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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.)

    Read: If the lab-leak theory is right, what next?

    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.

    Read: There is no evidence strong enough to end the pandemic-origins debate

    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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  • A Major Breed of Flu Has Gone Missing

    A Major Breed of Flu Has Gone Missing

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    In March 2020, Yamagata’s trail went cold.

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

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

    Read: The pandemic broke the flu

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

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

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

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

    Read: Eagles Are Falling, Bears Are Going Blind

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

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

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

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

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

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

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

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

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

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

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

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

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    Katherine J. Wu

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  • 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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