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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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  • Trying to Stop Long COVID Before It Even Starts

    Trying to Stop Long COVID Before It Even Starts

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    Three years into the global fight against SARS-CoV-2, the arsenal to combat long COVID remains depressingly bare. Being vaccinated seems to reduce people’s chances of developing the condition, but the only surefire option for avoiding long COVID is to avoid catching the coronavirus at all—a proposition that feels ever more improbable. For anyone who is newly infected, “we don’t have any interventions that are known to work,” says Akiko Iwasaki, an immunologist and long-COVID researcher at Yale.

    Some researchers are hopeful that the forecast might shift soon. A pair of recent preprint studies, both now under review for publication in scientific journals, hint that two long-COVID-preventing pills might already be on our pharmacy shelves: the antiviral Paxlovid and metformin, an affordable drug commonly used for treating type 2 diabetes. When taken early in infection, each seems to at least modestly trim the chance of developing long COVID—by 42 percent, in the case of metformin. Neither set of results is a slam dunk. The Paxlovid findings did not come out of a clinical trial, and were focused on patients at high risk of developing severe, acute COVID; the metformin data did come out of a clinical trial, but the study was small. When I called more than half a dozen infectious-disease experts to discuss them, all used hopeful, but guarded, language: The results are “promising,” “intriguing”; they “warrant further investigation.”

    At this point, though, any advance at all feels momentous. Long COVID remains the pandemic’s biggest unknown: Researchers still can’t even agree on its prevalence or the features that define it. What is clear is that millions of people in the United States alone, and countless more worldwide, have experienced some form of it, and more are expected to join them. “We’ve already seen early data, and we’ll continue to see data, that that will emphasize the impact that long COVID has on our society, on quality of life, on productivity, on our health system and medical expenditures,” says Susanna Naggie, an infectious-disease physician and COVID-drug researcher at Duke University. “This needs to be a high priority,” she told me. Researchers have to trim long COVID incidence as much as possible, as soon as possible, with whatever safe, effective options they can.

    By now, news of the inertia around preventive long-COVID therapies may not come as much of a shock. Interventions that stop disease from developing are, on the whole, a neglected group; big, blinded, placebo-controlled clinical trials—the industry gold standard—usually look to investigate potential treatments, rather than drugs that might keep future illness at bay. It’s a bias that makes research easier and faster; it’s a core part of the American medical culture’s reactive approach to health.

    Read: Long COVID has forced a reckoning for one of medicine’s most neglected diseases

    For long COVID, the terrain is even rougher. Researchers are best able to address prevention when they understand a disease’s triggers, the source of its symptoms, and who’s most at risk. That intel provides a road map, pointing them toward specific bodily systems and interventions. The potential causes of COVID, though, remain murky, says Adrian Hernandez, a cardiologist and clinical researcher at Duke. Years of research have shown that the condition is quite likely to comprise a cluster of diverse syndromes with different triggers and prognoses, more like a category (e.g., “cancer”) than a singular disease. If that’s the case, then a single preventive treatment shouldn’t be expected to cut its rates for everyone. Without a universal way to define and diagnose the condition, researchers can’t easily design trials, either. Endpoints such as hospitalization and death tend to be binary and countable. Long COVID operates in shades of gray.

    Still, some scientists might be making headway with vetted antiviral drugs, already known to slash the risk of developing severe COVID-19. A subset of long-COVID cases could be caused by bits of virus that linger in the body, prompting the immune system to wage an extended war; a drug that clears the microbe more quickly might lower the chances that any part of the invader sticks around. Paxlovid, which interferes with SARS-CoV-2’s ability to copy itself inside of our cells, fits that bill. “The idea here is really nipping it in the bud,” says Ziyad Al-Aly, a clinical epidemiologist and long-COVID researcher at Washington University in St. Louis, who led the recent Paxlovid work.

    Paxlovid has yet to hit the scientific jackpot: proof from a big clinical trial that shows it can prevent long COVID in newly infected people. But Al-Aly’s study, which pored over the electronic medical records of more than 56,000 high-risk patients, offers some early optimism. People who took the pills, he and his colleagues found, were 26 percent less likely to report lingering symptoms three months after their symptoms began than those who didn’t.

    Read: Inside the mind of an anti-Paxxer

    The pills’ main benefit remains the prevention of severe, acute disease. (In the recent study, Paxlovid-takers were also 30 percent less likely to be hospitalized and 48 percent less likely to die.) Al-Aly expects that the drug’s effectiveness at preventing long COVID—if it’s confirmed in other populations—will be “modest, not huge.” Though the two functions could yet be linked: Some long-COVID cases may result from severe infections that damage tissues so badly that the body struggles to recover. And should Paxlovid’s potential pan out, it could help build the case for testing other SARS-CoV-2 antivirals. Al-Aly and his colleagues are currently working on a similar study into molnupiravir. “The early results are encouraging,” he told me, though “not as robust as Paxlovid.” (Another study, run by other researchers, that followed hospitalized COVID patients found those who took remdesivir were less likely to get long COVID, but a later randomized clinical trial didn’t bear that out.)

    A clinical trial testing Paxlovid’s preventive potency against long COVID is still needed. Kit Longley, a spokesperson for Pfizer, told me in an email that the company doesn’t currently have one planned, though it is “continuing to monitor data from our clinical studies and real-world evidence.” (The company is collaborating with a research group at Stanford to study Paxlovid in new clinical contexts, but they’re looking at whether the pills  might treat long COVID that’s already developed. The RECOVER trial, a large NIH-funded study on long COVID, is also focusing its current studies on treatment.) But given the meager uptake rates for Paxlovid even among those in high-risk groups, Al-Aly thinks his new data could already serve a useful purpose: providing people with extra motivation to take the drug.

    The case for adding metformin to the anti-COVID tool kit might be a bit muddier. The drug isn’t the most intuitive medication to deploy against a respiratory virus, and despite its widespread use among diabetics, its exact effects on the body remain nebulous, says Stacey Schultz-Cherry, a virologist at St. Jude Children’s Research Hospital. But there are many reasons to believe it might be useful. Some research has shown that metformin can mess with the manufacture of viral proteins inside of human cells, Bramante told me, which may impede the ability of SARS-CoV-2 and other pathogens to reproduce. The drug also appears to rev up the disease-dueling powers of certain immune cells, and to stave off inflammation. Studies have shown that metformin can improve responses to certain vaccinations in humans and rodents, and researchers have found that people taking the drug seem less likely to get seriously sick from influenza. Even the diabetes-coronavirus connection may not be so tenuous: Metabolic disease is a risk factor for severe COVID; infection itself can put blood-sugar levels on the fritz. It’s certainly plausible that having a metabolically altered body, Schultz-Cherry told me, could make infections worse.

    Read: The promising treatment we’re not even trying for long COVID

    But the evidence that metformin helps prevent long COVID remains sparse. Carolyn Bramante, the scientist who led the metformin study, told me that when her team first set out in 2020 to investigate the drug’s effects on SARS-CoV-2 infections in a randomized, clinical trial, long COVID wasn’t really on their radar. Like many others in their field, they were hoping to repurpose established medicines to keep infected people out of the hospital; early studies of metformin—as well as the two other drugs in their trial, the antidepressant fluvoxamine and the antiparasitic ivermectin—hinted that they’d work. Ironically, two years later, their story flipped around. A large analysis, published last summer, showed that none of the three drugs were stellar at preventing severe COVID in the short term—a disappointing result (though Bramante contends that their data still indicate that metformin does some good). Then, when Bramante and her colleagues examined their data again, they found that study participants that had taken metformin for two weeks around the start of their illness were 42 percent less likely to have a long-COVID diagnosis from their doctor nearly a year down the road. David Boulware, an infectious-disease physician who helped lead the work, considers that degree of reduction pretty decent: “Is it 100 percent? No,” he told me. “But it’s better than zero.”

    Metformin may well prove to prevent long COVID but not acute, severe COVID (or vice versa). Plenty of people who never spend time in the hospital can still end up developing chronic symptoms. And Iwasaki points out that the demographics of long-haulers and people who get severe COVID don’t really overlap; the latter skew older and male. In the future, early-infection regimens may be multipronged: antivirals, partnered with metabolic drugs, in the hopes of keeping symptoms both mild and short-lived.

    But researchers are still a long way off from delivering that reality. It’s not yet clear, for instance, whether the drugs work additively when combined, Boulware told me. Nor is it a given that they’ll work across different demographics—age, vaccination status, risk factors, and more. Bramante and Boulware’s study cast a decently wide net: Although everyone enrolled in the trial was overweight or obese, many were young and healthy; a few were even pregnant. The study was not enormous, though—about 1,000 people. It also relied on patients’ individual doctors to deliver long-COVID diagnoses, likely leading to some inconsistencies, so other studies that follow up in the future could find different results. For now, this isn’t enough to “mean we should run out and use metformin,” Schultz-Cherry, who has been battling long COVID herself, told me.

    Other medications could still fill the long-COVID gaps. Hernandez, the Duke cardiologist, is hopeful that one of his ongoing clinical trials, ACTIV-6, might provide answers soon. He and his team are testing whether any of several drugs—including ivermectin, fluvoxamine, the steroid fluticasone, and, as a new addition, the anti-inflammatory montelukast—might cut down on severe, short-term COVID. But Hernandez and his colleagues, Naggie among them, appended a check-in at the 90-day mark, when they’ll be asking their patients whether they’re experiencing a dozen or so symptoms that could hint at a chronic syndrome.

    That check-in questionnaire won’t capture the full list of long-COVID symptoms, now more than 200 strong. Still, the three-month benchmark could give them a sense of where to keep looking, and for how long. Hernandez, Naggie, and their colleagues are considering whether to extend their follow-up period to six months, maybe farther. The need for long-COVID prevention, after all, will only grow as the total infection count does. “We’re not going to get rid of long COVID anytime soon,” Iwasaki told me. “The more we can prevent onset, the better off we are.”

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    Katherine J. Wu

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  • I’m Sorry, but This COVID Policy Is Ridiculous

    I’m Sorry, but This COVID Policy Is Ridiculous

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    Cases have surged in China since it dropped its zero-COVID policy in December, and the latest models now suggest that at least 1 million people may die as a result. Many countries have responded by policing their borders: Last week, the CDC announced that anyone entering the United States from China would be required to test negative within two days of departure; the U.K., Canada, and Australia quickly followed suit; and the European Union has urged its member states to do the same. (Taking a more extreme tack, Morocco has said it will ban travelers from China from entering altogether.) At a media briefing on Wednesday, World Health Organization Director-General Tedros Adhanom Ghebreyesus said, “It is understandable that some countries are taking steps they believe will protect their own citizens.”

    On Tuesday, a Chinese official denounced some of the new restrictions as having “no scientific basis.” She wasn’t wrong. If the goal is to “slow the spread of COVID” from overseas, as the CDC has stated, there is little evidence to suggest that the restrictions will be effective. More important, it wouldn’t matter if they were: COVID is already spreading unchecked in the U.S. and many of the other countries that have new rules in place, so imported cases wouldn’t make much of a difference. The risk is particularly low given the fact that 95 percent of China’s locally acquired cases are being caused by two Omicron lineages—BA.5.2 and BF.7—that are old news elsewhere. “The most dangerous new variant at the moment is from New York—XBB.1.5—which the U.S. is now busy exporting to the rest of the world,” Christina Pagel, a mathematician who studies health care at University College London, told me. “I’m sorry, but this is fucking ridiculous.”

    By now, it’s well known that travel restrictions can’t stop COVID from crossing borders. At best, they slow its entry. When Omicron was first detected, in South Africa in late November 2021, America blocked travel from southern-African countries in an attempt to prevent the variant from spreading; by mid-December, Omicron dominated the United States. Restrictions can delay the spread of a variant only if they are implemented while cases are low and before travelers have had a chance to spread it. Such policies were more effective early in the pandemic: A BMJ Global Health review concluded that the initial ban on all travel into or out of Wuhan, China, in January 2020 significantly reduced the number of cases exported to other countries and delayed outbreaks elsewhere by “up to a few weeks.” Later on, such restrictions lost value. The COVID Border Accountability Project, which tracks travel restrictions around the world, has found that border closures did not reduce COVID spread, at least through April 2021, Mary Shiraef, the project’s principal investigator and a political scientist at Notre Dame University, told me. (According to the study, domestic lockdowns did slow transmission.)

    At this stage of the pandemic, restrictions make sense only under two conditions, Pagel said: The country deploying them must have low levels of spread and good control policies, and the restrictions must be applied to all other nations, as opposed to just one. Neither of these conditions is being met right now by any country deploying travel measures against China. Even if a single-point ban did serve some useful purpose, the rules in place for China don’t add up. Predeparture testing likely won’t catch most infected travelers from China, Adam Kucharski, a professor of infectious-disease epidemiology at the London School of Hygiene and Tropical Medicine, told me. A person could test negative one day and then positive a few days later. If the point of restrictions is to slow local transmission, Kucharski said, calculations based on his research suggest that travelers should be tested twice: once before they arrive, then about three or four days afterward. Doing so would catch infected travelers who initially tested negative while limiting their window for spreading disease.

    Read: Why America scrapped its travel bans

    The best possible outcome of a travel restriction like the one the U.S. now has in place would be a very small delay before the arrival of a catastrophic new variant that has just emerged in China. In that scenario, any extra time might be used to intensify mitigation strategies and assess the degree to which current vaccines are expected to hold up. Historically, though, the time saved by travel bans has been wasted. After countries restricted travel from South Africa to keep Omicron at bay, governments responded by “not really doing much at all domestically,” Kucharski said. In any case, as my colleague Katherine J. Wu has pointed out, the virus is able to spread easily in China right now without any further changes to its genome. Population immunity there is modest, owing to the country’s low natural-infection rate and less effective vaccines, so the virus can infect people perfectly well as is.

    The travel restrictions on China will have little impact on the spread of COVID, but they do send a forceful political message. The U.S. measures are meant to pressure China, by slowing its economic rebound, into being transparent about its COVID situation, Stephen Morrison, the director of the Global Health Policy Center at the Center for Strategic and International Studies, a Washington, D.C.-based think tank, told me. China’s alleged official death count, for example—5,259 as of January 4—seems way too low to be believable, especially amid reports of overflowing Chinese hospitals and funeral homes. So long as the country isn’t more forthcoming, Morrison said, then Chinese tourists, who have only recently been allowed to travel internationally, will continue to be unwelcome.

    Expressing this message through a largely pointless public-health measure comes with a price. When that measure fails to keep COVID spread at bay, faith in public-health institutions could decline, which Pagel said is the “biggest danger” for the next pandemic. It also stokes the long-standing fear that Chinese people are more likely to carry disease than anyone else, whether foreign or American. “We are watching this policy so carefully to see if it will once again invite a racial backlash,” Manjusha Kulkarni, a co-founder of Stop AAPI Hate, told me. If a rise in anti-Asian hate and violence comes along with more transparency from China about its COVID situation, the cost of these restrictions hardly seems worth their benefits.

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    Yasmin Tayag

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