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Tag: virus

  • Avian flu is crippling California poultry farms. Will there be a surge in pricing?

    Avian flu is crippling California poultry farms. Will there be a surge in pricing?

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    December should have been the most profitable month of the year for Liberty Ducks, a poultry farm in Sonoma County. Instead, the 31-year-old business was suddenly face to face with a possible shutdown.

    “There was never going to be a good time for this to hit, but during the holidays was especially hard,” said Jennifer Reichardt of Liberty Ducks. The farm, she said, has been “crippled” by the outbreak.

    In December, the farm was one of nine locations in Sonoma County infected with highly pathogenic avian influenza, also known as bird flu. As a result, poultry farmers in the county have been forced to destroy more than 1 million birds while trying to quarantine their flocks to curb the outbreak.

    The outbreak has been ongoing since 2022, but its sudden surge in December has meant restaurants in the winery-rich region are seeing their supplies of poultry dwindle. Experts warn this may only be the beginning of a bird flu spike in California .

    “Restaurants are looking for product,” said Bill Mattos, president of the California Poultry Federation.

    The lingering disease has yet to affect prices or supply across the state as a whole, Mattos said, given the poultry available from other counties and outside the state. But restaurants, stores and wholesalers who prefer to use local sources are seeing their supply dwindle.

    “Everyone is looking to see what they can do to prevent it even more,” Mattos said.

    Liberty Ducks supplies Bay Area restaurants and more than 200 wholesalers. But because the company’s locations are under quarantine, the farm can’t start new production, Reichardt said.

    “Our business will be at a standstill for at least two months until the quarantine is lifted or we find other locations,” she said.

    Poultry companies have been feeling the effects of the avian flu since February 2022, when the U.S. Department of Agriculture first detected the virus in commercial and backyard flocks.

    Since then, more than 79 million birds across the U.S have been affected in 47 states. In California, the virus has affected 37 commercial and 22 backyard flocks, totaling 5.4 million birds, according to U.S. Department of Agriculture’s Animal and Plant Health Inspection Service.

    Since the outbreak began, the avian pandemic has not gone by unnoticed by consumers either.

    Last year, the outbreak helped make egg prices skyrocket across the country. According to the USDA, prices in California for a dozen large eggs jumped to $7.37 in January 2023, up from $2.35 the year before. The USDA said that while demand for eggs was surging in December 2022, the avian flu was cutting the supply; in the last week of that month, there were about 29% fewer eggs than at the beginning of 2022.

    A higher incidence of the highly pathogenic avian influenza is common during this time of year because of the migratory patterns of wild birds, which carry the virus as they fly from the Arctic to California, said Dr. Maurice Pitesky, associate professor at UC Davis School of Veterinary Medicine whose research focuses on the disease.

    Unfortunately, the same climate and geography that makes poultry farming popular in some areas is what draws in wild birds like ducks and geese, carrying the flu with them into the state. The virus can pass from one animal to another through saliva, mucus or feces.

    “Wildlife can bring this virus into their farms because the virus is so infectious,” Pitesky said.

    Farmers have tried to keep their flocks safe through bio-security practices, such requiring clean footwear before workers enter a farm to keep feces from contaminating the area under the shoes, Mattos said. Several big farms also try to reduce risk by prohibiting their workers from owning backyard flocks.

    This past month, however, poultry farmers in Northern California have been particularly hit by the virus.

    “I’m not sure if it’s a more virulent strain or what,” Mattos said. “The industry expects it to come and show up, we just didn’t expect it to be in big numbers.”

    According to the USDA, 11 flocks in California have tested positive for the virus in the past 30 days, affecting more than 3.3 million birds.

    In Sonoma County, the effect has been significant.

    Nine poultry in sites in southern Sonoma County have been infected with the virus, requiring more than a million birds to be euthanized to prevent further spread, according to the county.

    On Dec. 5, the Sonoma County Board of Supervisors declared a local emergency because of the disease. Flocks that have been infected have been put in quarantine, and county officials are hoping to curb the spread of the virus.

    The flu’s effect in the county and region is still unclear, but officials are concerned that the consequences could ripple through affected farms, workers, restaurants and markets that rely on the farms’ eggs, meat and jobs.

    A spokesperson for Sonoma County said officials have not yet done an economic impact study, but are focusing resources on containing the outbreak.

    According to the California Department of Food and Agriculture, five California counties — Fresno, Marin, Merced, San Joaquin and Sonoma — have active avian flu infections.

    The flu could be especially damaging to businesses like Liberty Ducks that are still recovering from the COVID-19 pandemic.

    “After COVID, we were already in such a tight financial space, this really could have been the final blow,” said Reichardt.

    She and her brother set up a GoFundMe campaign to keep the business afloat, and have raised more than $184,000 so far.

    “The community outreach is not only letting us continue on and help with cash flow, but also mentally gives us such a lift to fight on,” Reichardt said.

    Some farms can also apply for federal compensation for the value of lost birds, but Mattos said it is not enough to cover what farmers could have made from their flocks.

    For now, farmers and backyard flock owners are being urged to take precautions and keep their birds isolated from exposure.

    And depending on this year’s rains, poultry farmers may be seeing just the first effects of the outbreak this year, Pitesky warned.

    “If it’s a wet year, unfortunately, [wild birds] will probably stay here until April and May,” he said. “Most likely, they’ll be dealing with this for several more months.”

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    Salvador Hernandez

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  • Bird flu concerns grow in California as deadly virus infects more farms

    Bird flu concerns grow in California as deadly virus infects more farms

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    Federal and state officials have confirmed outbreaks in the last few weeks of a fast-spreading avian influenza strain — commonly known as bird flu — in four new California counties, sparking concerns about the possible agricultural and financial blow of the virus.

    The “highly pathogenic” bird flu was confirmed Wednesday at two commercial farms in Stanislaus County, joining recent outbreaks at poultry farms in Fresno, San Benito and Sonoma counties, according to updates from the California Department of Food and Agriculture. The strain is easily spread among birds and often fatal for them.

    “It is important to note that [the bird flu] is widespread in California and may also be present in other counties that are not listed,” the agency said in a statement Wednesday. “Enhanced biosecurity is critical in the face of ongoing disease outbreaks.”

    Surging egg prices earlier this year were blamed on an outbreak of the bird flu that killed millions of hens and left grocers struggling to keep shelves stocked.

    California agriculture officials said that in order to protect other flocks from the disease, the farms where outbreaks were reported are being quarantined and their birds euthanized.

    After cases were confirmed earlier this week at two Sonoma County poultry farms, officials there declared a state of emergency, calling the outbreak a local disaster.

    “We need to promote and protect our local food shed and the agricultural producers who dedicate their livelihoods to producing food for our local populations and beyond,” Sonoma County Agricultural Commissioner Andrew Smith said in a statement. “These producers are integral in maintaining and increasing food security in our communities.”

    Sonoma County Supervisor David Rabbitt said he is concerned about economic and supply-chain issues that could result from the emergency, noting that south Sonoma County has about “one million farm birds within a five-mile radius” of one of the facilities hit by the outbreak, and that they provide as many as hundreds of thousands of eggs daily.

    Rabbitt also said that more than 200 employees work at the two affected Sonoma County facilities, and will be hurt by the losses.

    In October, as cases of avian flu increased nationally and the first California outbreak of the season was detected in Merced County, the state veterinarian urged that California bird farmers move their flocks indoors for now.

    The Merced County outbreak was confirmed at a commercial turkey farm, home to about 30,000 birds, according to USDA data tracking the virus’ spread.

    The most recent outbreaks confirmed in Stanislaus County were at two commercial farms that are raising about 250,000 chickens each. The infected Sonoma County farms were a duck farm with 169,000 birds, and a commercial egg producer with more than 80,000 birds.

    The San Benito and Fresno county cases also included commercial duck farms, with 5,000 birds in San Benito and 23,000 in Fresno, according to the USDA data.

    State officials did not disclose the names of the companies involved, and USDA data was limited.

    Avian infuenza can be found in both wild and domesticated fowl, including chickens, turkeys, pheasants, quail, ducks and geese, and its typically spread through bird-to-bird contact, according to the state Department of Food and Agriculture.

    There have also been confirmed cases in wild birds over the last month in Sacramento and Santa Clara counties, according to the USDA.

    Officials noted this spring that continued spread of the virus could soon become a concern for the still-endangered California condor.

    According to the federal Centers for Disease Control and Protection, this bird flu strain is considered a low risk to humans. However, the World Health Organization has said there is some cause for worry due to some reports of the virus infecting humans.

    Californians can report unusual sick or dead pets or domesticated birds via the state Department of Food and Agriculture Sick Bird Hotline at (866) 922-2473. Any unusual or dead wild birds should be reported to the state Department of Fish and Wildlife online.

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    Grace Toohey

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  • What you need to know about the new RSV shot for babies

    What you need to know about the new RSV shot for babies

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    Ahead of the winter respiratory virus season, many parents were relieved the U.S. Food and Drug Administration approved a shot to combat respiratory syncytial virus, or RSV, for infants and toddlers this summer.

    But the shot is hard to come by.

    RSV is a common respiratory virus that usually causes mild, cold-like symptoms in most adults who recover in a week or two, according to the Centers for Disease Control and Prevention. But that’s not the case for infants and toddlers, who are at higher risk of the virus becoming severe or life-threatening.

    The first vaccine for RSV was approved in May and was targeted for older adults.

    Two months later, federal regulators approved the first long-lasting shot for infants younger than 8 months who are entering their first RSV season. According to the CDC, Nirsevimab, which is made by AstraZeneca and sold under the brand name Beyfortus, reduces the risk of severe RSV by 80%. One dose lasts about five months, the length of the average RSV season.

    The shot does not activate the immune system the way a vaccine would, but instead introduces antibodies to protect against RSV. Health officials with the CDC say once the antibodies are out of a baby’s system, the immunity is also gone.

    Amid the peak of RSV season, there has been unprecedented demand for the shot and not enough supplies to go around.

    The CDC recently announced the release of more than 77,000 additional doses to be distributed immediately to physicians and hospitals through the Vaccines for Children Program. The CDC and FDA are working with drug manufacturers to ensure availability through early next year.

    What preventive measures can parents can take?

    Children at high risk include those 6 months and younger, infants born prematurely, those younger than 2 with congenital heart disease and those with weakened immune systems who have neuromuscular disorders, according to the American Lung Assn.

    Previously, the only immunization against severe RSV for babies was a shot women could get during weeks 32 through 36 of pregnancy. That shot is still available and recommended September through January.

    There also are everyday preventive measures to help reduce the spread of RSV and other respiratory illnesses, according to health agencies such as the CDC, American Lung Assn. and the California Department of Public Health:

    • Stay home if you’re feeling sick.
    • If you need to leave your home, consider wearing a mask in crowded or indoor areas.
    • Wash your hands with soap and water for at least 20 seconds.
    • Avoid touching your face with unwashed hands.
    • Cover your mouth and nose when you cough and sneeze.
    • Avoid close contact with others, such as kissing, shaking hands and sharing cups and utensils.
    • Clean frequently touched surfaces, including doorknobs and mobile devices.

    What are the signs of RSV?

    RSV affects both the upper respiratory system, which includes the nose and throat, and the lower respiratory system, which includes the lungs.

    The virus is highly transmissible. You can catch it if the droplets from an infected person’s cough or sneeze get in your eyes, nose or mouth; if you touch a surface (such as a doorknob) that has the virus on it and then touch your face before washing your hands; or if you have direct contact with the virus (for example, by kissing the face of a child with RSV). Being in crowded places with people who may be infected or having exposure to other children or siblings who may be infected are common ways to pick up the virus.

    RSV can survive for many hours on hard surfaces such as tables and crib rails; it has a shorter life span on softer surfaces such as tissues and hands.

    A person infected with RSV is usually contagious for three to eight days. However, some infants and people with weakened immune systems can continue to spread the virus for as long as four weeks, even after their symptoms go away, according to the CDC.

    Virtually all children get an RSV infection by the time they are 2, but the virus can cause complications, the CDC said.

    Health agencies recommend parents reach out to their healthcare provider if their child is showing signs of infection.

    According to health officials at Cedars-Sinai Medical Center, the most common symptoms are runny nose; fever; cough; short periods without breathing; trouble eating, drinking or swallowing; wheezing, flaring of nostrils or straining of the chest or stomach while breathing; breathing faster than usual or trouble breathing; and turning blue around the lips and fingers.

    These symptoms can seem like other health conditions, so the hospital advises parents to have their child see a healthcare provider for a diagnosis.

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    Karen Garcia

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  • Smoking, Marijuana, Virus, Lung, Budweiser, Cannabis: Marijuana Plantation Unearthed | Vadodara News – Medical Marijuana Program Connection

    Smoking, Marijuana, Virus, Lung, Budweiser, Cannabis: Marijuana Plantation Unearthed | Vadodara News – Medical Marijuana Program Connection

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    Vadodara: The SOG of Panchmahal district police unearthed a marijuana plantation in the Shehra taluka of the district. One person was arrested.
    SOG sleuths had received information regarding marijuana plantations in the farm of Vikramsinh Pagi in the Dalwada village of Shehra taluka. A team of SOG personnel then raided the farm and discovered the plants.
    According to sources, the plants weighed 31.83 kg and were fully grown. The seizure is valued at Rs 31.83 lakh. tnn

    Original Author Link click here to read complete story..

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    MMP News Author

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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.

    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.

    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 Republican Lab-Leak Circus Makes One Important Point

    The Republican Lab-Leak Circus Makes One Important Point

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    For more than three hours yesterday, the House Select Subcommittee on the Coronavirus Pandemic grilled a pair of virologists about their participation in an alleged “cover-up” of the pandemic’s origins. Republican lawmakers zeroed in on evidence that the witnesses, Kristian Andersen and Robert Garry, and other researchers had initially suspected that the coronavirus spread from a Chinese lab. “Accidental escape is in fact highly likely—it’s not some fringe theory,” Andersen wrote in a Slack message to a colleague on February 2, 2020. When he laid out the same concern to Anthony Fauci in late January, that some features of the viral genome looked like they might be engineered, Fauci told him to consider going to the FBI.

    But days later, Andersen, Garry, and the other scientists were starting to coalesce around a different point of view: Those features were more likely to have developed via natural evolution. The scientists wrote up this revised assessment in an influential paper, published in the journal Nature Medicine in March 2020, called “The Proximal Origin of SARS-CoV-2.” The virus is clearly “not a laboratory construct or a purposefully manipulated virus,” the paper said; in fact, the experts now “did not believe that any type of laboratory-based scenario is plausible,” and that the pandemic almost certainly started with a “zoonotic event”—which is to say, the spillover of an animal virus into human populations. That analysis would be cited repeatedly by scientists and media outlets in the months that followed, in support of the idea that the lab-leak theory had been thoroughly debunked.

    The researchers’ rapid and consequential change of heart, as revealed through emails, witness interviews, and Slack exchanges, is now a wellspring for Republicans’ suspicions. “All of a sudden, you did a 180,” Representative Nicole Malliotakis of New York said yesterday morning. “What happened?”

    Based on the available facts, the answer seems clear enough: Andersen, Garry, and the others looked more closely at the data, and decided that their fears about a lab leak had been unwarranted; the viral features were simply not as weird as they’d first thought. The political conversation around this episode is not so easily summarized, however. Yesterday’s hearing was less preoccupied with the small, persistent possibility that the coronavirus really did leak out from a lab than with the notion of a conspiracy—a cover-up—that, according to Republicans, involved Fauci and others in the U.S. government swaying Andersen and Garry to leave behind their scientific judgment and endorse “pro-China talking points” instead. (Fauci has denied that he tried to disprove the lab-leak theory.)

    Barbed accusations of this kind have only added headaches to the question of how the pandemic really started. For all of its distractions, though, the House investigation still serves a useful purpose: It sheds light on how discussions of the lab-leak theory went so very, very wrong, and turned into an endless, stultifying spectacle. In that way, the hearing—and the story that it tells about the “Proximal Origin” paper—gestures not toward the true origin of COVID, but toward the origin of the origins debate.

    From the start, the problem has been that a “lab leak” could mean many things. The term may refer to the release of a manufactured bioweapon, or to an accident involving basic-science research; it could involve a germ with genes deliberately inserted, or one that was rapidly evolved inside a cage or in a dish, or even a virus from the wild, brought into a lab and released by accident (in unaltered form) in a city like Wuhan. Yet all these categories blurred together in the early days of the pandemic. The confusion was made plain when Senator Tom Cotton of Arkansas, a hard-core China hawk, aired a proto-lab-leak theory in a February 16, 2020 interview with Fox News. “This virus did not originate in the Wuhan animal market,” he told the network. He later continued, “just a few miles away from that food market is China’s only biosafety-level-4 super-laboratory that researches human infectious diseases. Now, we don’t have evidence that this disease originated there, but because of China’s duplicity and dishonesty from the beginning, we need to at least ask the question.”

    Cotton did not specifically suggest that the Chinese “super-laboratory” was weaponizing viruses, nor did he say that any laboratory accident would necessarily have involved a genetically engineered virus, as opposed to one that had been cultured or collected from a bat cave. Nevertheless, The New York Times and The Washington Post reported that the senator had repeated a “fringe theory” about the coronavirus that was going around in right-wing circles at the time, that it had been manufactured by the Chinese government as a bioweapon. It was hard for reporters to imagine that Cotton could have been suggesting anything but that: The idea that Chinese scientists might have been collecting wild viruses, and doing research just to understand them, was not yet thinkable in that chaotic, early moment of pandemic spread. “Lab leak” was simply understood to mean “the virus is a bioweapon.”

    Scientists knew better. On the same day that Cotton gave his interview, one of Andersen and Garry’s colleagues posted the “Proximal Origin” paper on the web as an unpublished manuscript. (“Important to get this out,” Garry wrote in an email sent to the group the following morning. He included a link to the Washington Post article about Cotton described above.) In this version, the researchers were quite precise about what, exactly, they were aiming to debunk: The authors said, specifically, that their analysis clearly showed the virus had not been genetically engineered. It might well have been produced through cell-culture experiments in a lab, they wrote, though the case for this was “questionable.” And as for the other lab-leak possibilities—that a Wuhan researcher was infected by the virus while collecting samples from a cave, or that someone brought a sample back and then accidentally released it—the paper took no position whatsoever. “We did not consider any of these scenarios,” Andersen explained in his written testimony for this week’s hearing. If a researcher had indeed been infected in the field, he continued, then he would not have counted it as a “lab leak” to begin with—because that would mean the virus jumped to humans somewhere other than a lab.

    Rather than settling the matter, however, all this careful parsing only led to more confusion. In the early days of the pandemic, and in the context of the Cotton interview and its detractors, too much specificity was deemed a fatal flaw. On February 20, Nature decided to reject the manuscript, at least partly on account of its being too soft in its debunking. A month later, when their paper finally did appear in Nature Medicine, a new sentence had been added near the end: the one discounting “any type of laboratory-based scenario.” At this crucial moment in the pandemic-origins debate, the researchers’ original, narrow claim—that SARS-CoV-2 had not been purposefully assembled—was broadened to include a blanket statement that could be read to mean the lab-leak theory was wrong in all its forms.

    Over time, this aggressive phrasing would cause problems of its own. At first, its elision of several different possible scenarios served the mainstream narrative: We know the virus wasn’t engineered; ergo, it must have started in the market. More recently, the same confusion has served the interests of the lab-leak theorists. Consider a report from the Office of the Director of National Intelligence on pandemic origins, declassified last month. American intelligence agencies have determined that SARS-CoV-2 was not developed as a bioweapon, it explains, and they are near-unanimous in saying that it was not genetically engineered. (This confirms what Andersen and colleagues said in the first version of their paper, way back in February 2020.) “Most” agencies, the report says, further judge that the virus was not created through cell-culture experiments. Yet the fact that two of the nine agencies nonetheless believe that “a laboratory-associated incident” of any kind is the most likely cause of the first human infection has been taken as a sign that all lab-leak scenarios are still on the table. Thus Republicans in Congress can rail against Facebook for removing posts about the “lab-leak theory,” while ignoring the fact that the platform’s rules only ever prohibited one particular and largely discredited idea, that SARS-CoV-2 was “man-made or manufactured.” (In any case, that prohibition was reversed some three months later.)

    Where does this leave us? The committee’s work does not reveal a cover-up of COVID’s source. At the same time, it does show that the authors of the “Proximal Origin” paper were aware of how their work might shape the public narrative. (In a Slack conversation, one of them referred to “the shit show that would happen if anyone serious accused the Chinese of even accidental release.”) At first they strived to phrase their findings as clearly as they could, and to separate the strong evidence against genetic engineering of the virus—and what Garry called “the bio weapon scenario”—from the lingering possibility that laboratory science might have been involved in some other way. In the final version of their paper, though, they added in language that was rather less precise. This may have helped to muffle the debate in early 2020, but the haze it left behind was noxious and long-lasting.

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    Daniel Engber

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  • Only the Emergency Has Ended

    Only the Emergency Has Ended

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    Emergency responses—being, well, emergency responses—aren’t designed to last forever, and this morning, the World Health Organization declared the one that’s been in place for the COVID-19 pandemic since January 2020 officially done. “This virus is here to stay. It is still killing, and it’s still changing,” Tedros Adhanom Ghebreyesus, the director general of the WHO, said at a press conference; although the coronavirus will continue to pose a threat, the time had simply come, he and his colleagues said, for countries to move away from treating it as a global crisis.

    And, really, they already have: The United States, for instance, ended its national emergency last month and will sunset its public-health emergency next week; countries around the world have long since shelved testing programs, lifted lockdowns, dispensed with masking mandates, and even stopped recommending frequent COVID shots to healthy people in certain age groups. In some ways, the WHO was already a straggler. Had it waited much longer, the power of its designation of COVID as a “public health emergency of international concern,” or PHEIC, “would have been undermined,” says Salim Abdool Karim, the director of the Centre for the AIDS Program of Research in South Africa.

    There’s no disputing that the virus’s threat has ebbed since the pandemic’s worst days. By and large, “we are in our recovery phase now”—not perfectly stabilized, but no longer in chaotic flux, says René Najera, the director of public health at the College of Physicians of Philadelphia. Still, ending the emergency doesn’t mean that the world has fully addressed the problems that made this an emergency. Global vaccine distribution remains wildly inequitable, leaving many people susceptible to the virus’s worst effects; deaths are still concentrated among those most vulnerable; the virus’s evolutionary and transmission patterns are far from predictable or seasonal. Now, ending the emergency is less an epidemiological decision than a political one: Our tolerance for these dangers has grown to the extent that most people are doing their best to look away from the remaining risk, and will continue to until the virus forces us to turn back.

    The end to the PHEIC, to be clear, isn’t a declaration that COVID is over—or even that the pandemic is. Both a PHEIC and a pandemic tend to involve the rapid and international spread of a dangerous disease, and the two typically do go hand in hand. But no set-in-stone rules delineate when either starts or ends. Plenty of diseases have met pandemic criteria—noted by many epidemiologists as an epidemic that’s rapidly spread to several continents—without ever being granted a PHEIC, as is the case with HIV. And several PHEICs, including two of the Ebola outbreaks of the past decade and the Zika epidemic that began in 2015, did not consistently earn the pan- prefix among experts. With COVID, the WHO called a PHEIC more than a month before it publicly labeled the outbreak a pandemic on March 11. Now the organization has bookended its declaration with a similar mismatch: one crisis designation on and the other off. That once again leaves the world in a bizarre risk limbo, with the threat everywhere but our concern for it on the wane.

    For other diseases with pandemic potential, understanding the start and end of crisis has been simpler. After a new strain of H1N1 influenza sparked a global outbreak in 2009, disrupting the disease’s normal seasonal ebb and flow, scientists simply waited until the virus’s annual transmission patterns went back to their pre-outbreak baseline, then declared that particular pandemic done. But “we don’t really have a baseline” to return to for SARS-CoV-2, says Sam Scarpino, an infectious-disease modeler at Northeastern University. This has left officials floundering for an end-of-pandemic threshold to meet. Once, envisioning that coda seemed more possible: In February 2021, when the COVID shots were still new, Alexis Madrigal wrote in The Atlantic that, in the U.S. at least, pandemic restrictions might end once the country reached some relatively high rate of vaccination, or drove daily deaths below 100—approximating the low-ish end of the flu’s annual toll.

    Those criteria aren’t perfect. Given how the virus has evolved, even, say, an 85 percent vaccination rate probably wouldn’t have squelched the virus in a way public-health experts were envisioning in 2021 (and wouldn’t have absolved us of booster maintenance). And even if the death toll slipped below 100 deaths a day, the virus’s chronic effects would still pose an immense threat. But thresholds such as those, flawed though they were, were never even set. “I’m not sure we ever set any goals at all” to designate when we’d have the virus beat, Céline Gounder, an infectious-disease physician at NYU and an editor-at-large for public health at KFF Health News, told me. And if they had been, we probably still would not have met them: Two years out, we certainly have not.

    Instead, efforts to mitigate the virus have only gotten laxer. Most individuals are no longer masking, testing, or staying up to date on their shots; on community scales, the public goods that once seemed essential—ventilation, sick leave, equitable access to insurance and health care—have already faded from most discourse. That COVID has been more muted in recent months feels “more like luck” than a product of concerted muffling from us, Scarpino told me. Should another SARS-CoV-2 variant sweep the world or develop resistance to Paxlovid, “we don’t have much in the way of a plan,” he said.

    If and when the virus troubles us again, our lack of preparedness will be a reflection of America’s classically reactive approach to public health. Even amid a years-long emergency declaration that spanned national and international scales, we squandered the opportunity “to make the system more resilient to the next crisis,” Gounder said. There is little foresight for what might come next. And individuals are still largely being asked to fend for themselves—which means that as this emergency declaration ends, we are setting ourselves up for another to inevitably come, and hit us just as hard.

    As the final roadblocks to declaring normalcy disappear, we’re unlikely to patch those gaps. The PHEIC, at this point, was more symbolic than practical—but that didn’t make it inconsequential. Experts worry that its end will sap what remaining incentive there was for some countries to sustain a COVID-focused response—one that would, say, keep vaccines, treatments, and tests in the hands of those who need them most. “Public interest is very binary—it’s either an emergency or it’s not,” says Saskia Popescu, an infection-prevention expert at George Mason University. With the PHEIC now gone, the world has officially toggled itself to “not.” But there’s no going back to 2019. Between that and the height of the pandemic is middle-ground maintenance, a level of concern and response that the world has still not managed to properly calibrate.

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    Katherine J. Wu

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  • Will COVID’s Spring Lull Last?

    Will COVID’s Spring Lull Last?

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    By all official counts—at least, the ones still being tallied—the global situation on COVID appears to have essentially flatlined. More than a year has passed since the world last saw daily confirmed deaths tick above 10,000; nearly a year and a half has elapsed since the population was pummeled by a new Greek-lettered variant of concern. The globe’s most recent winters have been the pandemic’s least lethal to date—and the World Health Organization is mulling lifting its COVID emergency declaration sometime later this year, as the final pandemic protections in the United States prepare to disappear. On the heels of the least-terrible winter since the pandemic’s onset, this spring in the U.S. is also going … kind of all right. “I am feeling less worried than I have been in a while,” Shweta Bansal, an infectious-disease modeler at Georgetown University, told me.

    That sense of phew, though, Bansal said, feels tenuous. The coronavirus’s evolution is not yet predictable; its effects are nowhere near benign. This might be the longest stretch of quasi-normalcy that humanity has had since 2020’s start, but experts can’t yet tell whether we’re at the beginning of post-pandemic stability or in the middle of a temporary reprieve. For now, we’re in a holding pattern, a sort of extended coda or denouement. Which means that our lived experience and scientific reality might not match up for a good while yet.

    There is, to be fair, reason to suspect that some current trends will stick. The gargantuan waves of seasons past were the rough product of three factors: low population immunity, genetic changes that allowed SARS-CoV-2 to skirt what immunity did exist, and upswings in behaviors that brought people and the virus into frequent contact. Now, though, just about everyone has had some exposure to SARS-CoV-2’s spike protein, whether by infection or injection. And most Americans have long since dispensed with masking and distancing, maintaining their exposure at a consistently high plateau. That leaves the virus’s shape-shifting as the only major wild card, says Emily Martin, an infectious-disease epidemiologist at the University of Michigan. SARS-CoV-2 could, for instance, make another evolutionary leap large enough to re-create the Omicron wave of early 2022—but a long time has passed since the virus managed such a feat. Tentatively, carefully, experts are hopeful that we’re at last in a “period that could be kind of indicative of what the new normal really is,” says Virginia Pitzer, an infectious-disease epidemiologist at Yale.

    Top American officials are already gambling on that guess. At a conference convened in late March by the Massachusetts Medical Society, Ashish Jha, the outgoing coordinator of the White House COVID-19 Response Team, noted that the relative tameness of this past winter was a major deciding factor in the Biden administration’s decision to let the U.S. public-health emergency lapse. The crisis-caliber measures that were essential at the height of the pandemic, Jha said, were no longer “critical at this moment” to keep the nation’s health-care system afloat. Americans could rely instead primarily on shots and antivirals to keep themselves healthy—“If you are up to date on your vaccines and you get treated with Paxlovid, if you get an infection, you just don’t die of this virus,” he said. (That math, of course, doesn’t hold up as well for certain vulnerable groups, including the elderly and the immunocompromised.) The pharmaceuticals-only strategy asks much less of people: Going forward, most Americans will need to dose up on their COVID vaccines only once a year in the fall, a la seasonal flu shots.

    Making sweeping assessments at this particular juncture, though, is tough. Experts expect SARS-CoV-2 cases to take a downturn as winter transitions into spring—as many other respiratory viruses do. And a half-ish year of relative quietude is, well, just a half-ish year of relative quietude—too little data for scientists to definitively declare the virus seasonal, or even necessarily stable in its annual patterns. One of the most telling intervals is yet to come: the Northern Hemisphere’s summer, says Alyssa Bilinski, a health-policy researcher at Brown University. In previous years, waves of cases have erupted pretty consistently during the warmer months, especially in the American South, as people flock indoors to beat the heat.

    SARS-CoV-2 might not end up being recognizably seasonal at all. So far, the virus has circulated more or less year-round, with erratic bumps in the winter and, to a lesser extent, the summer. “There is a consistency there that is very enticing,” Bansal told me. But many of the worst surges we’ve weathered were driven by a lack of immunity, which is less of an issue now. “So I like to be extremely careful about the seasonality argument,” she said. In future years, the virus may break from its summer-winter shuffle. How SARS-CoV-2 will continue to interact with other respiratory viruses, such as RSV and flu, also remains to be seen. After an extended hiatus, driven largely by pandemic mitigations, those pathogens came roaring back this past autumn—making it more difficult, perhaps, for the coronavirus to find unoccupied hosts. Experts can’t yet tell whether future winters will favor the coronavirus or its competitors. Either way, scientists won’t know until they’ve collected several more years of evidence—“I would want at least a handful, like four or five,” Bansal said.

    Amassing those numbers is only getting tougher, though, as data streams dry up, Martin told me. Virus-surveillance systems are being dismantled; soon, hospitals and laboratories will no longer be required to share their COVID data with federal officials. Even independent trackers have sunsetted their regular updates. Especially abysmal are estimates of total infections, now that so many people are using only at-home tests, if they’re testing at all—and metrics such as hospitalization and death don’t fully reflect where and when the virus is moving, and which new variants may be on the rise.

    Shifts in long-term approaches to virus control could also upend this period of calm. As tests, treatments, and vaccines become privatized, as people lose Medicaid coverage, as community-outreach programs fight to stay afloat, the virus will find the country’s vulnerable pockets again. Those issues aren’t just about the coming months: COVID-vaccination rates among children remain worryingly low—a trend that could affect the virus’s transmission patterns for decades. And should the uptake of annual COVID shots continue on its current trajectory—worse, even, than America’s less-than-optimal flu vaccination rates—or dip even further down, rates of severe disease may begin another upward climb. Experts also remain concerned about the ambiguities around long COVID, whose risks remain ill-defined.

    We could get lucky. Maybe 2023 is the start of a bona fide post-pandemic era; maybe the past few months are genuinely offering a teaser trailer of decades to come. But even if that’s the case, it’s not a full comfort. COVID remains a leading cause of death in the United States, where the virus continues to kill about 200 to 250 people each day, many of them among the population’s most vulnerable and disenfranchised. It’s true that things are better than they were a couple of years ago. But in some ways, that’s a deeply unfair comparison to make. Deaths would have been higher when immunity was low; vaccines, tests, and treatments were scarce; and the virus was far less understood. “I would hope our standard for saying that we’ve succeeded and that we don’t need to do more is not Are we doing better than some of the highest-mortality years in history?” Bilinski told me. Perhaps the better question is why we’re settling for the status quo—a period of possible stability that may be less a relief and more a burden we’ve permanently stuck ourselves with.

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    Katherine J. Wu

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  • A Major Breed of Flu Has Gone Missing

    A Major Breed of Flu Has Gone Missing

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    In March 2020, Yamagata’s trail went cold.

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

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

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

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


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

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

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

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

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

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


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

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

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

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

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

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

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

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

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    Katherine J. Wu

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  • The Strongest Evidence Yet That an Animal Started the Pandemic

    The Strongest Evidence Yet That an Animal Started the Pandemic

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    For three years now, the debate over the origins of the coronavirus pandemic has ping-ponged between two big ideas: that SARS-CoV-2 spilled into human populations directly from a wild-animal source, and that the pathogen leaked from a lab. Through a swirl of data obfuscation by Chinese authorities and politicalization within the United States, and rampant speculation from all corners of the world, many scientists have stood by the notion that this outbreak—like most others—had purely natural roots. But that hypothesis has been missing a key piece of proof: genetic evidence from the Huanan Seafood Wholesale Market in Wuhan, China, showing that the virus had infected creatures for sale there.

    This week, an international team of virologists, genomicists, and evolutionary biologists may have finally found crucial data to help fill that knowledge gap. A new analysis of genetic sequences collected from the market shows that raccoon dogs being illegally sold at the venue could have been carrying and possibly shedding the virus at the end of 2019. It’s some of the strongest support yet, experts told me, that the pandemic began when SARS-CoV-2 hopped from animals into humans, rather than in an accident among scientists experimenting with viruses.

    “This really strengthens the case for a natural origin,” says Seema Lakdawala, a virologist at Emory who wasn’t involved in the research. Angela Rasmussen, a virologist involved in the research, told me, “This is a really strong indication that animals at the market were infected. There’s really no other explanation that makes any sense.”

    The findings won’t fully silence the entrenched voices on either side of the origins debate. But the new analysis may offer some of the clearest and most compelling evidence that the world will ever get in support of an animal origin for the virus that, in just over three years, has killed nearly 7 million people worldwide.

    Read: The lab leak will haunt us forever

    The genetic sequences were pulled out of swabs taken in and near market stalls around the pandemic’s start. They represent the first bits of raw data that researchers outside of China’s academic institutions and their direct collaborators have had access to. Late last week, the data were quietly posted by researchers affiliated with the country’s Center for Disease Control and Prevention, on an open-access genomic database called GISAID. By almost pure happenstance, scientists in Europe, North America, and Australia spotted the sequences, downloaded them, and began an analysis.

    The samples were already known to be positive for the coronavirus, and had been scrutinized before by the same group of Chinese researchers who uploaded the data to GISAID. But that prior analysis, released as a preprint publication in February 2022, asserted that “no animal host of SARS-CoV-2 can be deduced.” Any motes of coronavirus at the market, the study suggested, had most likely been chauffeured in by infected humans, rather than wild creatures for sale.

    The new analysis, led by Kristian Andersen, Edward Holmes, and Michael Worobey—three prominent researchers who have been looking into the virus’s roots—shows that that may not be the case. Within about half a day of downloading the data from GISAID, the trio and their collaborators discovered that several market samples that tested positive for SARS-CoV-2 were also coming back chock-full of animal genetic material—much of which was a match for the common raccoon dog. Because of how the samples were gathered, and because viruses can’t persist by themselves in the environment, the scientists think that their findings could indicate the presence of a coronavirus-infected raccoon dog in the spots where the swabs were taken. Unlike many of the other points of discussion that have been volleyed about in the origins debate, the genetic data are “tangible,” Alex Crits-Christoph, a computational biologist and one of the scientists who worked on the new analysis, told me. “And this is the species that everyone has been talking about.”

    Finding the genetic material of virus and mammal so closely co-mingled—enough to be extracted out of a single swab—isn’t perfect proof, Lakdawala told me. “It’s an important step, I’m not going to diminish that,” she said. Still, the evidence falls short of, say, isolating SARS-CoV-2 from a free-ranging raccoon dog or, even better, uncovering a viral sample swabbed from a mammal for sale at Huanan from the time of the outbreak’s onset. That would be the virological equivalent of catching a culprit red-handed. But “you can never go back in time and capture those animals,” says Gigi Gronvall, a senior scholar at the Johns Hopkins Center for Health Security. And to researchers’ knowledge, “raccoon dogs were not tested at the market and had likely been removed prior to the authorities coming in,” Andersen wrote to me in an email. He underscored that the findings, while an important addition, are still not “direct evidence of infected raccoon dogs at the market.”

    Still, the findings don’t stand alone. “Do I believe there were infected animals at the market? Yes, I do,” Andersen told me. “Does this new data add to that evidence base? Yes.” The new analysis builds on extensive previous research that points to the market as the source of the earliest major outbreak of SARS-CoV-2: Many of the earliest known COVID-19 cases of the pandemic were clustered roughly in the market’s vicinity. And the virus’s genetic material was found in many samples swabbed from carts and animal processing equipment at the venue, as well as parts of nearby infrastructure, such as storehouses, sewage wells, and water drains. Raccoon dogs, creatures commonly bred for sale in China, are also already known to be one of many mammal species that can easily catch and spread the coronavirus. All of this left one main hole in the puzzle to fill: clear-cut evidence that raccoon dogs and the virus were in the exact same spot at the market, close enough that the creatures might have been infected and, possibly, infectious. That’s what the new analysis provides. Think of it as finding the DNA of an investigation’s main suspect at the scene of the crime.

    The findings don’t rule out the possibility that other animals may have been carrying SARS-CoV-2 at Huanan. Raccoon dogs, if they were infected, may not even be the creatures who passed the pathogen on to us. Which means the search for the virus’s many wild hosts will need to plod on. “Do we know the intermediate host was raccoon dogs? No,” Andersen wrote to me, using the term for an animal that can ferry a pathogen between other species. “Is it high up on my list of potential hosts? Yes, but it’s definitely not the only one.”

    On Tuesday, the researchers presented their findings at a hastily scheduled meeting of the World Health Organization’s Scientific Advisory Group for the Origins of Novel Pathogens, which was also attended by several of the Chinese researchers responsible for the original analysis, according to multiple researchers who were not present but were briefed about it before and after by multiple people who were there.

    Shortly after the meeting, the Chinese team’s preprint went into review at a Nature Research journal—suggesting that a new version was being prepared for publication. (I reached out to the WHO for comment and will update the story when I have more information.)

    At this point, it’s still unclear why the sequences were posted to GISAID last week. They also vanished from the database shortly after appearing, without explanation. When I emailed George Gao, the former China CDC director-general and the lead author on the original Chinese analysis, asking for his team’s rationale, I didn’t immediately receive a response. Given what was in the GISAID data, it does seem that raccoon dogs could have been introduced into and clarified the origins narrative far sooner—at least a year ago, and likely more.

    China has, for years, been keen on pushing the narrative that the pandemic didn’t start within its borders. In early 2020, a Chinese official suggested that the novel coronavirus may have emerged from a U.S. Army lab in Maryland. The notion that a dangerous virus sprang out from wet-market mammals echoed the beginnings of the SARS-CoV-1 epidemic two decades ago—and this time, officials immediately shut down the Huanan market, and vehemently pushed back against assertions that live animals being sold illegally in the the country were to blame; a WHO investigation in March 2021 took the same line. “No verified reports of live mammals being sold around 2019 were found,” the report stated. But just three months later, in June 2021, a team of researchers published a study documenting tens of thousands of mammals for sale in wet markets in Wuhan between 2017 and late 2019, including at Huanan. The animals were kept in largely illegal, cramped, and unhygienic settings—conditions conducive to viral transmission—and among them were more than 1,000 raccoon dogs. Holmes himself had been at the market in 2014 and snapped a photo at Stall 29, clearly showing a raccoon dog in a cage; another set of images from the venue, captured by a local in December 2019 and later shared on Weibo, caught the animals on film as well—right around the time that the first recorded SARS-CoV-2 infections in humans occurred.

    And yet, Chinese researchers maintained their stance. As Jon Cohen reported for Science magazine last year, scientists from several of China’s largest academic institutions posted a preprint in September 2021 concluding that a massive nationwide survey of bats—the likeliest original source of the coronavirus before it jumped into an intermediate host, such as raccoon dogs, and then into us—had turned up no relatives of SARS-CoV-2. The implication, the team behind the paper asserted, was that relatives of the coronavirus were “extremely rare” in the region, making it unlikely that the pandemic had started there. The findings directly contradicted others showing that cousins of SARS-CoV-2 were indeed circulating in China’s bats. (Local bats have also been found to harbor viruses related to SARS-CoV-1.)

    The original Chinese analysis of the Huanan market swabs, from February 2022, also stuck with China’s party line on the pandemic. One of the report’s graphs suggested that viral material at the market had been mixed up with genetic material of multiple animal species—a data trail that should have led to further inquiry or conclusions, but which the Chinese researchers appear to have ignored. Their report noted only humans as being linked to SARS-CoV-2, stating that its findings “highly” suggested that any viral material at the market came from people (at least one of whom, presumably, picked it up elsewhere and ferried it into the venue). The Huanan market, the study’s authors wrote, “might have acted as an amplifier” for the epidemic. But “more work involving international coordination” would be needed to suss out the “real origins of SARS-CoV-2.”

    The wording of that report baffled many scientists in Europe, North America, and Australia, several of whom had, almost exactly 24 hours after the release of the China CDC preprint, published early versions of their own studies, concluding that the Huanan market was the pandemic’s probable epicenter—and that SARS-CoV-2 might have made its hop into humans from the venue twice at the end of 2019. Itching to get their hands on China CDC’s raw data, some of the researchers took to regularly trawling GISAID, occasionally at odd hours—the only reason that Florence Débarre, an evolutionary biologist at the French National Centre for Scientific Research, spotted the sequences pinging onto the server late last Thursday night with no warning or fanfare.

    Within hours of downloading the data and starting their own analysis, the researchers found their suspicions confirmed. Several surfaces in and around one stall at the market, including a cart and a defeathering machine, produced virus-positive samples that also contained genetic material from raccoon dogs—in a couple of cases, at higher concentrations than of human genomes. It was Stall 29—the same spot where Holmes had snapped the photo of the raccoon dog, nearly a decade before.

    Slam-dunk evidence for a raccoon-dog host—or another animal—could still emerge. In the hunt for the wild source of MERS, another coronavirus that caused a deadly outbreak in 2012, researchers were eventually able to identify the pathogen in camels, which are thought to have caught their initial infection from bats—and which still harbor the virus today; a similar story has played out for Nipah virus, which hopscotched from bats to pigs to us.

    Read: Bird flu leaves the world with an existential choice

    Proof of that caliber, though, may never turn up for SARS-CoV-2. (Nailing wild origins is rarely simple: Despite a years-long search, the wild host for Ebola still has not been definitively pinpointed.) Which leaves just enough ambiguity to keep debate about the pandemic’s origins running, potentially indefinitely. Skeptics will likely be eager to poke holes in the team’s new findings—pointing out, for instance, that it’s technically possible for genetic material from viruses and animals to end up sloshed together in the environment even if an infection didn’t take place. Maybe an infected human visited the market and inadvertently deposited viral RNA near an animal’s crate.

    But an infected animal, with no third-party contamination, still seems by far the most plausible explanation for the samples’ genetic contents, several experts told me; other scenarios require contortions of logic and, more important, additional proof. Even prior to the reveal of the new data, Gronvall told me, “I think the evidence is actually more sturdy for COVID than it is for many others.” The strength of the data might even, in at least one way, best what’s available for SARS-CoV-1: Although scientists have isolated SARS-CoV-1-like viruses from a wet-market-traded mammal host, the palm civet, those samples were taken months after the outbreak began—and the viral variants found weren’t exactly identical to the ones in human patients. The versions of SARS-CoV-2 tugged out of several Huanan-market samples, meanwhile, are a dead ringer for the ones that sickened humans with COVID early on.

    The debate over SARS-CoV-2’s origins has raged for nearly as long as the pandemic itself—outlasting lockdowns, widespread masking, even the first version of the COVID vaccines. And as long as there is murkiness to cling to, it may never fully resolve. While evidence for an animal spillover has mounted over time, so too have questions about the possibility that the virus escaped from a laboratory. When President Biden asked the U.S. intelligence community to review the matter, four government agencies and the National Intelligence Council pointed to a natural origin, while two others guessed that it was a lab leak. (None of these assessments were made with high confidence; a bill passed in both the House and Senate would, 90 days after it becomes a law, require the Biden administration to declassify underlying intelligence.)

    If this new level of scientific evidence does conclusively tip the origins debate toward the animal route, it will be, in one way, a major letdown. It will mean that SARS-CoV-2 breached our borders because we once again mismanaged our relationship with wildlife—that we failed to prevent this epidemic for the same reason we failed, and could fail again, to prevent so many of the rest.

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    Katherine J. Wu

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  • The COVID Question That Will Take Decades to Answer

    The COVID Question That Will Take Decades to Answer

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    To be a newborn in the year 2023—and, almost certainly, every year that follows—means emerging into a world where the coronavirus is ubiquitous. Babies might not meet the virus in the first week or month of life, but soon enough, SARS-CoV-2 will find them. “For anyone born into this world, it’s not going to take a lot of time for them to become infected,” maybe a year, maybe two, says Katia Koelle, a virologist and infectious-disease modeler at Emory University. Beyond a shadow of a doubt, this virus will be one of the very first serious pathogens that today’s infants—and all future infants—meet.

    Three years into the coronavirus pandemic, these babies are on the leading edge of a generational turnover that will define the rest of our relationship with SARS-CoV-2. They and their slightly older peers are slated to be the first humans who may still be alive when COVID-19 truly hits a new turning point: when almost everyone on Earth has acquired a degree of immunity to the virus as a very young child.

    That future crossroads might not sound all that different from where the world is currently. With vaccines now common in most countries and the virus so transmissible, a significant majority of people have some degree of immunity. And in recent months, the world has begun to witness the consequences of that shift. The flux of COVID cases and hospitalizations in most countries seems to be stabilizing into a seasonal-ish sine wave; disease has gotten, on average, less severe, and long COVID seems to be somewhat less likely among those who have recently gotten shots. Even the virus’s evolution seems to be plodding, making minor tweaks to its genetic code, rather than major changes that require another Greek-letter name.

    But today’s status quo may be more of a layover than a final destination in our journey toward COVID’s final form. Against SARS-CoV-2, most little kids have fared reasonably well. And as more babies have been born into a SARS-CoV-2-ridden world, the average age of first exposure to this coronavirus has been steadily dropping—a trend that could continue to massage COVID-19 into a milder disease. Eventually, the expectation is that the illness will reach a stable nadir, at which point it may truly be “another common cold,” says Rustom Antia, an infectious-disease modeler at Emory.

    The full outcome of this living experiment, though, won’t be clear for decades—well after the billions of people who encountered the coronavirus for the first time in adulthood are long gone. The experiences that today’s youngest children have with the virus are only just beginning to shape what it will mean to have COVID throughout a lifetime, when we all coexist with it from birth to death as a matter of course.


    At the beginning of SARS-CoV-2’s global tear, the coronavirus was eager to infect all of us, and we had no immunity to rebuff its attempts. But vulnerability wasn’t just about immune defenses: Age, too, has turned out to be key to resilience. Much of the horror of the disease could be traced to having not only a large population that lacked protection against the virus—but a large adult population that lacked protection against the virus. Had the entire world been made up of grade-schoolers when the pandemic arrived, “I don’t think it would have been nearly as severe,” says Juliet Pulliam, an infectious-disease modeler at Stellenbosch University, in South Africa.

    Across several viral diseases—polio, chicken pox, mumps, SARS, measles, and more—getting sick as an adult is notably more dangerous than as a kid, a trend that’s typically exacerbated when people don’t have any vaccinations or infections to those pathogens in their rearview. The manageable infections that strike toddlers and grade-schoolers may turn serious when they first manifest at older ages, landing people in the hospital with pneumonia, brain swelling, even blindness, and eventually killing some. When scientists plot mortality data by age, many curves bend into “a pretty striking J shape,” says Dylan Morris, an infectious-disease modeler at UCLA.

    The reason for that age differential isn’t always clear. Some of kids’ resilience probably comes from having a young, spry body, far less likely to be burdened with chronic medical conditions that raise severe disease risk. But the quick-wittedness of the young immune system is also likely playing a role. Several studies have found that children are much better at marshaling hordes of interferon—an immune molecule that armors cells against viruses—and may harbor larger, more efficient cavalries of infected-cell-annihilating T cells. That performance peaks sometime around grade school or middle school, says Janet Chou, a pediatrician at Boston Children’s Hospital. After that, our molecular defenses begin a rapid tumble, growing progressively creakier, clumsier, sluggish, and likelier to launch misguided attacks against the tissues that house them. By the time we’re deep into adulthood, our immune systems are no longer sprightly, or terribly well calibrated. When we get sick, our bodies end up rife with inflammation. And our immune cells, weary and depleted, are far less unable to fight off the pathogens they once so easily trounced.

    Whatever the explanations, children are far less likely to experience serious symptoms, or to end up in the hospital or the ICU after being infected with SARS-CoV-2. Long COVID, too, seems to be less prevalent in younger cohorts, says Alexandra Yonts, a pediatrician at Children’s National Hospital. And although some children still develop MIS-C, a rare and dangerous inflammatory condition that can appear weeks after they catch the virus, the condition “seems to have dissipated” as the pandemic has worn on, says Betsy Herold, the chief of pediatric infectious disease at the Children’s Hospital at Montefiore, in the Bronx.

    Should those patterns hold, and as the age of first exposure continues to fall, COVID is likely to become less intense. The relative mildness of childhood encounters with the virus could mean that almost everyone’s first infection—which tends, on average, to be more severe than the ones that immediately follow—could rank low in intensity, setting a sort of ceiling for subsequent bouts. That might make concentrating first encounters “in the younger age group actually a good thing,” says Ruian Ke, an infectious-disease modeler at Los Alamos National Laboratory.

    COVID will likely remain capable of killing, hospitalizing, and chronically debilitating a subset of adults and kids alike. But the hope, experts told me, is that the proportion of individuals who face the worst outcomes will continue to drop. That may be what happened in the aftermath of the 1918 flu pandemic, Antia, of Emory, told me: That strain of the virus stuck around, but never caused the same devastation again. Some researchers suspect that something similar may have even played out with another human coronavirus, OC43: After sparking a devastating pandemic in the 19th century, it’s possible that the virus no longer managed to wreak much more havoc than a common cold in a population that had almost universally encountered it early in life.


    Such a fate for COVID, though, isn’t a guarantee. The virus’s propensity to linger in the body’s nooks and crannies, sometimes causing symptoms that last many months or years, could make it an outlier among its coronaviral kin, says Melody Zeng, an immunologist at Cornell University. And even if the disease is likely to get better than what it is now, that is not a very high bar to clear.

    Some small subset of the population will always be naive to the virus—and it’s not exactly a comfort that in the future, that cohort will almost exclusively be composed of our kids. Pediatric immune systems are robust, UCLA’s Morris told me. But “robust is not the same as infallible.” Since the start of the pandemic, more than 2,000 Americans under the age of 18 have died from COVID—a small fraction of total deaths, but enough to make the disease a leading cause of death for children in the U.S. MIS-C and long COVID may not be common, but their consequences are no less devastating for the children who experience them. Some risks are especially concentrated among our youngest kids, under the age 5, whose immune defenses are still revving up, making them more vulnerable than their slightly older peers. There’s especially little to safeguard newborns just under six months, who aren’t yet eligible for most vaccines—including COVID shots—and who are rapidly losing the antibody-based protection passed down from their mothers while they were in the womb.

    A younger average age of first infection will also probably increase the total number of exposures people have to SARS-CoV-2 in a typical lifetime—each instance carrying some risk of severe or chronic disease. Ke worries the cumulative toll that this repetition could exact: Studies have shown that each subsequent tussle with the virus has the potential to further erode the functioning or structural integrity of organs throughout the body, raising the chances of chronic damage. There’s no telling how many encounters might push an individual past a healthy tipping point.

    Racking up exposures also won’t always bode well for the later chapters of these children’s lives. Decades from now, nearly everyone will have banked plenty of encounters with SARS-CoV-2 by the time they reach advanced age, Chou, from Boston Children’s Hospital, told me. But the virus will also continue to change its appearance, and occasionally escape the immunity that some people built up as kids. Even absent those evasions, as their immune systems wither, many older people may not be able to leverage past experiences with the disease to much benefit. The American experience with influenza is telling. Despite a lifetime of infections and available vaccines, tens of thousands of people typically die annually of the disease in the United States alone, says Ofer Levy, the director of the Precision Vaccines Program at Boston Children’s Hospital. So even with the expected COVID softening, “I don’t think we’re going to reach a point where it’s, Oh well, tra-la-la,” Levy told me. And the protection that immunity offers can have caveats: Decades of research with influenza suggest that immune systems can get a bit hung up on the first versions of a virus that they see, biasing them against mounting strong attacks against other strains; SARS-CoV-2 now seems to be following that pattern. Depending on the coronavirus variants that kids encounter first, their responses and vulnerability to future bouts of illness may vary, says Scott Hensley, an immunologist at the University of Pennsylvania.

    Early vaccinations—that ideally target multiple versions of SARS-CoV-2—could make a big difference in reducing just about every bad outcome the virus threatens. Severe disease, long COVID, and transmission to other children and vulnerable adults all would likely be “reduced, prevented, and avoided,” Chou told me. But that’s only if very young kids are taking those shots, which, right now, isn’t at all the case. Nor are they necessarily getting protection passed down during gestation or early life from their mothers, because many adults are not up to date on COVID shots.

    Some of these issues could, in theory, end up moot. A hundred or so years from now, COVID could simply be another common cold, indistinguishable in practice from any other. But Morris points out that this reality, too, wouldn’t fully spare us. “When we bother to look at the burden of the other human coronaviruses, the ones who have been with us for ages? In the elderly, it’s real,” he told me. One study found that a nursing-home outbreak of OC43—the purported former pandemic coronavirus—carried an 8 percent fatality rate; another, caused by NL63, killed three out of the 20 people who caught it in a long-term-care facility in 2017. These and other “mild” respiratory viruses also continue to pose a threat to people of any age who are immunocompromised.

    SARS-CoV-2 doesn’t need to follow in those footsteps. It’s the only human coronavirus against which we have vaccines—which makes the true best-case scenario one in which it ends up even milder than a common cold, because we proactively protect against it. Disease would not need to be as inevitable; the vaccine, rather than the virus, could be the first bit of intel on the disease that kids receive. Tomorrow’s children probably won’t live in a COVID-free world. But they could at least be spared many of the burdens we’re carrying now.

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    Katherine J. Wu

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  • We Have a Mink Problem

    We Have a Mink Problem

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    Bird flu, at this point, is somewhat of a misnomer. The virus, which primarily infects birds, is circulating uncontrolled around much of the world, devastating not just birds but wide swaths of the animal kingdom. Foxes, bobcats, and pigs have fallen ill. Grizzly bears have gone blind. Sea creatures, including seals and sea lions, have died in great numbers.

    But none of the sickened animals has raised as much concern as mink. In October, a bird-flu outbreak erupted at a Spanish mink farm, killing thousands of the animals before the rest were culled. It later became clear that the virus had spread between the animals, picking up a mutation that helped it thrive in mammals. It was likely the first time that mammal-to-mammal spread drove a huge outbreak of bird flu. Because mink are known to spread certain viruses to humans, the fear was that the disease could jump from mink to people. No humans got sick from the outbreak in Spain, but other infections have spread from mink to humans before: In 2020, COVID outbreaks on Danish mink farms led to new mink-related variants that spread to a small number of humans.

    As mammals ourselves, we have good reason to be concerned. Outbreaks on crowded mink farms are an ideal scenario for bird flu to mutate. If, in doing so, it picks up the ability to spread between humans, it could potentially start another global pandemic. “There are many reasons to be concerned about mink,” Tom Peacock, a flu researcher at Imperial College London, told me. Right now, mink are a problem we can’t afford to ignore.

    For two animals with very different body types, mink and humans have some unusual similarities. Research suggests that we share similar receptors for COVID, bird flu, and human flu, through which these viruses can gain entry into our bodies. The numerous COVID outbreaks on mink farms during the early pandemic, and the bird-flu outbreak in Spain, gravely illustrate this point. It’s “not surprising” that mink can get these respiratory diseases, James Lowe, a veterinary-medicine professor at the University of Illinois at Urbana-Champaign, told me. Mink are closely related to ferrets, which are so well known for their susceptibility to human flu that they’re the go-to model for flu research.

    Mink wouldn’t get sick as often, and wouldn’t be as big an issue for humans, if we didn’t keep farming them for fur in the perfect conditions for outbreaks. Many barns used to raise mink are partially open-air, making it easy for infected wild birds to come in contact with the animals, sharing not only air but potentially food. Mink farms are also notoriously cramped: The Spanish farm, for example, kept tens of thousands of mink in about 30 barns. Viral transmission would be all but guaranteed in those conditions, but the animals are especially vulnerable. Because mink are normally solitary creatures, they face significant stress in packed barns, which may further predispose them to disease, Angela Bosco-Lauth, a biomedical-sciences professor at Colorado State University, told me. And because they’re often inbred so their coats look alike, an entire population may share a similar genetic susceptibility to disease. The frequency of outbreaks among mink, Bosco-Lauth said, “may actually have less to do with the animals and more to do with the fact that we raise them in the same way … we would an intensive cattle farm or chickens.”

    So far, there’s no evidence that mink from the Spanish farm spread bird flu to humans: None of the workers tested positive for the virus, and since then, no other mink farms have reported outbreaks. “We’re just not very susceptible” to bird flu, Lowe said. Our bird-flu receptors are tucked deep in our lungs, but when we’re exposed, most of the virus gets caught in the nose, throat, and other parts of the upper respiratory tract. This is why bird-flu infection is less common in people but is often pneumonia-level severe when it does happen. Indeed, a few humans have gotten sick and died from bird flu in the 27 years that the current strain of bird flu, known as H5N1, has circulated. This month, a girl in Cambodia died from the virus after potentially encountering a sick bird. The more virus circulating in an environment, the higher the chances a person will get infected. “It’s a dose thing,” Lowe said.

    But our susceptibility to bird flu could change. Another mink outbreak would give the virus more opportunities to keep mutating. The worry is that this could create a new variant that’s better at binding to the human flu receptors in our upper respiratory tract, Stephanie Seifert, a professor at Washington State University who studies zoonotic pathogens, told me. If the virus gains the ability to infect the nose and throat, Peacock, at Imperial College London, said, it would be better at spreading. Those mutations “would worry us the most.” Fortunately, the mutations that arose on the Spanish mink farm “were not as bad as many of us worried about,” he added, “but that doesn’t mean that the next time this happens, this will also be the case.”

    Because mink carry the receptors for both bird flu and human flu, they could serve as “mixing vessels” for the viruses to combine, researchers wrote in 2021. (Ferrets, pigs, and humans share this quality too.) Through a process called reassortment, flu viruses can swap segments of their genome, resulting in a kind of Frankenstein pathogen. Although viruses remixed in this way aren’t necessarily more dangerous, they could be, and that’s not a risk worth taking. “The previous three influenza pandemics all arose due to mixing between avian and human influenza viruses,” Peacock said.

    While there are good reasons to be concerned about mink, it is hard to gauge just how concerned we should be—especially given what we still don’t know about this changing virus. After the death of the young girl in Cambodia, the World Health Organization called the global bird flu situation “worrying,” while the CDC maintains that the risk to the public is low. Lowe said “it’s certainly not very risky” that bird flu will spill over into humans, but is worth keeping an eye on. H5N1 bird flu is not new, he added, and it hasn’t affected people en masse yet. But the virus has already changed in ways that make it better at infecting wild birds, and as it spreads in the wild, it may continue to change to better infect mammals, including humans. “We don’t understand enough to make strong predictions of public-health risk,” Jonathan Runstadler, an infectious-diseases professor at Tufts University, told me.

    As bird flu continues to spread among birds and in domestic and wild animal populations, it will only become harder to control. The virus, formally seasonal, is already present year-round in parts of Europe and Asia, and it is poised to do the same in the Americas. Breaking the chain of transmission is vital to preventing another pandemic. An important step is to avoid situations where humans, mink, or any other animal could be infected with both human and bird flu at the same time.

    Since the COVID outbreaks, mink farms have generally beefed up their biosecurity: Farm workers are often required to wear masks and protective gear, such as disposable overalls. To limit the risk to mink—and other susceptible hosts—farms need to reduce their size and density, reduce contact between mink and wild birds, and monitor the virus, Runstadler said. Some nations, including Mexico, Ecuador, have recently embraced bird-flu vaccines for poultry in light of the outbreaks. H5N1 vaccines are also available for humans, though they aren’t readily available.  Still, one of the most obvious options is to shut mink farms down. “We probably should have done that after SARS-CoV-2,” Bosco-Lauth, at Colorado State, said. Doing so is controversial, however, because the global mink industry is valuable, with a huge market in China. Denmark, which produces up to 40 percent of the world’s mink pelts, temporarily banned mink breeding in 2020 after a spate of COVID outbreaks, but the ban expired last month, and farms are returning, albeit in a limited capacity.

    But mink  are far from the only animal that poses a bird-flu risk to humans. “Frankly, with what we’re seeing with other wildlife species, there really aren’t any mammals that I would discount at this point in time,” Bosco-Lauth said. Any mammal species repeatedly infected by the virus is a potential risk, including marine mammals, such as seals. But we should be most concerned about the ones humans frequently come into close contact with, especially animals that are raised in high density, such as pigs, Runstadler said. This doesn’t pose just a human public-health concern, he said, but the potential for “ecological disruption.” Bird flu can be a devastating disease for wildlife, killing animals swiftly and without mercy.

    Whether bird flu makes the jump into humans, it isn’t the last virus that will threaten us—or mink. The era we live in has become known as the “Pandemicene,” as my colleague Ed Yong has called it, one defined by the regular spillover of viruses into humans, caused by our disruption of the normal trajectories of viral movement in nature. Mink may never pass bird flu to us. But that doesn’t mean they won’t be a risk the next time a novel influenza or coronavirus comes around. Doing nothing about mink essentially means choosing luck as a public-health strategy. Sooner or later, it will run out.

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    Yasmin Tayag

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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    Katherine J. Wu

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  • Are Colds Really Worse, or Are We All Just Weak Babies Now?

    Are Colds Really Worse, or Are We All Just Weak Babies Now?

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    For the past few weeks, my daily existence has been scored by the melodies of late winter: the drip of melting ice, the soft rustling of freshly sprouted leaves—and, of course, the nonstop racket of sneezes and coughs.

    The lobby of my apartment building is alive with the sounds of sniffles and throats being cleared. Every time I walk down the street, I’m treated to the sight of watery eyes and red noses. Even my work Slack is rife with illness emoji, and the telltale pings of miserable colleagues asking each other why they feel like absolute garbage. “It’s not COVID,” they say. “I tested, like, a million times.” Something else, they insist, is making them feel like a stuffed and cooked goose.

    That something else might be the once-overlooked common cold. After three years of largely being punted out of the limelight, a glut of airway pathogens—among them, adenovirus, RSV, metapneumovirus, parainfluenza, common-cold coronaviruses, and rhinoviruses galore—are awfully common again. And they’re really laying some people out. The good news is that there’s no evidence that colds are actually, objectively worse now than they were before the pandemic started. The less-good news is that after years of respite from a bunch of viral nuisances, a lot of us have forgotten that colds can be a real drag.

    Once upon a time—before 2020, to be precise—most of us were very, very used to colds. Every year, adults, on average, catch two to three of the more than 200 viral strains that are known to cause the illnesses; young kids may contract half a dozen or more as they toddle in and out of the germ incubators that we call “day cares” and “schools.” The sicknesses are especially common during the winter months, when many viruses thrive amid cooler temps, and people tend to flock indoors to exchange gifts and breath. When the pandemic began, masks and distancing drove several of those microbes into hiding—but as mitigations have eased in the time since, they’ve begun their slow creep back.

    For the majority of people, that’s not really a big deal. Common-cold symptoms tend to be pretty mild and usually resolve on their own after a few days of nuisance. The virus infiltrates the nose and throat, but isn’t able to do much damage and gets quickly swept out. Some people may not even notice they’re infected at all, or may mistake the illness for an allergy—snottiness, drippiness, and not much more. Most of us know the drill: “Sometimes, it’s just congestion for a few days and feeling a bit tired for a while, but otherwise you’ll be just fine,” says Emily Landon, an infectious-disease physician at the University of Chicago. As a culture, we’ve long been in the habit of dismissing these symptoms as just a cold, not enough of an inconvenience to skip work or school, or to put on a mask. (Spoiler: The experts I spoke with were adamant that we all really should be doing those things when we have a cold.)

    The general infectious-disease dogma has always been that colds are a big nothing, at least compared with the flu. But gentler than the flu is not saying much. The flu is a legitimately dangerous disease that hospitalizes hundreds of thousands of Americans each year, and, like COVID, can sometimes saddle people with long-term symptoms. Even if colds are generally less severe, people can end up totally clobbered by headaches, exhaustion, and a burning sore throat; their eyes will tear up; their sinuses will clog; they’ll wake up feeling like they’ve swallowed serrated razor blades, or like their heads have been pumped full of fast-hardening concrete. It’s also common for cold symptoms to stretch out beyond a week, occasionally even two; coughs, especially, can linger long after the runny nose and headache resolve. At their worst, colds can lead to serious complications, especially in the very young, very old, and immunocompromised. Sometimes, cold sufferers end up catching a bacterial infection on top of their viral disease, a one-two punch that can warrant a trip to the ER. “The fact of the matter is, it’s pretty miserable to have a cold,” Landon told me. “And that’s how it’s always been.”

    As far as experts can tell, the average severity of cold symptoms hasn’t changed. “It’s about perception,” says Jasmine Marcelin, an infectious-disease physician at the University of Nebraska Medical Center. After skipping colds for several years, “experiencing them now feels worse than usual,” she told me. Frankly, this was sort of a problem even before COVID came onto the scene. “Every year, I have patients who call me with ‘the worst cold they’ve ever had,’” Landon told me. “And it’s basically the same thing they had last year.” Now, though, the catastrophizing might be even worse, especially since pandemic-brain started prompting people to scrutinize every sniffle and cough.

    There’s still a chance that some colds this season might be a shade more unpleasant than usual. Many people falling sick right now are just coming off of bouts with COVID, flu, or RSV, each of which infected Americans (especially kids) by the millions this past fall and winter. Their already damaged tissues may not fare as well against another onslaught from a cold-causing virus.

    It’s also possible that immunity, or lack thereof, could be playing a small role. Many people are now getting their first colds in three-plus years, which means population-level vulnerability might be higher than it normally is this time of year, speeding the rate at which viruses spread and potentially making some infections more gnarly than they’d otherwise be. But higher-than-usual susceptibility seems unlikely to be driving uglier symptoms en masse, says Roby Bhattacharyya, an infectious-disease physician and microbiologist at Massachusetts General Hospital. Not all cold-causing viruses leave behind good immunity—but many of those that do are thought to prompt the body to mount relatively durable defenses against truly severe infections, lasting several years or more.

    Plus, for a lot of viruses going around right now, the immunity question is largely moot, Landon told me. So many different pathogens cause colds that a recent exposure to one is unlikely to do much against the next. A person could catch half a dozen colds in a five-year time frame and not even encounter the same type of virus twice.

    It’s also worth noting that what some people are categorizing as the worst cold they’ve ever had might actually be a far more menacing virus, such as SARS-CoV-2 or a flu virus. At-home rapid tests for the coronavirus often churn out false-negative results in the early days of infection, even after symptoms start. And although the flu can sometimes be distinguished from a cold by its symptoms, they’re often pretty similar. The illnesses can only be definitively diagnosed with a test, which can be difficult to come by.

    The pandemic has steered our perception of illness into a false binary: Oh no, it’s COVID or Phew, it’s not. COVID is undoubtedly still more serious than a run-of-the-mill cold—more likely to spark severe disease or chronic, debilitating symptoms that can last months or years. But the range of severity between them overlaps more than the binary implies. Plus, Marcelin points out, what truly is “just” a cold for one person might be an awful, weeks-long slog for someone else, or worse—which is why, no matter what’s turning your face into a snot factory, it’s still important to keep your germs to yourself. The current outbreak of colds may not be any more severe than usual. But there’s no need to make it bigger than it needs to be.

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    Katherine J. Wu

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  • Get Used to Expensive Eggs

    Get Used to Expensive Eggs

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    Over the past week, my breakfast routine has been scrambled. I have had overnight oats, beans on sourdough, corned-beef hash and fried rice, and, on a particularly weird morning, leftover cream-of-broccoli soup. Under normal circumstances, I would be eating eggs. But right now, I’m in hoarding mode, jealously guarding the four that remain from a carton purchased indignantly for six dollars. For that price—50 damn cents each!—my daily sunny-side-up eggs will have to wait. The perfect moment beckons: Maybe a toasted slab of brioche will call for a luxurious soft scramble, or maybe I will cave to a powerful craving for an egg-salad sandwich.

    Eggs, that quintessential cheap food, have gotten very, very expensive in the United States. In December, the average price for a dozen eggs in U.S. cities hit an all-time high of $4.25, up from $1.78 a year earlier. Though the worst now seems to be behind us, there’s still a way to go before consumer prices hit reasonable levels, and now Americans are starting to crack. Online, the shortage has recently hatched endless memes: In some posts, people pretend to portion out eggs in plastic baggies, like drug dealers (Pablo Eggscobar, anyone?); another recurring bit suggests painting potatoes to hunt at Easter. The high prices have even led to egg smuggling, and raised the profile of “rent-a-chicken” services where customers can borrow hens, chicken feed, and a coop for a couple hundred bucks.

    Surging egg prices are partly a familiar story of pandemic-era inflation. Producing eggs costs more because fuel, transportation, feed, and packaging are more expensive now, Jada Thompson, an agricultural economist at the University of Arkansas, told me. And it doesn’t help that there are no great substitutes for eggs. But a big reason that prices are so high right now is because of the avian flu—a virus that infects many types of birds and is deadly for some. Right now, we’re facing the worst-ever wave in the U.S., which has decimated chicken flocks and dented America’s egg inventory. Just over the past year, more than 57 million birds have died from the flu. Some much-needed relief from sky-high egg prices is likely coming, but don’t break out the soufflé pans yet. All signs suggest that avian flu is here to stay. If such rampant spread of the virus continues, “these costs are not going to come down to pre-2022 levels,” Thompson told me. Cheap eggs may soon become a thing of the past.

    This isn’t the first time American egg producers have encountered the avian flu, but dealing with it is still a challenge. For one thing, the virus keeps changing. It has long infected but not killed waterfowl and shorebirds, such as ducks and geese, but by 1996, it had mutated into the “highly pathogenic” H5N1, a poultry-killing strain that is named for the nasty versions of its “H” and “N” proteins. (They form spikes on the virus’s surface—sound familiar?) In 2014 and 2015, H5N1 ignited a terrible outbreak of avian flu, which gave U.S. poultry farmers their first taste of just how bad egg shortages could get.

    But this outbreak is like nothing we’ve seen before. The strain of avian flu that’s behind this wave is indeed new, and in the U.S. the virus has been circulating for a full year now—far longer than during the last big outbreak. The virus has become “host-adapted,” meaning that it can infect its natural hosts without killing them, so wild waterfowl are ruthlessly efficient at spreading the virus to chickens, Richard Webby, the director of the World Health Organization Collaborating Center for Studies on the Ecology of Influenza in Animals and Birds, told me.

    Many of these wild birds are migratory, and during their long journeys between Canada and South America, they descend on waterways and poop virus from the sky over poultry farms. Chickens stand no chance: The fleshy flaps on their heads may turn blue, their eyes and neck may swell, and, in rare instances, paralysis occurs. An entire poultry flock can be wiped out in 48 hours. Death is swift and vicious.

    Everything about this current wave has aligned to put a serious dent in our egg supply. Most eggs in the United States are hatched in jam-packed industrial egg farms, where transmission is next to impossible to stop, so the go-to move when the flu is detected is to “depopulate,” the preferred industry term for killing all of the birds. Without such a brutal tactic, Bryan Richards, the emerging-disease coordinator at the U.S. Geological Survey, told me, the current wave would be much worse.

    But this strategy also means fewer eggs, at least until new chicks grow into hens. That takes about six months, so there just haven’t been enough hens lately—especially for all the holiday baking people wanted to do, Thompson said. By the end of 2022, U.S. egg inventory was 29 percent lower than it had been at the beginning of the year. The chicken supply, in contrast, is robust because avian flu tends to affect older birds, like egg layers, Thompson said; at six to eight weeks old, the birds we eat, known as broilers, are not as susceptible. Also, she added, wild-bird migration pathways are not as concentrated in the Southeast, where most broiler production happens.

    Egg eaters should be able to return to their normal breakfast routines soon enough. New hens are now replenishing the U.S. egg supply—while waterfowl are wintering in the warmer climes of South America rather than lingering in the U.S. Since the holidays, “the price paid to the farmers for eggs has been decreasing rapidly, and usually, in time, the consumer price follows,” Maro Ibarburu, a business analyst at Iowa State University’s Egg Industry Center, told me.

    Still, going forward, it may be worth rethinking our relationship with eggs. There’s no guarantee that eggs will go back to being one the cheapest and most nutritious foods. When the weather warms, the birds will return, and “it’s highly likely that upon spring migration, we could see yet another wave,” said Richards. Europe, which experienced the H5N1 wave about six months before the Americas did, offers a glimpse of the future. “They went from being in a situation where the virus would come and go to a position where essentially it came and stayed,” Webby told me. If we’re lucky, though, birds will develop natural immunity to the virus, making it harder to spread, or the U.S. could start vaccinating poultry against the flu, which the country has so far been reluctant to do.

    Omelets aside, curbing the spread of avian flu is in our best interest, not just to help prevent $6 egg cartons, but also to avoid a much scarier possibility—the virus spilling over and infecting people. All viruses from the influenza-A family have an avian origin, noted Webby; a chilling example is the H1N1 strain behind the 1918 flu pandemic. Fortunately, though some people have been infected with H5N1, very few cases of human-to-human spread have been documented. But continued transmission, over a long enough period, could change that. The fact that the virus has recently jumped from birds into mammals, such as seals and bears, and has spread among mink, is troubling because that means that it is evolving to infect species that are more closely related to us. “The risk of this particular virus [spreading among humans] as it is now is low, but the consequences are potentially high,” said Webby. “If there is a flu virus that I don’t want to catch, this one would be it.”

    More than anything, the egg shortage is a reminder that the availability of food is not something we can take for granted going forward. Shortages of staple goods seem to be striking with more regularity, not only due to pandemic-related broken supply chains and inflation but also to animal and plant disease. In 2019, swine fever decimated China’s pork supply; the ongoing lettuce shortage, which rapper Cardi B bemoaned earlier this month, is due to both a plant virus and a soil disease. Last September, California citrus growers detected a virus known to reduce crop yields. By creating cozier conditions for some diseases, climate change is expected to raise risk of infection for both animals and plants. And as COVID has illustrated, any situation in which different species are forced into abnormally close quarters with one another is likely to encourage the spread of disease.

    Getting used to intermittent shortages of staple foods such as eggs and lettuce will in all likelihood become a normal part of meal planning, barring some sort of huge shift away from industrial farming and its propensity for fostering disease. These farms are a major reason that these foods are so inexpensive and widely available in the first place; if cheap eggs seemed too good to be true, it’s because they were. Besides, there are always alternatives: May I suggest cream-of-broccoli soup?

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    Yasmin Tayag

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  • Is COVID Immunity Hung Up on Old Variants?

    Is COVID Immunity Hung Up on Old Variants?

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    In the two-plus years that COVID vaccines have been available in America, the basic recipe has changed just once. The virus, meanwhile, has belched out five variants concerning enough to earn their own Greek-letter names, followed by a menagerie of weirdly monikered Omicron subvariants, each seeming to spread faster than the last. Vaccines, which take months to reformulate, just can’t keep up with a virus that seems to reinvent itself by the week.

    But SARS-CoV-2’s evolutionary sprint might not be the only reason that immunity can get bogged down in the past. The body seems to fixate on the first version of the virus that it encountered, either through injection or infection—a preoccupation with the past that researchers call “original antigenic sin,” and that may leave us with defenses that are poorly tailored to circulating variants. In recent months, some experts have begun to worry that this “sin” might now be undermining updated vaccines. At an extreme, the thinking goes, people may not get much protection from a COVID shot that is a perfect match for the viral variant du jour.

    Recent data hint at this possibility. Past brushes with the virus or the original vaccine seem to mold, or even muffle, people’s reactions to bivalent shots—“I have no doubt about that,” Jenna Guthmiller, an immunologist at the University of Colorado School of Medicine, told me. The immune system just doesn’t make Omicron-focused antibodies in the quantity or quality it probably would have had it seen the updated jabs first. But there’s also an upside to this stubbornness that we could not live without, says Katelyn Gostic, an immunologist and infectious-disease modeler who has studied the phenomenon with flu. Original antigenic sin is the reason repeat infections, on average, get milder over time, and the oomph that enables vaccines to work as well as they do. “It’s a fundamental part,” Gostic told me, “of being able to create immunological memory.”

    This is not just basic biology. The body’s powerful first impressions of this coronavirus can and should influence how, when, and how often we revaccinate against it, and with what. Better understanding of the degree to which these impressions linger could also help scientists figure out why people are (or are not) fighting off the latest variants—and how their defenses will fare against the virus as it continues to change.


    The worst thing about “original antigenic sin” is its name. The blame for that technically lies with Thomas Francis Jr., the immunologist who coined the phrase more than six decades ago after noticing that the initial flu infections people weathered in childhood could bias how they fared against subsequent strains. “Basically, the flu you get first in life is the one you respond to most avidly for the long term,” says Gabriel Victora, an immunologist at Rockefeller University. That can become somewhat of an issue when a very different-looking strain comes knocking.

    In scenarios like these, original antigenic sin may sound like the molecular equivalent of a lovesick teen pining over an ex, or a student who never graduates out of immunological grade school. But from the immune system’s point of view, never forgetting your first is logically sound. New encounters with a pathogen catch the body off guard—and tend to be the most severe. A deep-rooted defensive reaction, then, is practical: It ups the chances that the next time the same invader shows up, it will be swiftly identified and dispatched. “Having good memory and being able to boost it very quickly is sometimes a very good thing,” Victora told me. It’s the body’s way of ensuring that it won’t get fooled twice.

    These old grudges come with clear advantages even when microbes morph into new forms, as flu viruses and coronaviruses often do. Pathogens don’t remake themselves all at once, so immune cells that home in on familiar snippets of a virus can still in many cases snuff out enough invaders to prevent an infection’s worst effects. That’s why even flu shots that aren’t perfectly matched to the season’s most prominent strains are usually still quite good at keeping people out of hospitals and morgues. “There’s a lot of leniency in how much the virus can change before we really lose protection,” Guthmiller told me. The wiggle room should be even bigger, she said, with SARS-CoV-2, whose subvariants tend to be far more similar to one another than, say, different flu strains are.

    With all the positives that immune memory can offer, many immunologists tend to roll their eyes at the negative and bizarrely moralizing implications of the phrase original antigenic sin. “I really, really hate that term,” says Deepta Bhattacharya, an immunologist at the University of Arizona. Instead, Bhattacharya and others prefer to use more neutral words such as imprinting, evocative of a duckling latching onto the first maternal figure it spots. “This is not some strange immunological phenomenon,” says Rafi Ahmed, an immunologist at Emory University. It’s more a textbook example of what an adaptable, high-functioning immune system does, and one that can have positive or negative effects, depending on context. Recent flu outbreaks have showcased a little bit of each: During the 2009 H1N1 pandemic, many elderly people, normally more susceptible to flu viruses, fared better than expected against the late-aughts strain, because they’d banked exposures to a similar-looking H1N1—a derivative of the culprit behind the 1918 pandemic—in their youth. But in some seasons that followed, H1N1 disproportionately sickened middle-aged adults whose early-life flu indoctrinations may have tilted them away from a protective response.

    The backward-gazing immune systems of those adults may have done more than preferentially amplify defensive responses to a less relevant viral strain. They might have also actively suppressed the formation of a response to the new one. Part of that is sheer kinetics: Veteran immune cells, trained up on past variants and strains, tend to be quicker on the draw than fresh recruits, says Scott Hensley, an immunologist at the Perelman School of Medicine at the University of Pennsylvania. And the greater the number of experienced soldiers, the more likely they are to crowd out rookie fighters—depriving them of battlefield experience they might otherwise accrue. Should the newer viral strain eventually return for a repeat infection, those less experienced immune cells may not be adequately prepared—leaving people more vulnerable, perhaps, than they might otherwise have been.

    Some researchers think that form of imprinting might now be playing out with the bivalent COVID vaccines. Several studies have found that the BA.5-focused shots are, at best, moderately more effective at producing an Omicron-targeted antibody response than the original-recipe jab—not the knockout results that some might have hoped for. Recent work in mice from Victora’s lab backs up that idea: B cells, the manufacturers of antibodies, do seem to have trouble moving past the impressions of SARS-CoV-2’s spike protein that they got from first exposure. But the findings don’t really trouble Victora, who gladly received his own bivalent COVID shot. (He’ll take the next update, too, whenever it’s ready.) A blunted response to a new vaccine, he told me, is not a nonexistent one—and the more foreign a second shot recipe is compared with the first, the more novice fighters should be expected to participate in the fight. “You’re still adding new responses,” he said, that will rev back up when they become relevant. The coronavirus is a fast evolver. But the immune system also adapts. Which means that people who receive the bivalent shot can still expect to be better protected against Omicron variants than those who don’t.

    Historical flu data support this idea. Many of the middle-aged adults slammed by recent H1N1 infections may not have mounted perfect attacks on the unfamiliar virus, but as immune cells continued to tussle with the pathogen, the body “pretty quickly filled in the gaps,” Gostic told me. Although it’s tempting to view imprinting as a form of destiny, “that’s just not how the immune system works,” Guthmiller told me. Preferences can be overwritten; biases can be undone.


    Original antigenic sin might not be a crisis, but its existence does suggest ways to optimize our vaccination strategies with past biases in mind. Sometimes, those preferences might need to be avoided; in other instances, they should be actively embraced.

    For that to happen, though, immunologists would need to fill in some holes in their knowledge of imprinting: how often it occurs, the rules by which it operates, what can entrench or alleviate it. Even among flu viruses, where the pattern has been best-studied, plenty of murkiness remains. It’s not clear whether imprinting is stronger, for instance, when the first exposure comes via infection or vaccination. Scientists can’t yet say whether children, with their fiery yet impressionable immune systems, might be more or less prone to getting stuck on their very first flu strain. Researchers don’t even know for certain whether repetition of a first exposure—say, through multiple doses of the same vaccine, or reinfections with the same variant—will more deeply embed a particular imprint.

    It does seem intuitive that multiple doses of a vaccine could exacerbate an early bias, Ahmed told me. But if that’s the case, then the same principle might also work the other way: Maybe multiple exposures to a new version of the virus could help break an old habit, and nudge the immune system to move on. Recent evidence has hinted that people previously infected with an early Omicron subvariant responded more enthusiastically to a bivalent BA.1-focused vaccine—available in the United Kingdom—than those who’d never encountered the lineage before. Hensley, at the University of Pennsylvania, is now trying to figure out if the same is true for Americans who got the BA.5-based bivalent shot after getting sick with one of the many Omicron subvariants.

    Ahmed thinks that giving people two updated shots—a safer approach, he points out, than adding an infection to the mix—could untether the body from old imprints too. A few years ago, he and his colleagues showed that a second dose of a particular flu vaccine could help shift the ratio of people’s immune responses. A second dose of the fall’s bivalent vaccine might not be practical or palatable for most people, especially now that BA.5 is on its way out. But if next autumn’s recipe overlaps with BA.5 in ways that it doesn’t with the original variant—as it likely will to at least some degree, given the Omicron lineage’s continuing reign—a later, slightly different shot could still be a boon.

    Keeping vaccine doses relatively spaced out—on an annual basis, say, à la flu shots—will likely help too, Bhattacharya said. His recent studies, not yet published, hint that the body might “forget” old variants, as it were, if it’s simply given more time: As antibodies raised against prior infections and injections fall away, vaccine ingredients could linger in the body rather than be destroyed by prior immunity on sight. That slightly extended stay might offer the junior members of the immune system—lesser in number, and slower on the uptake—more of an opportunity to cook up an Omicron-specific response.

    In an ideal world, researchers might someday know enough about imprinting to account for its finickiness whenever they select and roll out new shots. Flu shots, for instance, could be personalized to account for which strains babies were first exposed to, based on birth year; combinations of COVID vaccine doses and infections could dictate the timing and composition of a next jab. But the world is not yet living that reality, Gostic told me. And after three years of an ever-changing coronavirus and a fluctuating approach to public health, it’s clear that there won’t be a single vaccine recipe that’s ideal for everyone at once.

    Even Thomas Francis Jr. did not consider original antigenic sin to be a total negative, Hensley told me. According to Francis, the true issue with the “sin” was that humans were missing out on the chance to imprint on multiple strains at once in childhood, when the immune system is still a blank slate—something that modern researchers could soon accomplish with the development of universal vaccines. Our reliance on first impressions can be a drawback. But the same phenomenon can be an opportunity to acquaint the body with diversity early on—to give it a richer narrative, and memories of many threats to come.

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    Katherine J. Wu

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  • Will Nasal COVID Vaccines Save Us?

    Will Nasal COVID Vaccines Save Us?

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    Since the early days of the coronavirus pandemic, a niche subset of experimental vaccines has offered the world a tantalizing promise: a sustained slowdown in the spread of disease. Formulated to spritz protection into the body via the nose or the mouth—the same portals of entry most accessible to the virus itself—mucosal vaccines could head SARS-CoV-2 off at the pass, stamping out infection to a degree that their injectable counterparts might never hope to achieve.

    Now, nearly three years into the pandemic, mucosal vaccines are popping up all over the map. In September, India authorized one delivered as drops into the nostrils; around the same time, mainland China green-lit an inhalable immunization, and later on, a nasal-spray vaccine, now both being rolled out amid a massive case wave. Two more mucosal recipes have been quietly bopping around in Russia and Iran for many months. Some of the world’s largest and most populous countries now have access to the technology—and yet it isn’t clear how well that’s working out. “Nothing has been published; no data has been made available,” says Mike Diamond, an immunologist at Washington University in St. Louis, whose own approach to mucosal vaccines has been licensed for use in India via a company called Bharat. If mucosal vaccines are delivering on their promise, we don’t know it yet; we don’t know if they will ever deliver.

    The allure of a mucosal vaccine is all about geography. Injectable shots are great at coaxing out immune defenses in the blood, where they’re able to cut down on the risk of severe disease and death. But they aren’t as good at marshaling a protective response in the upper airway, leaving an opening for the virus to still infect and transmit. When viral invaders throng the nose, blood-borne defenses have to scamper to the site of infection at a bit of a delay—it’s like stationing guards next to a bank’s central vault, only to have them rush to the entrance every time a robber trips an external alarm. Mucosal vaccines, meanwhile, would presumably be working at the door.

    That same logic drives the effectiveness of the powerful oral polio vaccine, which bolsters defenses in its target virus’s preferred environment—the gut. Just one mucosal vaccine exists to combat a pathogen that enters through the nose: a nasal spray made up of weakened flu viruses, a version of which is branded as FluMist. The up-the-nose spritz is reasonably protective in kids, in some cases even outperforming its injected counterparts (though not always). But FluMist is much less potent for adults: The immunity they accumulate from a lifetime of influenza infections can wipe out the vaccine before it has time to lay down new protection. When it comes to cooking up a mucosal vaccine for a respiratory virus, “we don’t have a great template to follow,” says Deepta Bhattacharya, an immunologist at the University of Arizona.

    To circumvent the FluMist problem, some researchers have instead concocted viral-vector-based vaccines—the same group of immunizations to which the Johnson & Johnson and AstraZeneca COVID shots belong. China’s two mucosal vaccines fall into this category; so does India’s nose-drop concoction, as well as a nasal version of Russia’s Sputnik V shot. Other researchers are cooking up vaccines that contain ready-made molecules of the coronavirus’s spike protein, more akin to the shot from Novavax. Among them are Iran’s mucosal COVID vaccine and a newer, still-in-development candidate from the immunologist Akiko Iwasaki and her colleagues at Yale. The Yale group is also testing an mRNA-based nasal recipe. And the company Vaxart has been tinkering with a COVID-vaccine pill that could be swallowed to provoke immune cells in the gut, which would then deploy fighters throughout the body’s mucosal surfaces, up through the nose.

    Early data in animals have spurred some optimism. Trial versions of Diamond’s vaccine guarded mice, hamsters, and monkeys from the virus, in some cases seeming to stave off infection entirely; a miniaturized version of Vaxart’s oral vaccine was able to keep infected hamsters from spreading the coronavirus through the air. Iwasaki is pursuing an approach that deploys mucosal vaccines exclusively as boosters to injected shots, in the hopes that the initial jab can lay down bodywide immunity, a subset of which can then be tugged into a specialized compartment in the nose. Her nasal-protein recipe seems to trim transmission rates among rodents that have first received an in-the-muscle shot.

    But attempts to re-create these results in people yielded mixed results. After an intranasal version of the AstraZeneca vaccine roused great defenses in animals, a team at Oxford moved the immunization into a small human trial—and last month, published results showing that it hardly triggered any immune response, even as a booster to an in-the-arm shot. Adam Ritchie, one of the Oxford immunologists behind the study, told me the results don’t necessarily spell disaster for other mucosal attempts, and that with more finagling, AstraZeneca’s vaccine might someday do better up the nose. Still, the results “definitely put a damper on the excitement around intranasal vaccines,” says Stephanie Langel, an immunologist at Case Western Reserve University, who’s partnering with Vaxart to develop a COVID-vaccine pill.

    The mucosal COVID vaccines in India and China, at least, have reportedly shown a bit more promise in small, early human trials. Bharat’s info sheet on its nasal-drop vaccine—the Indian riff on Diamond’s recipe—says it bested another locally made vaccine, Covaxin, at tickling out antibodies, while provoking fewer side effects. China’s inhaled vaccine, too, seems to do reasonably well on the human-antibody front. But antibodies aren’t the same as true effectiveness: Vaccine makers and local health ministries, experts told me, have yet to release large-scale, real-world data showing that the vaccines substantially cut down on transmission or infection. And although some studies have hinted that nasal protection can stick around in animals for many, many months, there’s no guarantee the same will be true in humans, in whom mucosal antibodies, in particular, “are kind of known to wane pretty quickly,” Langel told me.

    SARS-CoV-2 infections have offered sobering lessons of their own. The nasal immune response to the virus itself is neither impenetrable nor particularly long-lived, says David Martinez, a viral immunologist at the University of North Carolina at Chapel Hill. Even people who have been both vaccinated and infected can still get infected again, he told me, and it would be difficult for a nasal vaccine to do much better. “I don’t think mucosal vaccines are going to be the deus ex machina that some people think they’re going to be.”

    Mucosal vaccines don’t need to provide a perfect blockade against infection to prove valuable. Packaged into sprays, drops, or pills, immunizations tailor-made for the mouth or the nose might make COVID vaccines easier to ship, store, and distribute en masse. “They often don’t require specialized training,” says Gregory Poland, a vaccinologist at the Mayo Clinic—a major advantage for rural or low-resource areas. The immunizing experience could also be easier for kids or anyone else who’d rather not endure a needle. Should something like Vaxart’s encapsulated vaccine work out, Langel told me, COVID vaccines could even one day be shipped via mail, in a form safe and easy enough to swallow with a glass of water at home. Some formulations may also come with far fewer side effects than, say, the mRNA-based shots, which “really kick my ass,” Bhattacharya told me. Even if mucosal vaccines weren’t a transmission-blocking knockout, “if it meant I didn’t have to get the mRNA vaccine, I would consider it.”

    But the longer that countries such as the U.S. have gone without mucosal COVID vaccines, the harder it’s gotten to get one across the finish line. Transmission, in particular, is tough to study, and Langel pointed out that any new immunizations will likely have to prove that they can outperform our current crop of injected shots to secure funding, possibly even FDA approval. “It’s an uphill battle,” she told me.

    Top White House advisers remain resolute that transmission-reducing tech has to be part of the next generation of COVID vaccines. Ideally, those advancements would be paired with ingredients that enhance the life span of immune responses and combat a wider swath of variants; skimp on any of them, and the U.S. might remain in repeat-vaccination purgatory for a while yet. “We need to do better on all three fronts,” Anthony Fauci, the outgoing director of the National Institute of Allergy and Infectious Diseases, told me. But packaging all that together will require another major financial investment. “We need Warp Speed 2.0,” says Shankar Musunuri, the CEO of Ocugen, the American company that has licensed Diamond’s recipe. “And so far, there is no action.” When I asked Fauci about this, he didn’t seem optimistic that this would change. “I think that they’ve reached the point where they feel, ‘We’ve given enough money to it,’” he told me. In the absence of dedicated government funds, some scientists, Iwasaki among them, have decided to spin off companies of their own. But without more public urgency and cash flow, “it could be years to decades to market,” Iwasaki told me. “And that’s if everything goes well.”

    Then there’s the issue of uptake. Musunuri told me that he’s confident that the introduction of mucosal COVID vaccines in the U.S.—however long it takes to happen—will “attract all populations, including kids … people like new things.” But Rupali Limaye, a behavioral scientist at Johns Hopkins University, worries that for some, novelty will drive the exact opposite effect. The “newness” of COVID vaccines, she told me, is exactly what has prompted many to adopt an attitude of “wait and see” or even “that’s not for me.” An even newer one that jets ingredients up into the head might be met with additional reproach.

    Vaccine fatigue has also set in for much of the public. In the United States, hospitalizations are once again rising, and yet less than 15 percent of people eligible for bivalent shots have gotten them. That sort of uptake is at odds with the dream of a mucosal vaccine that can drive down transmission. “It would have to be a lot of people getting vaccinated in order to have that public-health population impact,” says Ben Cowling, an epidemiologist at the University of Hong Kong. And there’s no guarantee that even a widely administered mucosal vaccine would be the population’s final dose. The pace at which we’re doling out shots is driven in part by “the virus changing so quickly,” says Ali Ellebedy, an immunologist at Washington University in St. Louis. Even a sustained encampment of antibodies in the nose could end up being a poor match for the next variant that comes along, necessitating yet another update.

    The experts I spoke with worried that some members of the scientific community—even some members of the public—have begun to pin all their hopes about stopping the spread of SARS-CoV-2 on mucosal vaccines. It’s a recipe for disappointment. “People love the idea of a magic pill,” Langel told me. “But it’s just not reality.” The virus is here to stay; the goal continues to be to make that reality more survivable. “We’re trying to reduce infection and transmission, not eliminate it; that would be almost impossible,” Iwasaki told me. That’s true for any vaccine, no matter how, or where, the body first encounters it.

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    Katherine J. Wu

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  • 8 Ways You Can Save Yourself and Others From Being Scammed

    8 Ways You Can Save Yourself and Others From Being Scammed

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    Opinions expressed by Entrepreneur contributors are their own.

    Statistics on the number of scam websites that litter the internet are disturbing. During 2020, Google registered more than 2 million phishing websites alone. That means more than 5,000 new phishing sites popped up every day — not to mention the ones that avoided Google’s detection. In 2021, the U.S. Federal Bureau of Investigation (FBI) reported nearly $7 billion in losses from cybercrime that is perpetrated through these sites.

    What exactly are scam websites? Scam websites refer to any illegitimate website that is used to deceive users into fraud or malicious attacks. Many scammers operate these fake websites and will download viruses onto your computer or steal passwords or other personal information.

    Reporting these sites as they are encountered is an important part of fighting back. In other words, if you see something, say something. Keeping quiet, even if you avoid falling prey, allows the scammers to aim at another target.

    Perhaps you’ve received a suspicious link in an email? Or maybe a strange text message that you haven’t clicked on. Fortunately, there are many organizations out there that have launched efforts aimed at reducing the threat that they pose. In general, these organizations put scam websites on the radar by collecting and sharing information about them. In some cases, they prompt an investigation into the scammers behind the sites.

    Related: Learn How to Protect Your Business From Cybercrime

    It’s free to report a suspicious website you’ve encountered, and it takes just a minute. Here are eight ways you can report a suspected scam website to stop cyber criminals and protect yourself and others online.

    1. The Internet Crime Complaint Center

    The IC3, as it is known, is an office of the FBI that receives complaints from those who have been the victims of internet-related crime. The IC3 defines the internet crimes that it addresses to include illegal activity involving websites. Complaints filed with the IC3 are reviewed and researched by trained FBI analysts.

    2. Cybersecurity and Infrastructure Security Agency

    CISA, which is an agency of the U.S. Department of Homeland Security, targets a wide range of malicious cyber activity. It specifically requests reports on phishing activity utilizing fraudulent websites. Information provided to CISA is shared with the Anti-Phishing Working Group, a non-profit focused on reducing the impact of phishing-related fraud around the world.

    3. econsumer.gov

    The econsumer.gov site, run by the International Consumer Protection and Enforcement Network, is for reporting international scams. It is supported by consumer protection agencies and related offices in more than 65 countries. A secure version of their site is used by law enforcement agencies to share info on scams.

    4. Google Safe Browsing

    While Google does not have a mechanism for reporting all varieties of website scams, there is a form for reporting sites that are suspected of being used to carry out phishing. Reports made via the form are managed by Google’s Safe Browsing team. Google’s Transparency Report provides information on the sites that it has determined to be “currently dangerous to visit.”

    Related: Is That Instagram Email a Phishing Attack? Now You Can Find Out.

    5. PhishTank

    This service was founded by Cisco Talos Intelligence Group to “pour sunshine on some of the dark alleys of the Internet.” Phishtank includes an ever-growing list of URLs reported as being involved in phishing scams. To date, it has received more than 7.5 million reports of potential phishing sites. It says that more than 100,000 of the sites are still online.

    Related: 6 Ways Better Business Bureau Accreditation Can Boost Your Business

    6. Antivirus Apps

    Antivirus providers such as Norton, Kaspersky, and McAfee have forms that can be used to identify pages that users feel should be blocked. Scam sites would definitely fall under that category. With some antivirus platforms, reporting forms can only be accessed by registered users. Norton’s is open to anyone.

    7. Web host

    There is a chance that the DNS service hosting the scam site will take action to shut it down. There are a variety of online resources that can help you to find the DNS of a particular site. Once you identify it, send a message to their customer service reporting the site in question and the experience that you had.

    8. Share your experience on social media

    This is actually more like sounding an alarm than filing a report, but it might protect one of your connections who stumbles upon the same site or is targeted by the same type of scam. At the very least, it could draw attention to the fact that scam sites affect real people. A post on Facebook about a close call you had with a scam might better equip your network to avoid any dangerous entanglements. If it does, they’ll thank you.

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    Jay Feldman, DO

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  • Will We Get Omicron’d Again?

    Will We Get Omicron’d Again?

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    In COVID terms, the middle of last autumn looked a lot like this one. After a rough summer, SARS-CoV-2 infections were down; hospitalizations and deaths were in a relative trough. Kids and workers were back in schools and offices, and another round of COVID shots was rolling out. Things weren’t great … but they weren’t the most terrible they’d ever been. There were vaccines; there were tests; there were drugs. The worst winter development the virus might produce, some experts thought, might involve the spawning of some nasty Delta offshoot.

    Then, one year ago this week, Omicron appeared. The first documented infection with the variant was identified from a specimen collected in South Africa on November 9, 2021; by December 1, public-health officials had detected cases in countries all around the globe, including the United States. Twenty days later, Omicron had unseated Delta as America’s dominant SARS-CoV-2 morph. The new, highly mutated variant could infect just about anyone it encountered—even if they’d already caught a previous version of the virus or gotten several shots of a vaccine. At the beginning of December, and nearly two years into the pandemic, researchers estimated that roughly one-third of Americans had contracted SARS-CoV-2. By the middle of February this year, that proportion had nearly doubled.

    Omicron’s arrival and rapid spread around the world was, and remains, this crisis’s largest inflection point to date. The variant upended scientists’ expectations about SARS-CoV-2’s evolution; it turned having COVID into a horrific norm. Now, as the U.S. approaches its Omicronniversary, conditions may seem ripe for an encore. Some experts worry that the emergence of another Greek-letter variant is overdue. “I’m at a loss as to why we haven’t seen Pi yet,” says Salim Abdool Karim, an epidemiologist at the Centre for the AIDS Programme of Research in South Africa. “I think there’s a chance we still will.”

    A repeat of last winter seems pretty unlikely, experts told me. But with a virus this unpredictable, there’s no guarantee that we won’t see disaster unspool again.

    A lot has changed since last year. For one thing, population immunity to SARS-CoV-2 is higher. Far more people have received additional doses of vaccine, many of them quite recently, with an updated formula that’s better tailored to the variants du jour. Plus, at this point, nearly every American has been infected at least once—and most of them with at least some subvariant of Omicron, says Shaun Truelove, an epidemiologist and a modeler at Johns Hopkins University. These multiple layers of protection make it more challenging for the average SARS-CoV-2 spin-off to severely sicken people. They also raise transmission obstacles for the coronavirus in whatever form it takes.

    Omicron does seem to have ushered in “a different phase of the pandemic,” says Verity Hill, an evolutionary virologist at Yale. The variants that took over different parts of the world in 2021 rose in a rapid succession of monarchies: Alpha, Beta, Gamma, Delta. But in the U.S. and elsewhere, 2022 has so far been an oligarchy of Omicron offshoots. Perhaps the members of the Omicron lineage are already so good at moving among hosts that the virus hasn’t needed a major upgrade since.

    If that’s the case, SARS-CoV-2 may end up a victim of its own success. The Omicron subvariants BQ.1 and BQ1.1 appear capable of spreading up to twice as fast as BA.5, according to laboratory data. But their takeover in the U.S. has been slow and halting, perhaps because they’re slogging through a morass of immunity to the Omicron family. That alone makes it less likely that any single Omicron subvariant will re-create the sudden surge of late 2021 anytime soon. In South Africa and the United Kingdom, for instance, different iterations of Omicron seem to have triggered just modest bumps in sickness in recent months. (That said, those countries—with their distinct demographics and vaccination and infection histories—aren’t a perfect bellwether for the U.S.)

    For an Omicron 2021 redux to happen, SARS-CoV-2 might need to undergo a substantial genetic makeover—which Abdool Karim thinks would be very difficult for the virus to manage. In theory, there are only so many ways that SARS-CoV-2 can scramble its appearance while retaining its ability to latch onto our cells; by now, its options should be somewhat slimmed. And the longer the Omicron line of succession persists, the tougher it may be to upend. “It’s just getting harder to compete,” Hill told me.

    But the world has gotten overconfident before. Even if SARS-CoV-2 doesn’t produce a brand-new version of itself, low uptake of the bivalent vaccine could allow our defenses to wither, driving a surge all the same, Truelove told me. Our transmission-dampening behaviors too are slacker than they’ve been since the pandemic’s start. This time last year, 50 to 60 percent of Americans were regularly wearing masks. The latest figures, many of them several months old, are closer to 30 percent. “The more opportunities you give the virus to get into somebody,” Hill said, “the more chances you give it to get the group of mutations that could help it take off.” Immunocompromised people who remain chronically infected with older variants, such as Alpha or Delta, could also become the sites of new viral offshoots. (That may be how the world got Omicron to begin with.)

    Going on probability alone, “it seems more likely that we’ll keep going with these subvariants of Omicron rather than dealing with something wholly brand-new,” says Maia Majumder, an epidemiologist at Boston Children’s Hospital. But Lauren Ancel Meyers, an infectious-disease modeler at the University of Texas at Austin, warns that plenty of uncertainty remains. “What we don’t have is a really data-driven model right now that tells us if, when, where, and what kind of variants will be emerging in the coming months and years,” she told me. Our window into the future is only getting foggier too as fewer people submit their test results—or take any test at all—and surveillance systems continue to go offline.

    It wouldn’t take another Omicron-type event to hurl us into disarray. Maybe none of the Omicron subvariants currently jockeying for control will surge ahead of the pack. But several of them might yet drive regional epidemics, Majumder told me, depending on the local nitty-gritty of who’s susceptible to what. And as winter looms, some of the biggest holes in our COVID shield remain unpatched. People who are immunocompromised are losing their last monoclonal-antibody treatments, and although powerful drugs exist to slash the risk of severe disease and death, useful preventives and treatments for long COVID remain sparse.

    Our nation’s capacity to handle new COVID cases is also low, Majumder said. Already, hospitals around the country are being inundated with other respiratory viruses—RSV, flu, rhinovirus, enterovirus—all while COVID is still kicking in the background. “If flu has taken over hospital beds,” says Srini Venkatramanan, an infectious-disease modeler at the University of Virginia, even a low-key wave will “feel like it’s having a much bigger impact.”

    As the country approaches its second holiday season with Omicron on deck, this version of the virus may “feel familiar,” Majumder pointed out. “I think people perceive the current circumstances to be safer than they were last year,” she said—and certainly, some of them are. But the fact that Omicron has lingered is not entirely a comfort. It is also, in its way, a reminder of how bad things once were, and how bad they could still get.

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    Katherine J. Wu

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  • What Happened to Hand-Washing?

    What Happened to Hand-Washing?

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    Way back in the early, whirlwind days of the pandemic, surfaces were the thing to worry about. The prevailing scientific wisdom was that the coronavirus spread mainly via large droplets, which fell onto surfaces, which we then touched with our hands, with which we then touched our faces. (Masks, back then, were said by public health authorities to be unnecessary for the general public.) So we washed our hands until they were raw. We contorted ourselves to avoid touching doorknobs. We went through industrial quantities of hand sanitizer, and pressed elevator buttons with keys and pens, and disinfected our groceries and takeout orders and mail.

    And then we learned we’d had it all backwards. The virus didn’t spread much via surfaces; it spread through the air. We came to understand the danger of indoor spaces, the importance of ventilation, and the difference between a cloth mask and an N95. Meanwhile, we mostly stopped talking about hand-washing. The days when you could hear people humming “Happy Birthday” in public restrooms quickly disappeared. And wiping down packages and ostentatious workplace-disinfection protocols became a matter of lingering hygiene theater.

    This whole episode was among the stranger and more disorienting shifts of the pandemic. Sanitization, that great bastion of public health, saved lives; actually, no, it didn’t matter that much for COVID. On one level, this about-face should be seen as a marker of good scientific progress, but it also raises a question about the sorts of acts we briefly thought were our best available defense against the virus. If hand-washing isn’t as important as we thought it was in March 2020, how important is it?

    Any public-health expert will be quick to tell you that, please, yes, you should still wash your hands. Emanuel Goldman, a microbiologist at Rutgers New Jersey Medical School, considers it “commonsense hygiene” for protecting us against a range of viruses spread through close contact and touch, such as gastrointestinal viruses. Also, let’s be honest: It’s gross to use the bathroom and then refuse to wash, whether or not you’re going to give someone COVID.

    Even so, the pandemic has piled on evidence that the transmission of the coronavirus via fomites—that is, inanimate contaminated objects or surfaces—plays a much smaller role, and airborne transmission a much larger one, than we once thought. And the same likely goes for other respiratory pathogens, such as influenza and the coronaviruses that cause the common cold, Linsey Marr, an environmental engineer and aerosols expert at Virginia Tech, told me.

    This realization is not an entirely new one: A 1987 study by researchers at the University of Wisconsin found that a group of men playing poker with “soggy,” rhinovirus-contaminated cards were not infected, while a group playing with other sick players were. Now Goldman intends to push this point even further. At a conference in December, he is going to present a paper arguing that, with rare exceptions, such as RSV, all respiratory pathogens are transmitted predominantly through the air. The reason we’ve long thought otherwise, he told me, is that our understanding has been founded on faulty assumptions. Generally speaking, the studies pointing toward fomite-centric theories of transmission were virus-survival studies, which measure how long a virus can survive on a surface. Many of them either used unrealistically large amounts of virus or measured only the presence of the virus’s genetic material, not whether it remained infectious. “The design” of these experiments, he said, “was not appropriate for being able to extrapolate to real-life conditions.”

    The upshot, for Goldman, is that surface transmission of respiratory pathogens is “negligible,” probably accounting for less than .01 percent of all infections. If correct, this would mean that your chance of catching the flu or a cold by touching something in the course of daily life is virtually nonexistent. Goldman acknowledged that there’s a “spectrum of opinion” on the matter. Marr, for one, would not go quite so far: She’s confident that more than half of respiratory-pathogen transmission is airborne, though she said she wouldn’t be surprised if the proportion is much, much higher—the only number she would rule out is 100 percent.

    For now, it’s important to avoid binary thinking on the matter, Saskia Popescu, an epidemiologist at George Mason University, told me. Fomites, airborne droplets, smaller aerosol particles—all modes of transmission are possible. And the proportional breakdown will not be the same in every setting, Seema Lakdawa, a flu-transmission expert at Emory University, told me. Fomite transmission might be negligible at a grocery store, but that doesn’t mean it’s negligible at a day care, where kids are constantly touching things and sneezing on things and sticking things in their mouths. The corollary to this idea is that certain infection-prevention strategies prove highly effective in one context but not in another: Frequently disinfecting a table in a preschool classroom might make a lot of sense; frequently disinfecting the desk in your own private cubicle, less so.

    Much of the conspicuous cleaning we did early in the pandemic was excessive, Popescu said, but she worries that we may have slightly overcorrected, lumping some useful behaviors—targeted disinfection, even hand-washing in some cases—into the category of hygiene theater. Whatever the setting, the experts I spoke with all agreed that these behaviors remain important for contending with non-respiratory pathogens. Recently, when several members of Marr’s family came down with norovirus, an extremely unpleasant stomach bug that causes vomiting, diarrhea, and stomach cramping, she disinfected a number of high-touch surfaces around the house. Picture that: one of the country’s foremost experts on airborne transmission wiping down doorknobs and light switches.

    Marr isn’t convinced we’ve overcorrected. Hand sanitizer still abounds, businesses still tout their surface-cleaning protocols, and air quality still gets comparatively little attention. Recently, she watched a person use their shirt to open the door of a visitor center without touching the handle … then proceed inside unmasked. There’s nothing wrong with taking certain precautions to prevent fomite transmission, she said—these should not all be dismissed en masse as hygiene theater—as long as they don’t come at the expense of efforts to block airborne transmission. “If you’re doing extra hand washing … then you should also be wearing a good mask in crowded indoor environments,” Marr said. “If you’re bothering to clean the surfaces, then you should be bothering to clean the air.”

    On Friday, with respiratory-virus season looming, CDC Director Rochelle Walensky tweeted out three pieces of advice for staying healthy: “Get an updated COVID-19 vaccine & get your annual flu vaccine,” “Stay home if you are sick,” and—not to be forgotten—“Practice good hand hygiene.” She made no mention of masks or ventilation.

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    Jacob Stern

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