imitates the shapes of artificial plants nearby and another study that examined whether the hair on people’s heads in the Northern Hemisphere swirled in the same direction as someone’s hair in the Southern Hemisphere.

Other winners include a group of scientists who showed that fake medicine that causes side effects can be more effective than fake medicine that doesn’t cause side effects and one showing that some mammals are cable of breathing through their anus.

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September 12, 2024
The ‘Unthinkable’ New Reality About Bedbugs

This article was originally published by Knowable Magazine.

The stories have become horribly familiar: houses so overrun by bedbugs that the bloodsucking insects pile an inch deep on the floor. An airport shutting down gates for deep cleaning after the parasites were spotted. Fear and loathing during Fashion Week 2023 in Paris, with bedbug-detection dogs working overtime when the insects turned up in movie theaters and trains.

For reasons that almost certainly have to do with global travel and poor pest management, bedbugs have resurfaced with a vengeance in 50 countries since the late 1990s. But recently, the resurgence has brought an added twist: When exterminators swarm out to hunt these pests, they might encounter not just one but two different kinds of bugs.

Besides the common bedbug, Cimex lectularius, which has always made its home in the Northern Hemisphere, there are now sightings of its relative, the tropical bedbug, Cimex hemipterus, in temperate regions. Historically, this species didn’t venture that far from the equator, write the entomologists Stephen Doggett and Chow-Yang Lee in the 2023 issue of the Annual Review of Entomology. But in recent years, tropical bedbugs have turned up in the United States, Sweden, Italy, Norway, Finland, China, Japan, France, Central Europe, Spain—“even in Russia, which would have once been unthinkable,” says Lee, a professor of urban entomology at UC Riverside.

Like the common bedbug, the tropical version has grown resistant to many standard pesticides—to the point where some experts say they wouldn’t bother spraying should their own home become infested. It has been estimated that the fight against bedbugs is costing the world economy billions annually.

This all adds up to a sobering new reality: For many people, bedbugs are becoming a fact of life again, much as they used to be throughout humanity’s history. But as scientists race to find new strategies to combat these pests—everything from microfabricated surfaces that entrap the insects to fungal spores that invade and kill them—they also learn more about the often-bizarre biology of bedbugs, which might one day reveal the parasite’s Achilles’ heel.

Genomics shows that bedbugs emerged 115 million years ago, before the dinosaurs went extinct. When the first humans appeared and moved into caves, the ancestors of today’s bedbugs were ready and waiting. It is thought that these insects initially fed on bats. But bats reduce their blood circulation during their sleeplike torpor state, likely making it harder for the bloodsucking parasite to feed. Presumably, then, at least some bedbug ancestors happily switched to humans.

Since then, the bugs have followed humankind across the globe, tagging along on ancient shipping routes and modern plane rides. Preserved bedbugs were found in the quarters used by workers in ancient Egypt some 3,550 years ago.

Bedbugs can survive a year or more without feeding. About as big as flattened apple seeds, they squeeze into tiny cracks in walls or in the joints of bed frames during the day; they crawl out at night, attracted by a sleeper’s exhaled carbon dioxide and body warmth. At the turn of the 20th century, an estimated 75 percent of homes in the U.K. contained bedbugs. Bizarre prescriptions for remedies have circulated down the years, including a recipe for “cat juice” in a pest-control guide from 1725. The formula called for suffocating and skinning a cat, roasting it on a spit, mixing the drippings with egg yolk and oil, and smearing the concoction into crevices around the bed.

DDT (dichlorodiphenyltrichloroethane) and the pesticides that followed helped bring a few decades’ worth of respite from the 1940s to the 1990s—enough that most people forgot about the insects and didn’t recognize them when they reappeared around the turn of the millennium.

Doggett and Lee hypothesize that the bloodsuckers’ comeback started in areas of Africa, where common and tropical bedbugs naturally coexist, and where DDT (and, later, other insecticides) were sprayed in bedrooms against malaria-carrying mosquitoes. Initially, this would have killed the majority of bed bugs too. But some resistant ones survived and multiplied.

Read: Animals of the future

Bedbugs suck up more than three times their body weight in blood. As they do, they also take in any viruses or other infectious agents that might circulate in the body of their prey, such as hepatitis B and HIV. They have never been found to transmit these pathogens in the wild—but this doesn’t mean that the parasites are benign. “Bedbugs produce some of the most irritating bites of all insects,” says Doggett, a medical entomologist at Westmead Hospital, in Sydney, Australia. “If I receive one, I don’t sleep, as I react so badly. If there are lots of bedbugs, the bites are horrendous.” There have been cases where people have accidentally set mattresses on fire in desperate attempts to chase off the bugs, sometimes burning down their home in the process.

Humans aren’t the only ones to react so strongly. The Cimicidae family, to which bedbugs belong, comprises about 100 species. Almost all prefer to bite nonhuman animals, such as birds. Biologists have observed cliff-swallow chicks jumping to their death from heavily infested nests rather than enduring the bites.

Infestations in which hundreds of bugs may descend upon a bed at night can cause a human sleeper to become anemic. Victims can even develop insomnia, anxiety, and depression. They may find themselves shunned by friends, blacklisted by landlords, and—being sleep-deprived—more prone to car accidents and problems at work.

Read: The psychological toll of bedbugs

Indirectly, at least, bedbugs may cause human deaths. Doggett has noticed that some people in Africa are giving up the bed nets that protect them from mosquitoes and life-threatening malaria infections because bedbugs hide in them. “In some regions, malaria cases are on the rise, and we think that bedbugs are contributing to this,” he says.

By now, bedbug resistance has been reported against most of the prevalent insecticides, including organochlorines, organophosphates, carbamates, neonicotinoids, aryl pyrroles, and pyrethroids. Some of today’s bedbug strains tolerate pesticide doses that are many thousands of times higher than those that used to consistently kill them. Resistant bedbugs have either developed gene mutations that prevent pesticides from binding effectively to their cells or they produce enzymes that quickly break down the toxins in their body. Others are growing thicker exoskeletons that the poisons can’t easily penetrate.

An investigation some years back into a hospital in Cleveland discovered that new bedbugs showed up in the facility every 2.2 days on average. And tropical bedbugs seem just as happy in our modern indoors as the common variety does. “Heating and air-conditioning have made our living environments more standardized,” Lee says. “If a tropical bedbug happens to be introduced to a house in Norway, it can now survive there even in winter.”

Currently, the only bedbug sprays that still tend to work are certain combination products that blend different classes of pesticides. But it’s only a matter of time before these, too, will fail, experts say: Reports of resistance have already been documented. More and more, exterminators incorporate nonchemical approaches such as heat treatments, in which trained professionals warm up rooms to more than 120 degrees Fahrenheit for several hours. They sometimes sprinkle a floury dust called diatomaceous earth around rooms, which clings to those bugs that hide from the heat in wall cracks or under mattresses. The dust abrades the insect’s exoskeleton, dehydrating it to death.

Such measures—combined with more awareness—have helped plateau, or even partly reverse, the spread of bedbugs in some places. In New York City, for example, bedbug complaints fell by half from 2014 to 2020, from 875 complaints a month to 440, on average. To be sure, that’s still 14 complaints a day.

But although effective, nonchemical methods tend to work slowly. “It’s very common that an elimination takes one to two or even three months,” says Changlu Wang, an entomologist at Rutgers University. Meanwhile, residents must keep living in their infested quarters.

Nonchemical measures may also be expensive, because they can require laborious steps such as sealing cracks in walls and physically removing bugs by vacuuming. Although a quick (but increasingly futile) spraying of pesticides may cost a few hundred dollars, mechanical eradications can run as high as several thousand dollars. This puts effective bedbug control out of many people’s reach, making them vulnerable to entrenched infestations that can spread through communities.

The result is that the epidemic has shifted to the poor, says Michael Levy, an epidemiologist at the University of Pennsylvania: “While many cities now have bedbug policies, very few provide much assistance to those who cannot afford treatment.” A 2016 report on 2,372 low-income apartment units in 43 buildings across four New Jersey cities found that 3.8 percent to 29.5 percent were infested with bedbugs.

The northward spread of tropical bedbugs complicates matters further. Although the two species look alike, tropical bedbugs have more hair on their legs, which allows them to climb out of many of the smooth-walled traps that are used to monitor homes. This means that infestations could stay undetected longer, Lee says. And the larger a population grows, the harder it is to get rid of.

To fight back, researchers find inspiration in traditional wisdom. In the Balkan region, homeowners used to spread the leaves of the bean plant Phaseolus vulgaris L. around their beds. The leaves possess tiny hooks on their surface that trap the bugs. Now scientists at UC Irvine are developing a “physical insecticide” in the shape of a synthetic material sporting sharply curved microstructures that mimic those on the bean leaves. These irreversibly impale the feet of the bedbugs, Catherine Loudon, a biology professor at UC Irvine, wrote in a 2022 paper in Integrative and Comparative Biology: “The bugs are unable to get away once they are pierced.”

Other recent approaches are also rooted in nature. Scientists have found, for example, that essential oils can repel bedbugs. However, the effect is mostly temporary. Certain fungal spores, on the other hand, work permanently. “Basically, the spores go into the body of the bedbug and kill it,” Wang says. At least one product containing the insect-killing fungus Beauveria bassiana is now available in the United States.

Read: A better bed bug trap

Researchers continue to be fascinated by the biology of this insect, particularly its sex life. Although female bedbugs possess a normal set of genitalia, the males typically mate by stabbing a needle-sharp penis straight into the female’s abdomen to inject sperm. They usually do this just after a female bedbug has fed, because this makes her too engorged to protect herself.

Having to cope with these frequent injuries has led female bedbugs to evolve the only immunity organ in the insect kingdom, says Klaus Reinhardt, a zoologist at the Dresden University of Technology, in Germany. They have also evolved a remarkably elastic material that covers the parts of their abdomen most likely to be stabbed. “It resembles one of those self-sealing injection bottles that close up again when you pull the needle,” Reinhardt says.

Although this knowledge will likely do little to combat these pests directly, answering another question might: Why don’t bedbugs stay on their host’s body, as lice do? As it turns out, bedbugs don’t like our smell. Certain lipids in human skin repel the bugs, according to a 2021 study in Scientific Reports. This makes them retreat to daytime hiding places, marking their trails with pheromones.

Already, exterminators try to trap bedbugs with fake trail markings. And one day, we might deter the insects from spreading by treating suitcases with smells they despise.

But for now, caution remains the best approach. Experts advise that travelers check accommodations for bedbug-defecation stains: on mattress seams and furniture, and behind headboards. (The insects poop as frequently as a few dozen times after every blood meal, often right next to their victims.) Suitcases should be kept in the hotel bathtub or wrapped in a plastic bag. Upon arrival back home, the luggage’s contents should be put into the clothes dryer for at least 30 minutes at the highest setting, or into a very cold freezer for several days.

If bedbugs do invade a home, “the biggest mistake is to try and get rid of them on one’s own,” Doggett says. “The average person doesn’t appreciate how challenging it is to control bedbugs and will use supermarket insecticides that are labeled for bedbugs but don’t work. The infestation will spread, and the costs escalate.”

Ute Eberle

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February 10, 2024
Flu Shots Need to Stop Fighting ‘Something That Doesn’t Exist’

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In Arnold Monto’s ideal vision of this fall, the United States’ flu vaccines would be slated for some serious change—booting a major ingredient that they’ve consistently included since 2013. The component isn’t dangerous. And it made sense to use before. But to include it again now, Monto, an epidemiologist and a flu expert at the University of Michigan, told me, would mean vaccinating people “against something that doesn’t exist.”

That probably nonexistent something is Yamagata, a lineage of influenza B viruses that hasn’t been spotted by global surveyors since March of 2020, shortly after COVID mitigations plummeted flu transmission to record lows. “And it isn’t for lack of looking,” Kanta Subbarao, the director of the WHO’s Collaborating Centre for Reference and Research on Influenza, told me. In a last-ditch attempt to find the missing pathogen, a worldwide network of monitoring centers tested nearly 16,000 influenza B virus samples collected from February to August of last year. Not a single one of them came up Yamagata. “The consensus is that it’s gone,” Cheryl Cohen, the head of South Africa’s Centre for Respiratory Diseases and Meningitis, told me. Officially removing an ingredient from flu vaccines will codify that sentiment, effectively publishing Yamagata’s obituary.

Read: The flu may never be the same

Last year around this time, Subbarao told me, the WHO was already gently suggesting that the world might want to drop Yamagata from vaccines; by September, the agency had grown insistent, describing the ingredient as “no longer warranted” and urging that “every effort should be made to exclude it as soon as possible.” The following month, an advisory committee to the FDA unanimously voted to speedily adopt that same change.

But the switch from a four-flu vaccine to a trivalent one, guarding against only three, isn’t as simple as ordering the usual, please, just hold the Yams. Trivalent vaccines require their own licensure, which some manufacturers may have allowed to lapse—or never had at all; manufacturers must also adhere to the regulatory pipelines specific to each country. “People think, ‘They change the strains every season; this should be no big deal,’” Paula Barbosa, the associate director of vaccine policy at the International Federation of Pharmaceutical Manufacturers and Associations, which represents vaccine manufacturers, told me. This situation is not so simple: “They need to change their whole manufacturing process.” At the FDA advisory-committee meeting in October, an industry representative cautioned that companies might need until the 2025–26 season to fully transition to trivalents in the Northern Hemisphere, a timeline that Barbosa, too, considers realistic. The South could take until 2026.

In the U.S., though, where experts such as Monto have been pushing for expedient change, a Yamagata-less flu vaccine could be coming this fall. When I reached out to CSL Seqirus and GSK, two of the world’s major flu-vaccine producers, a spokesperson from each company told me that their firm was on track to deliver trivalent vaccines to the U.S. in time for the 2024–25 flu season, should the relevant agencies recommend and request it. (The WHO’s annual meeting to recommend the composition of the Northern Hemisphere’s flu vaccine isn’t scheduled until the end of February; an FDA advisory meeting on the same topic will follow shortly after.) Sanofi, another vaccine producer, was less definitive, but told me that, with sufficient notice from health authorities, its plans would allow for trivalent vaccines this year, “if there is a definitive switch.” AstraZeneca, which makes the FluMist nasal-spray vaccine, told me that it was “engaging with the appropriate regulatory bodies” to coordinate the shift to a trivalent vaccine “as soon as possible.”

Quadrivalent flu vaccines are relatively new. Just over a decade ago, the world relied on immunizations that included two flu A strains (H1N1 and H3N2), plus one B: either Victoria or Yamagata, whichever scientists predicted might be the bigger scourge in the coming flu season. “Sometimes the world got it wrong,” Mark Jit, an epidemiologist at the London School of Hygiene & Tropical Medicine, told me. To hedge their bets, experts eventually began to recommend simply sticking in both. But quadrivalent vaccines typically cost more to manufacture, experts told me. And although several countries, including the U.S., quickly transitioned to the heftier shots, many nations—especially those with fewer resources—never did.

Now “the extra component is a waste,” Vijay Dhanasekaran, a virologist at the University of Hong Kong, told me. It’s pointless to ask people’s bodies to mount a defense against an enemy that will never attack. Trimming Yamagata out of flu-vaccine recipes should also make them cheaper, Dhanasekaran said, which could improve global access. Plus, continuing to manufacture Yamagata-focused vaccines raises the small but serious risk that the lineage could be inadvertently reintroduced to the world, Subbarao told me, as companies grow gobs of the virus for their production pipeline. (Some vaccines, such as FluMist, also immunize people with live-but-weakened versions of flu viruses.)

Some of the researchers I spoke with for this article weren’t ready to rule out the possibility—however slim—that Yamagata is still biding its time somewhere. (Victoria, a close cousin of Yamagata, and the other B lineage that pesters people, once went mostly quiet for about a decade, before roaring back in the early aughts.) But most experts, at this point, are quite convinced. The past couple of flu seasons have been heavy enough to offer even a rather rare lineage the chance to reappear. “If it had been circulating in any community, I’m pretty sure that global influenza surveillance would have detected it by now,” Dhanasekaran said. Plus, even before the pandemic began, Yamagata had been the wimpiest of the flu bunch, Jit told me: slow to evolve, crummy at transmitting, and already dipping in prevalence. When responses to the pandemic starved all flu viruses of hosts, he said, this lineage was the likeliest to be lost.

Read: The pandemic broke the flu

Eventually, companies may return to including four types of flu in their products, swapping in, say, another strain of H3N2, the most severe and fastest-evolving of the bunch—a change that Subbarao and Monto both told me might actually be preferable. But incorporating a second H3N2 is even more of a headache than returning to a trivalent vaccine: Researchers would likely first need to run clinical trials, experts told me, to ensure that the new components played nicely with each other and conferred additional benefits.

For the moment, a slimmed-down vaccine is the quickest way to keep up with the flu’s current antics. And in doing so, those vaccines will also reflect the strange reality of this new, COVID-modified world. “A whole lineage of flu has probably been eliminated through changes in human behavior,” Jit told me. Humanity may not have intended it. But our actions against one virus may have forever altered the course of another.

Katherine J. Wu

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February 5, 2024
Risking Their Lives to Ski While They Can

There’s something fundamentally excessive about winter sports. Instead of curling up with a book or Netflix when the weather turns cold, winter athletes wrestle with inordinate layers and high-tech gear just to make it through the day without frostbite. They sprint across ice with knives strapped to their feet and hurtle down mountains at speeds generally reserved for interstate highways. They fall off ski lifts—or are trapped overnight in them. Show me an experienced winter recreationalist, and I’ll show you someone who has slipped, skidded, and crashed their way to a broken tailbone or torqued knee, and more likely than not a concussion or two.

But over the past few years, climate change, social media, and a pandemic-era obsession with the outdoors have combined to make these already intense sports even more extreme. Seasoned athletes have long considered bunny slopes and indoor ice rinks to be mere gateways to backcountry skiing (zooming through the tree line on untouched powder—and sometimes jumping out of a helicopter to get there) or “wild” ice skating over remote glaciers and freshly frozen lakes. Now a growing crowd of beginners has started to follow them—and the consequences can be fatal.

Since the rise of remote work enabled an exodus from big cities in 2020 and 2021, a record number of people have visited U.S. ski areas each winter. Resorts can be so crowded that people wait 45 minutes for a chair lift that, four years ago, might have only had a three-minute line. No wonder skiers are searching farther and farther afield to get their fix. Greg Poschman, the county commissioner chairman of Colorado’s Pitkin County, told me that in just the past few seasons, he’s seen more people up in the backcountry and out on frozen lakes and rivers than he has in a lifetime living near Aspen. That sentiment is echoed by athletes and officials across the United States. All it takes is a sufficiently impressive stunt posted to social media, and once-deserted corners of the natural world will be inundated with hobbyists a few days later.

In the wilderness, or even the “sidecountry” just outside resort bounds, athletes are exposed to dangers that are rare in more controlled settings. Miles from civilization, no one is policing the landscape for holes in the ice, buried rocks and twigs, and surprise cliffs, not to mention avalanches and ice dams. Perhaps most crucially, pushing out farther from roads and services means being farther from rescue when things go wrong. “You may be doing something that’s a low-risk sport”—ice-skating, snowshoeing, and the like—“but the consequences are very high,” Poschman said.

Photos: The insanity of downhill ice cross racing

Even sports that have never relied on curated resorts to thrive are becoming more treacherous. Kale Casey, a five-time Team USA co-captain for sled-dog sports, told me that unpredictable winter seasons are forcing teams away from traditional routes across Alaska that have become unsafe. Portions of the famous roughly 1,000-mile Iditarod race have been rerouted. Mushers are strategically running certain portions of races at night so their dogs—bred for temperatures around –20 degrees—don’t overheat. As the planet warms, and snow coverage of Alaska’s tundra contracts, other winter sports are converging with the mushers on the little snow that’s left. This season, five dogs have been hit and killed by people riding snowmobiles (known locally as snow machines); five more dogs were also injured in these collisions. “During the lockdown, there wasn’t a snow machine available in Alaska,” Casey told me. “Everybody bought them—and they’ve got to go places. Where do they go? They go where we go.”

Climate change isn’t just pushing winter athletes into more crowded or remote territory. It’s also making that territory less predictable. From across the Northern Hemisphere, the near-identical refrain I heard went something like this: As recently as five years ago, the snow season used to begin sometime around Thanksgiving. It started slowly, with the odd storm or two, building up ice and snowpack gradually as temperatures fell. On a given day, you could be fairly certain of the quality of whatever frigid surface you were skiing on, climbing up, or skating over. And if the weather wasn’t good, well, the snow and ice would be there for you the next day.

But now everyone I spoke with—whether in Iceland or in alpine California—said the first storms don’t come until January. The weather is unpredictable: Record-setting blizzards are interspersed with snow-melting rain. A dry early season followed by rain and wet snow is the perfect recipe for avalanches, Poschman said. Shannon Finch, who was an avalanche-rescue dog handler in Utah for 12 years before turning to heli-ski guiding, told me that even experts are now “perplexed, confused, and getting caught off guard” in environments they’d previously navigated with ease. Her dog, Lēif, struggled in these new conditions: When someone is buried by an avalanche, their scent is less likely to rise through wetter snow and warmer air temperatures. Consequently, Lēif needed to cover considerably more ground before making a rescue.

The shorter seasons also create havoc for a uniquely human reason: FOMO. “People are chomping at the bit to get out there” and are willing to take greater risks for good snow or ice, Travis White, who runs a tourism fishing business in the Upper Peninsula of Michigan, told me. The result is that even a relatively leisurely activity such as ice fishing suddenly becomes an extreme sport. With fewer waterways icing over, more people from places that no longer freeze regularly are suddenly crowding onto just a few lakes. These newcomers aren’t around to watch the water slowly freeze; they don’t know where to watch out for eddies and currents that may make the ice unstable, or how to avoid the most recently frozen patches, which are also the most dangerous.

Stories of ice fishers, figure skaters, and hockey players falling in—even dying—abound. Incidents on the snow are common too. Earlier this month, 23 people needed rescuing in Killington, Vermont, after ducking a boundary rope to ski and snowboard out-of-bounds on a particularly good powder day—the kind that’s getting vanishingly rare in the Northeast.

Read: How skiing went from the Alps to the masses

White, like many of the other winter enthusiasts I spoke with, also blames social media for the extremification of his sport. Inexperienced ice fishers might see a cool spot posted on Instagram and find it easily, thanks to geolocation. The same goes for wild ice-skating, snowmobiling, and backcountry skiing. Athletes also worry that impressive, engagement-oriented stunts posted online could inspire inexperienced people to try extreme moves in those remote sites. “The only thing that I see on social media is people jumping off cliffs on their skis,” Ben Graves, a Colorado-based outdoor educator and an avid backcountry skier, told me. But only a tiny fraction of skiers who can find said cliffs are good enough to jump off them with something approximating safety.

That fraction could soon get even smaller. Ívar Finnbogason, a manager at Icelandic Mountain Guides, is deeply concerned by the decline in skill he’s witnessed over the past decade. He stepped away from a career as an ice climber when he became a father, in part because of the danger but mostly because waiting and waiting for the right conditions meant that he simply couldn’t train effectively. “That’s no way for you as an athlete—as someone with ambition—to build up your momentum,” he told me.

By the end of the century, snow and ice may be so scarce that only the most well-resourced and committed athletes can even attempt these new extremes. With just a degree or two Celsius more warming, much of the Northern Hemisphere can expect massive snow loss. If this happens, the only way to reach the snow might be with a helicopter or a days-long hike.

Read: The threshold at which snow starts irreversibly disappearing

A dramatic collapse in winter sports might well result in fewer accidents. But we would also lose something intrinsically human. For many winter-recreation devotees, these sports are more than just activities to pass the time. They are a way of life, dating as far back as 8000 B.C.E. Perhaps those who test their skills against the strength of Mother Nature have it right. Maybe now is the time for winter athletes to take their passions to dangerous new heights, before they lose the option forever.

Talia Barrington

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January 31, 2024
What To Know About The Winter Solstice

For the Northern Hemisphere, especially the northern Northern, it is a dark, cold day – and the turning point of light…Winter Solstice is upon us.

The Winter Solstice is upon us. The Northern Hemisphere’s winter solstice falls on December 21 at 10:27 p.m. EST. South of the Equator, this same moment marks the unofficial beginning of summer. Solstices occur at the same time around the world, but their local times vary with time zones. But whether you are in Tirupattur, India or Mobile, Alabama, it is an ancient and scientific key moment. For the Southern hemisphere, summer is about to begin and for the Northern, winter – and is the shortest day of the year.

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Cultures around the world have long held feasts and celebrated holidays around the winter solstice. Fire and light are traditional symbols of celebrations held on the darkest day of the year. Here are few celebrations

Soyal is the winter solstice celebration of the Hopi Indians of northern Arizona. Ceremonies and rituals include purification, dancing, and sometimes gift-giving. At the time of the solstice, Hopi welcome the kachinas, protective spirits from the mountains. Prayer sticks are crafted and used for various blessings and other rituals.

The Persian festival Yalda, or Shab-e Yalda is a celebration of the winter solstice in Iran that started in ancient times. It marks the last day of the Persian month of Azar. Yalda is viewed traditionally as the victory of light over dark, and the birthday of the sun god Mithra. Families celebrate together with special foods like nuts and pomegranates and some stay awake all night long to welcome the morning sun.

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Even Antarctica gets its share of solstice celebration, thanks to the researchers staying there over the long, dangerously cold season. While those of us in the Northern Hemisphere are enjoying the most daylight hours, in the Southern Hemisphere they are celebrating Midwinter. Festivities include special meals, films, and sometimes even handmade gifts.

St. Lucia’s Day is a festival of lights celebrated in Scandinavia around the time of the winter solstice. Although it is now meant to honor St. Lucia, a Christian martyr, it has been incorporated with earlier Norse solstice traditions, such as lighting fires to ward off spirits during the longest night. Girls dress up in white gowns with red sashes and wear wreaths of candles on their heads in honor of St. Lucia.

Top four ways most people celebrate winter solstice: drinking, complaining about lack of light, consuming cannabis, and prepping for the holiday season.

Anthony Washington

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December 20, 2023
One More COVID Summer?

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.

Katherine J. Wu

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July 29, 2023
Pandemic Babies’ Microbiomes Are Bound to Be Different

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.”

Katherine J. Wu

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December 5, 2022
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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November 23, 2022