The writers on The Atlantic’s Science, Technology, and Health desks have learned a lot this year. Our coverage of the ongoing coronavirus pandemic has continued, but this year, more so than in 2020 and 2021, we’ve also had the chance to report on topics that have filled us with awe and delight. Though the past 12 months have not been free of concerns about infectious disease, climate change, and even nuclear war, we’ve embraced more fascination and curiosity in our coverage this year, and we wanted to share and reflect on some of the most compelling tidbits we’ve stumbled across. We hope you find these facts as mind-blowing as we did.
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Max Hamilton found out that his roommate had been exposed to the coronavirus shortly after Thanksgiving. The dread set in, and then, so did her symptoms. Wanting to be cautious, she tested continuously, remaining masked in all common areas at home. But after three negative rapid tests in a row, she and Hamilton felt like the worst had passed. At the very least, they could chat safely across the kitchen table, right? Wrong. More than a week later, another test finally sprouted a second line: bright, pink, positive. Five days after that, Hamilton was testing positive as well. This was his second bout of COVID since the start of the pandemic, and he wasn’t feeling so great. Congestion and fatigue aside, he was “just very frustrated,” he told me. He felt like they had done everything right. “If we have no idea if someone has COVID, how are we supposed to avoid it?” Now he has a different take on rapid tests: They aren’t guarantees. When he and his roommate return from their Christmas and New Year’s holidays, he said, they’ll steer clear of friends who show any symptoms whatsoever. Hamilton and his roommate are just two of many who have been wronged by the rapid. Since the onset of Omicron, for one reason or another, false negatives seem to be popping up with greater frequency. That leaves people stuck trying to figure out when, and if, to bank on the simplest, easiest way to check one’s COVID status. At this point, even people who work in health care are throwing up their hands. Alex Meshkin, the CEO of the medical laboratory Flow Health, told me that he spent the first two years of the pandemic carefully masking in social situations and asking others to get tested before meeting with him. Then he came down with COVID shortly after visiting a friend who didn’t think that she was sick. Turns out, she’d only taken a rapid test. “That’s my wonderful personal experience,” Meshkin told me. His takeaway? “I don’t trust the antigen test at all.” [Read: Should everyone be masking again?] That might be a bit extreme. Rapid antigen tests still work, and we’ve known about the problem of delayed positivity for ages. In fact, the tests are about as good at picking up the SARS-CoV-2 virus now as they’ve ever been, Susan Butler-Wu, a clinical microbiologist at the University of Southern California’s Keck School of Medicine, told me. Their limit of detection––the lowest quantity of viral antigen that will register reliably as a positive result––didn’t really change as new variants emerged. At the same time, the Omicron variant and its offshoots seem to take longer, after the onset of infection, to accumulate that amount of virus in the nose, says Wilbur Lam, a professor of pediatrics and biomedical engineering at Emory University who is also one of the lead investigators assessing COVID diagnostic tests for the federal government. Lam told me that this delay, between getting sick and reaching the minimum detectable concentration of the viral antigen, could be contributing to the spate of false-negative results. That problem isn’t likely to be solved anytime soon. The same basic technology behind COVID rapid tests, called “lateral flow,” has been around for years; it’s even used for standard pregnancy tests, Emily Landon, an infectious-disease physician at the University of Chicago, told me. Oliver Keppler, a virology researcher at the Ludwig Maximilian University of Munich who was involved in a study comparing the performance of rapid tests between variants, says there isn’t really a way to tweak the tests so that they’ll be any more sensitive to newer variants. “Conceptually, there’s little we can do.” In the meantime, he told me, we have to accept that “in the first one or two days of infection with Omicron, on average, antigen tests are very poor.” Of course, Hamilton (and his roommate) would point out that the tests can fail even several days after symptoms start. That’s why he and others are feeling hesitant to trust them again. “It’s not just about the utility or accuracy of the test. It’s also about the willingness to even do the test,” Ng Qin Xiang, a resident in preventative medicine at Singapore General Hospital who was involved in a study examining the performance of rapid antigen tests, told me. “Even within my circle of friends, a lot of people, when they have respiratory symptoms, just stay home and rest,” he said. They just don’t see the point of testing. [Read: COVID science is moving backwards] Landon recently got COVID for the first time since the start of the pandemic. When her son came home with the virus, she decided to perform her own experiment. She kept track of her rapids, testing every 12 hours and even taking pictures for proof. Her symptoms started on a Friday night and her initial test was negative. So was Saturday morning’s. By Saturday evening, though, a faint line had begun to emerge, and the next morning—36 hours after symptom onset—the second line was dark. Her advice for those who want the most accurate result and don’t have as many tests to spare is to wait until you’ve had symptoms for two days before testing. And if you’ve been exposed, have symptoms, and only have one test? “You don’t even need to bother. You probably have COVID.” from https://ift.tt/1X5I9bd Check out http://natthash.tumblr.com Roughly a century ago, a new fad diet began to sweep the United States. Hollywood starlets such as Ethel Barrymore supposedly swore by it; the citrus industry hopped on board. All a figure-conscious girl had to do was eat a lot of grapefruit for a week, or two, or three. The Grapefruit Diet, like pretty much all other fad diets, is mostly bunk. If people were losing weight with the regimen, that’s because the citrus was being recommended as part of a portion-controlled, low-calorie, low-carbohydrate diet—not because it had exceptional flab-blasting powers. And yet, the diet has survived through the decades, spawning a revival in the 1970s and ’80s, a dangerous juice-exclusive spin-off called the grapefruit fast, and even a shout-out from Weird Al; its hype still plagues nutritionists today. [Read: Why science can be so indecisive about nutrition] But for every grapefruit evangelist, there is a critic warning of its dangers—probably one with a background in pharmacology. The fruit, for all its tastiness and dietetic appeal, has another, more sinister trait: It raises the level of dozens of FDA-approved medications in the body, and for a select few drugs, the amplification can be potent enough to trigger a life-threatening overdose. For most people, chowing down on grapefruit is completely safe; it would take “a perfect storm” of factors—say, a vulnerable person taking an especially grapefruit-sensitive medication within a certain window of drinking a particular amount of grapefruit juice—for disaster to unfurl, says Emily Heil, an infectious-disease pharmacist at the University of Maryland. But that leaves grapefruit in a bit of a weird position. No one can agree on exactly how much the world should worry about this bittersweet treat whose chemical properties scientists still don’t fully understand. Grapefruit’s medication-concentrating powers were discovered only because of a culinary accident. Some three decades ago, the clinical pharmacologist David Bailey (who died earlier this year) was running a trial testing the effects of alcohol consumption on a blood-pressure medication called felodipine. Hoping to mask the distinctive taste of booze for his volunteers, Bailey mixed it with grapefruit juice, and was shocked to discover that blood levels of felodipine were suddenly skyrocketing in everyone—even those in the control group, who were drinking virgin grapefruit juice. After running experiments on himself, Bailey confirmed that the juice was to blame. Some chemical in grapefruit was messing with the body’s natural ability to break down felodipine in the hours after it was taken, causing the drug to accumulate in the blood. It’s the rough physiological equivalent of jamming a garbage disposal: Waste that normally gets flushed just builds, and builds, and builds. In this case, the garbage disposal is an enzyme called cytochrome P450 3A4—CYP3A4 for short—capable of breaking down a whole slate of potentially harmful chemicals found in foods and meds. And the jamming culprit is a compound found in the pulp and peel of grapefruit and related citrus, including pomelos and Seville oranges. It doesn’t take much: Even half a grapefruit can be enough to trigger a noticeable interaction, says George Dresser, a pharmacologist at Western University, in Ontario. The possible consequences of these molecular clogs can sometimes get intense. “On the list of concerning food-drug interactions,” Dresser told me, “arguably, this is the most important one.” When paired with certain heart medications, grapefruit could potentially cause arrhythmias; with some antidepressants, it might induce nausea, vomiting, and an elevated heart rate. Grapefruit can also raise blood levels of the cholesterol drugs atorvastatin and simvastatin, prompting muscle pain and, eventually, muscle breakdown. One of the fruit’s most worrying interactions occurs with an immunosuppressive drug called tacrolimus, frequently prescribed to organ-transplant patients, that may, when amped up by grapefruit, spark headaches, tremors, hypoglycemia, and kidney problems. The citrus even has the ability to lift blood levels of drugs of abuse, including fentanyl, oxycodone, and ketamine. The full list of potential interactions is long. “More than 50 percent of drugs on the market are metabolized by CYP3A4,” which inhabits both the liver and the gut, says Mary Paine, a pharmacologist at Washington State University. That said, grapefruit can really affect only intestinal CYP3A4, and will cause only a small fraction of those medications to reach notably higher concentrations in the blood (and sometimes only when fairly large quantities of juice are consumed—a quart or more). And only a small fraction of those medications will, when amassed, threaten true toxicity. Our bodies are always making more CYP3A4; stop eating grapefruit and, within a day or two, levels of the protein should more or less reset. Professionals disagree on how to characterize grapefruit’s risks. To Shirley Tsunoda, a pharmacist at UC San Diego, “it’s definitely a big deal,” especially for the organ-transplant patients to whom she prescribes tacrolimus. Her advice to them is to indulge in grapefruit exactly never—and ideally, tacrolimus-takers should skip related citrus too. Tsunoda even advises people to check the labels of mixed-fruit juices, just in case the makers sneaked some grapefruit in, and she thinks twice when considering noshing on it herself. Paul Watkins, a pharmacologist at the University of North Carolina at Chapel Hill, is much less worried; his bigger concern, he told me, is that the fruit’s reputation as a nemesis of oral medications has been way overblown. He used to study grapefruit-drug interaction but abandoned it years ago, after “I came to the conclusion that it wasn’t very important,” he told me. Some concern is absolutely warranted for certain people on certain meds, he noted. But “I think the actual incidence of patients who have gotten into any kind of trouble or had serious adverse reactions due to taking their drugs with grapefruit juice is very, very small.” Even the FDA seems a bit unsure of how it feels about the fruit. The agency has stamped the documentation of several grapefruit-sensitive medications with official warnings. But fact sheets for other drugs merely mention that they can interact with grapefruit, say to consult a health-care professional, or just counsel people to avoid drinking the juice in “large amounts.” And as Dan Nosowitz has reported for Atlas Obscura, several interacting drugs that bear warnings in Canada—among them, Viagra, oxycodone, the HIV antiviral Edurant, and the blood pressure medication verapamil--don’t mention any issues with grapefruit in the United States. (When I asked the agency about these discrepancies, a spokesperson wrote, “The FDA is continuously reviewing new information about approved drugs, including studies and reports of adverse events. If the FDA determines there is a safety concern, the agency will take appropriate action.”) Very little solid data can precisely quantify grapefruit’s perils. Over the years, researchers have documented a number of isolated cases of citrus-drug interactions that prompted urgent medical care. But some of them involved truly exceptional amounts of juice. And citrus stans aren’t constantly dropping dead in clinical trials or nursing homes. Even when Bailey first presented his findings to the greater medical community, “people asked, ‘Where are all the bodies?’” Dresser, who was mentored by Bailey, told me. The paucity of data, Dresser contends, stems in part from health-care workers neglecting to check their patients for a history of juice-chugging. For now, the conversation has mostly stalled, while grapefruit has served up even more mysteries. In the years since Bailey’s discovery, researchers have found that the fruit might lower the concentration of certain drugs, such as the allergy med fexofenadine, perhaps by keeping the lining of the intestines from absorbing certain compounds. New drugs are a particularly murky area, especially because grapefruit interactions aren’t a typical first priority when a new medication hits the market. The popular COVID antiviral pill Paxlovid, for instance, contains the CYP3A4-susceptible ingredient ritonavir. A Pfizer representative told me that the company is not concerned about toxicity. But Heil wonders whether grapefruit could mildly aggravate some of Paxlovid’s irksome side effects: diarrhea, for instance, or maybe the sour, metallic taste that reminds many people of … well, grapefruit. [Read: Paxlovid mouth is real—and gross] That said, most grapefruit lovers need not despair. The fruit is still healthy—chock-full of vitamins and flavor—and yet is often overlooked, says Heidi Silver, a nutrition scientist at Vanderbilt University. Silver and researchers have shown that consuming grapefruit flesh or juice might be able to slightly lower levels of triglycerides and cholesterol. Technically, it can even play a role in weight loss: Snacking on a small portion before a meal can help people feel full faster. Then again, a glass of water will too. Just as grapefruit is not a miraculous vanquisher of fat, it isn’t a ubiquitous killer. Even people on certain medications may be able to enjoy it if they consult an expert first. Heil’s own father absolutely adores grapefruit, and also happens to take an oral medication that can interact. Swallow them too close together, and he risks dizziness and fatigue. But he and Heil have found a compromise: He can have small portions of grapefruit or its juice in the morning, spaced about 12 hours out from when he takes his meds at bedtime. A few weeks ago, Heil (who thinks grapefruit is disgusting) even gave her dad the green light to enjoy a dinnertime cocktail that contained a small splash of the juice. Maybe the smidge of fruit affected his meds that day. But “it wasn’t going to be the end of the world,” Heil told me. To say that, after all, would have been an exaggeration. from https://ift.tt/54WxgcR Check out http://natthash.tumblr.com No country has a perfect COVID vaccination rate, even this far into the pandemic, but America’s record is particularly dismal. About a third of Americans—more than a hundred million people—have yet to get their initial shots. You can find anti-vaxxers in every corner of the country. But by far the single group of adults most likely to be unvaccinated is Republicans: 37 percent of Republicans are still unvaccinated or only partially vaccinated, compared with 9 percent of Democrats. Fourteen of the 15 states with the lowest vaccination rates voted for Donald Trump in 2020. (The other is Georgia.) We know that unvaccinated Americans are more likely to be Republican, that Republicans in positions of power led the movement against COVID vaccination, and that hundreds of thousands of unvaccinated Americans have died preventable deaths from the disease. The Republican Party is unquestionably complicit in the premature deaths of many of its own supporters, a phenomenon that may be without precedent in the history of both American democracy and virology. Obviously, nothing about being a Republican makes someone inherently anti-vaccine. Many Republicans—in fact, most of them—have gotten their first two shots. But the wildly disproportionate presence of Republicans among the unvaccinated reveals an ugly and counterintuitive aspect of the GOP campaign against vaccination: At every turn, top figures in the party have directly endangered their own constituents. Trump disparaged vaccines while president, even after orchestrating Operation Warp Speed. Other politicians, such as Texas Governor Greg Abbott, made all COVID-vaccine mandates illegal in their state. More recently, Florida Governor Ron DeSantis called for a grand jury to investigate the safety of COVID vaccines. The right-wing media have leaned even harder into vaccine skepticism. On his prime-time Fox News show, Tucker Carlson has regularly questioned the safety of vaccines, inviting guests who have called for the shots to be “withdrawn from the market.” Breaking down the cost of vaccine hesitancy would be simple if we could draw a causal relationship between Republican leaders’ anti-vaccine messaging and the adoption of those ideas by Americans, and then from those ideas to deaths due to non-vaccination. Unfortunately, we don’t have the data to do so. Individual vaccine skepticism cannot be traced back to a single source, and even if it could, we don’t know exactly who is unvaccinated and what their political affiliations are. What we do have is a patchwork of estimations and correlations that, taken together, paint a blurry but nevertheless grim picture of how Republican leaders spread the vaccine hesitancy that has killed so many people. We know that as of April 2022, about 318,000 people had died from COVID because they were unvaccinated, according to research from Brown University. And the close association between Republican vaccine hesitancy and higher death rates has been documented. One study estimated that by the fall of 2021, vaccine uptake accounted for 10 percent of the total difference between Republican and Democratic deaths. But that estimate has changed—and even likely grown—over time. Partisanship affected outcomes in the pandemic even before we had vaccines. A recent study found that from October 2020 to February 2021, the death rate in Republican-leaning counties was up to three times higher than that of Democratic-leaning counties, likely because of differences in masking and social distancing. Even when vaccines came around, these differences continued, Mauricio Santillana, an epidemiology expert at Northeastern University and a co-author of the study, told me. Follow-up research published in Lancet Regional Health Americas in October looked at deaths from April 2021 to March 2022 and found a 26 percent higher death rate in areas where voters leaned Republican. “There are subsequent and very serious [partisan] patterns with the Delta and Omicron waves, some of which can be explained by vaccination,” Bill Hanage, a co-author of the paper and an epidemiologist at Harvard, told me in an email. But to understand why Republicans have died at higher rates, you can’t look at vaccine status alone. Congressional districts controlled by a trifecta of Republican leaders—state governor, Senate, and House—had an 11 percent higher death rate, according to the Lancet study. A likely explanation, the authors write, could be that in the post-vaccine era, those leaders chose policies and conveyed public-health messages that made their constituents more likely to die. Although we still can’t say these decisions led to higher death rates, the association alone is jarring. One of the most compelling studies comes from researchers at Yale, who published their findings as a working paper in November. They link political party and excess-death rate—the percent increase in deaths above pre-COVID levels—among those registered as either Democrats or Republicans, providing a more granular view. They chose to analyze data from Florida and Ohio from before and after vaccines were available. Looking at the period before the vaccine, researchers found a 1.6 percentage-point difference in excess death rate among Republicans and Democrats, with a higher rate among Republicans. But after vaccines became available, that gap widened dramatically to 10.4 percentage points, again with a higher Republican excess death rate. “When we compare individuals who are of the same age, who live in the same county in the same month of the pandemic, there are differences correlated with your political-party affiliation that emerge after vaccines are available,” Jacob Wallace, an assistant professor of public health at Yale who co-authored the paper, told me. “That’s a statement we can confidently make based on the study and we couldn’t before.” Even with this new research, it is difficult to determine just how many people died as a result of their political views. In the “excess death” study, researchers dealt only with rates of excess death, not actual death-toll numbers. Overall, excess deaths represent a small share of deaths. “On the scale of national registration for both parties,” Wallace said, “we’re talking about relatively small numbers and differences in deaths” when you look at excess death rates alone. The absolute number of Republican deaths is less important than the fact that they happened needlessly. Vaccines could have saved lives. And yet, the party that describes itself as pro-life campaigned against them. Democrats are not without fault, though. The Biden administration’s COVID blunders are no doubt to blame for some of the nation’s deaths. But on the whole, Democratic leaders have mostly not promoted ideas or enforced policies around COVID that actively chip away at life expectancy. It is a tragedy that the Republican push against basic lifesaving science has cut lives short and continues to do so. The partisan divide in COVID deaths, Hanage said, is just “another example of how the partisan politics of the U.S. has poisoned the well of public health.” What’s most concerning about all of this is that partisan disparities in death rates were also apparent before COVID. People living in Republican jurisdictions have been at a health disadvantage for more than 20 years. From 2001 to 2019, the death rate in Democratic counties decreased by 22 percent, according to a recent study; in Republican counties, it declined by only 11 percent. In the same time period, the political gap in death rates increased sixfold. Health outcomes have been diverging at the state level since the ’90s, Steven Woolf, an epidemiologist at Virginia Commonwealth University, told me. Woolf’s work suggests that over the decades, state policy decisions on health issues such as Medicaid, gun legislation, tobacco taxes, and, indeed, vaccines have likely had a stronger impact on state health trajectories than other factors. COVID’s high Republican death rates are not an isolated phenomenon but a continuation of this trend. As Republican-led states pushed back on lockdowns, the impact on population death rates was observed within weeks, Woolf said. If the issue is indeed systemic, that doesn’t bode well for the future. Other factors could explain the higher death rate in Republican-leaning places—more poverty, less education, worse socioeconomic conditions—, though Woolf said isn’t convinced that those factors aren’t related to bad state health policy too. In any case, the long-term decline of health in red states indicates that there is an ongoing problem at a high level in Republican-led places, and that something has gone awry. “If you happen to live in certain states, your chances for living a long life are going to be much higher than if you’re an American living in a different state,” Woolf said. Unfortunately, this trend shows no signs of breaking. The anti-science messaging that fuels such a divide is popular with Republican leaders because it plays so well with their constituents. Far-right crowds cheer for missed vaccine targets and jokes about executing scientific leaders. In an environment where partisanship trumps all—including trying to save people’s lives—such messaging is both politically effective and morally abhorrent. The data, however imperfect, demand a reckoning with the consequences of such a strategy not only during the pandemic but over the past few decades, and in the years to come. But to acknowledge how many Republicans didn’t have to die would mean giving credence to scientific and medical expertise. So long as America remains locked in a poisonous partisan battle in which science is wrongly dismissed as being associated with the left, the death toll will only rise. from https://ift.tt/Aw4I9uE Check out http://natthash.tumblr.com Winter is here, and so, once more, are mask mandates. After last winter’s crushing Omicron spike, much of America did away with masking requirements. But with cases once again on the rise and other respiratory illnesses such as RSV and influenza wreaking havoc, some scattered institutions have begun reinstating them. On Monday, one of Iowa’s largest health systems reissued its mandate for staff. That same day, the Oakland, California, city council voted unanimously to again require people to mask up in government buildings. A New Jersey school district revived its own mandate, and the Philadelphia school district announced that it would temporarily do the same after winter break. The reinstated mandates are by no means widespread, and that seems unlikely to change any time soon. But as we trudge into yet another pandemic winter, they do raise some questions. What role should masking play in winters to come? Is every winter going to be like this? Should we now consider the holiday season … masking season? These questions don’t have simple answers. Regardless of what public-health research tells us we should do, we’ve clearly seen throughout the pandemic that limits exist to what Americans will do. Predictably, the few recent mandates have elicited a good deal of aggrievement and derision from the anti-masking set. But even many Americans who diligently masked earlier in the pandemic seem to have lost their appetite for this sort of intervention as the pandemic has eased. In its most recent national survey of health behavior, the COVID States Project found that only about a quarter of Americans still mask when they go out, down from more than 80 percent at its peak. Some steadfast maskers have started feeling awkward: “I have personally felt like I get weird looks now wearing a mask,” Saskia Popescu, an epidemiologist at George Mason University, told me. Even so, masking remains one of the best and least obtrusive infection-prevention measures we have at our disposal. We haven’t yet been slammed this winter by another Omicronlike variant, but the pandemic is still here. COVID cases, hospitalizations, and deaths are all rising nationally, possibly the signs of another wave. Kids have been hit especially hard by the unwelcome return of influenza, RSV, and other respiratory viruses. All of this is playing out against the backdrop of low COVID-19-booster uptake, leaving people more vulnerable to death and severe disease if they get infected. All of which is to say: If you’re only going to mask for a couple of months of the year, now is a good time. “Should people be masking? Absolutely yes, right now,” Seema Lakdawala, a flu-transmission expert at Emory University, told me. That doesn’t mean masking everywhere all the time. Lakdawala masks at the grocery store, at the office, and while using public transportation, but not when she goes out to dinner or attends parties. Those activities pose a risk of infection, but Lakdawala’s goal is to reduce her risk, not to minimize it at all costs. A strategy that prevents you from enjoying the things you love most is not sustainable. Both Lakdawala and Popescu were willing to go so far as to suggest that masking should indeed become a seasonal fixture—just like skiing and snowmen, only potentially lifesaving and politically radioactive. Even before the pandemic, influenza alone killed tens of thousands of Americans every year, and more masking, even if only in certain targeted settings, could go a long way toward reducing the toll. “If we could just say, Hey, from November to February, we should all just mask indoors,” Lakdawala said, that would do a lot of good. “The idea of the unknown and the perpetualness of two years of things coming on and off, and then the confusing CDC county-by-county guideline—it just sort of makes it harder for everybody than if we had a simple message.” Universal mandates or recommendations that people mask at small social gatherings are probably too much to ask, Lakdawala told me. Instead, she favors some limited, seasonal mandates, such as on public transportation or in schools dealing with viral surges. David Dowdy, an epidemiologist at the Johns Hopkins Bloomberg School of Public Health, is all for masking season, he told me, but he’d be more hesitant to resort to mandates. “It’s hard to impose mandates without a very strong public-health rationale,” he said, especially in our current, hyperpolarized climate. And although that rationale clearly existed for much of the past two crisis-ridden years, it’s less clear now. “COVID is no longer this public-health emergency, but it’s still killing thousands of people every week, hundreds a day … so it becomes a more challenging balancing act,” Dowdy said. Rather than requirements, he favors broad recommendations. The CDC, for instance, could suggest that during flu season, people should consider wearing masks in crowded indoor spaces, the same way it recommends that everyone old enough get a flu shot each year. (Although the agency has hardly updated its “Interim Guidance” on masks and the flu since 2004, Director Rochelle Walensky has encouraged people to mask up this winter.) Another strategy, Dowdy said, could be making masks more accessible to people, so that every time they enter a public indoor space, they have the option of grabbing an N95. The course of the pandemic has both demonstrated the efficacy of widespread masking and rendered that strategy so controversial in America as to be virtually impossible. The question now is how to negotiate those two realities. Whatever answer we come up with this year, the question will remain next year, and for years after that. The pandemic will fade, but the coronavirus, like the other surging viruses this winter, will continue to haunt us in one form or another. “These viruses are here,” Lakdawala said. “They’re not going anywhere.” from https://ift.tt/t2Un9ox Check out http://natthash.tumblr.com 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.” [Read: America’s flu-shot problem is also its next COVID-shot problem] 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.” [Read: The three COVID developments I’m still holding out hope for] 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. from https://ift.tt/5DgXEw2 Check out http://natthash.tumblr.com Barack Obama did it. Donald Trump did it. Joe Biden, of course, has done it too. But each of them was wrong: Kissing another person’s baby is just not a good idea. That rule of lip, experts told me, should be a top priority during the brisk fall and winter months, when flu, RSV, and other respiratory viruses tend to go hog wild (as they are doing right this very moment). “But actually, this is year-round advice,” says Tina Tan, a pediatrician at Lurie Children’s Hospital of Chicago. Rain, wind, or shine, outside of an infant’s nuclear family, people should just keep their mouths to themselves. Leave those soft, pillowy cheeks alone! A moratorium on infant smooching might feel like a bit of a downer—even counterintuitive, given how essential it is for infants and caregivers to touch. But kissing isn’t the only way to show affection to a newborn, and the rationale for cutting back on it specifically is one that most can get behind: keeping those same wee bebes safe. An infant’s immune system is still fragile and unlearned; it struggles to identify infectious threats and can’t marshal much of a defense even when it does. Annette Cameron, a pediatrician at Yale, told me she usually advises parents to avoid public places—church, buses, stores—until their baby is about six weeks old, and able to receive their first big round of immunizations. (And even then, shots take a couple of weeks to kick in.) The situation grows far less perilous once kids’ vaccine cards start to get more full; past, say, six months of age or so, they’re in much better shape. But risk remains a spectrum, especially when lips get involved. The mouth, I am sorry to tell you, is a weird and gross place, chock-full of saliva, half-chewed flecks of food, and microbes galore; all that schmutz is apt to drool and dribble onto whatever surfaces we drag our faces across. Flu, RSV, rhinovirus, SARS-CoV-2, and the coronaviruses that lead to common colds are among the many respiratory pathogens that hang out in and around our mouth. Although these viruses don’t usually make adults very sick, they can clobber young, unvaccinated kids, whose airways are still small. Health-care workers are seeing a lot of those illnesses now: Cameron recently treated a two-week-old who’d caught rhinovirus and ended up in the ICU. Also on the list of smoochable threats is herpes simplex 1, the virus responsible for cold sores. “That’s the one I worry about the most,” says Annabelle de St. Maurice, a pediatric-infectious-disease specialist at UCLA and the mother of a 1-year-old daughter. Most American adults harbor chronic HSV-1 infections in their mouth with no symptoms at all, save for maybe the occasional lesion. But the super-transmissible virus can spread throughout the body of an infant, triggering high fevers and seizures bad enough to require a visit to the hospital. For the first few weeks of a baby’s life, anyone with an active cold sore—blood relative, presidential candidate, or both—would do well to keep away. (Even a history of cold sores might warrant extra caution.) The lip-restraining guidance is most pertinent to people outside an infant’s household, experts told me, which can include extended family. Ideally, even grandparents “should not be kissing on the baby for at least the first few months,” Tan told me. Within a home, siblings attending day care and school—where it’s easy to pick up germs—might also want to sheathe their smackeroos at first. Years ago, Cameron’s own son had to be admitted to the hospital with RSV when he was six weeks old after catching the virus from his 4-year-old sister. Lakshmi Ganapathi, a pediatric-infectious-disease specialist at Boston Children’s Hospital, told me that she didn’t kiss her own two sons on the face before they hit the six-week mark—though experts told me that they don’t expect most parents to get this puritanical about puckering up. [Read: The worst pediatric-care crisis in decades] Baby-kissing—especially outside families and tight-knit social circles—isn’t a universal impulse: A few of my friends were rather shocked to hear that such a PSA was even necessary. But people’s threshold for instigating a loving lunge is far lower when it comes to babies than to older kids or adults. One colleague told me that strangers have reached into his daughter’s stroller to stroke her hair; another mentioned that randos have swooped in to tickle his son’s feet. When de St. Maurice takes strolls around her neighborhood with her daughter, she’s surprised by how often casual acquaintances will try to dive-bomb her baby with pursed lips. Then again, there is perhaps no lure more powerful than a tiny human. Babies snare us visually, with their wide eyes, round cheeks, and button noses; their scent wafts toward us like the heady perfume of a fresh cream scone. (One colleague with kids told me that inhaling that particular odor was, for him, “like huffing glue.”) Among primates, human infants are born especially vulnerable, in desperate need of help, and so we go into overdrive providing it, even to others’ babies, who—at least in our social species—might benefit from communal care. “It’s programmed into us,” Oriana Aragón, a social psychologist at the University of Cincinnati, told me. “I’m able to get really strong reactions out of people with just a photograph.” Even the urge to plant a wet one on someone else’s baby may have adaptive roots in kiss feeding, the practice of delivering pre-chewed meals to an infant lip to lip, says Shelly Volsche, an anthropologist at Boise State University. Kiss-feeding isn’t very popular in the United States today, but it’s still practiced by many groups around the globe. [Read: Pregnancy is a war; birth is a cease-fire] But as important as these acts are for babies, they can also be at odds with an infant’s health when a bunch of respiratory viruses are swirling about. Those costs aren’t always top of mind when a stranger locks eyes with a tiny human across the way, and it can be “a really awkward conversation,” de St. Maurice told me, to deter someone who just wants to shower affection on your child. Cameron recommends being frank: “I’m just trying to protect my baby.” Physical deterrents can help, too. “Put them in the stroller, put the canopy up, buckle the baby in, make it as difficult as possible,” she said. That’s a lot of barriers for even the most dedicated baby kissers to surmount. De St. Maurice also likes to point out that her little infant, as adorable as she is, “could also potentially transmit something to you.” Plus, by the time they’re six months old, babies may be experiencing their first whiffs of stranger danger and react negatively to unfamiliar hands and mouths. “That’s not particularly good for the baby, and the stranger wouldn’t get anything out of it either,” says Ann Bigelow, a developmental psychologist at St. Francis Xavier University, in Canada. Again, this advice isn’t meant to starve infants of tactile stimulation. Kids need to be exposed to the outside world and all of its good-germiness. More than that, they need a lot of physical touch. “The skin is our largest sense organ,” Bigelow told me. Skin-to-skin contact stimulates the release of oxytocin, and cements the bond between a caregiver and an infant. Kissing doesn’t have to be the means for giving that affection, though it certainly can be. “Heck, when I’m a grandparent, I’m going to be kissing my grandchild,” Cameron told me. “Just try and stop me.” from https://ift.tt/wX4dz2y Check out http://natthash.tumblr.com This past spring, Amanda Goldberg crouched in the leafy undergrowth of a southwestern Virginia forest and attempted to swab a mouse for COVID. No luck; its nose was too tiny for her tools. “You never think about nostrils until you start having to swab an animal,” Goldberg, a conservation biologist at Virginia Tech University, told me. Larger-nosed creatures that she and her team had trapped, such as raccoons and foxes, had no issue with nose swabs—but for mice, throat samples had to do. The swabs fit reasonably well into their mouths, she said, though they endured a fair bit of munching. Goldberg’s throat-swabbing endeavors were part of a study she and her colleagues devised to answer an unexplored question: How common is COVID in wildlife? Of the 333 forest animals her team swabbed around Blacksburg, Virginia, spanning 18 species, one—an opossum—tested positive. This was to be expected, Goldberg said; catching a wild animal that happened to have an active infection right when it was swabbed was like finding Waldo. But the researchers also collected blood samples, and those were more telling about whether the animals had experienced previous bouts with COVID. Analysis by the Molecular Diagnostics Lab and the Fralin Biomedical Research Institute at Virginia Tech revealed antibodies across 24 animals spanning six species, including the opossum, the Eastern gray squirrel, and two types of mice. “Our minds were blown,” Goldberg said. “It was basically every species we sent” to the lab. That animals can get COVID is one of the earliest things we learned about the virus. Despite the endless debate over its origins, SARS-CoV-2 most likely jumped from an animal through an intermediate host to humans in Wuhan. Since then, it has since spread back to a range of animals. People have passed it to household pets, such as dogs and cats, and to a Disney movie’s worth of beasts, including lions, hippos, hyenas, tigers, mink, and hamsters. Three years into the pandemic, animals are still falling sick with COVID, just as we are. COVID is likely circulating more widely in animals than we are aware of, Edward Holmes, a biologist at the University of Sydney, told me. “In all my 30-plus years of doing work on this subject, I have never seen a virus that can infect so many animal species,” he said. More than 500 other mammal species are predicted to be highly susceptible to infection. Given that most people nowadays aren’t fretting too much about human-to-human spread, it makes sense that animal-to-human spread has largely been forgotten. But even when there are so many other pandemic concerns, animal COVID can’t be ignored. The consequences of sustained animal transmission are exactly the same as they are in people: The more COVID spreads, the more opportunities the virus has to evolve into new variants. What’s most alarming is the chance that one of those variants could spill back into humans. As we’ve known since the pandemic started, SARS-CoV-2 is not a human virus, but one that can infect multiple animals, including humans. As long as animals are still getting COVID, we’re not out of the doghouse either. Perhaps part of the reason COVID in animals has been overlooked—apart from the fact that they’re not people—is that most species don’t seem to get very sick. Animals that have gotten infected generally exhibit mild symptoms—typically some coughing and sluggishness, as in pumas and lions. But our research has gone only fur-deep. “We certainly can’t ask them, ‘Are you feeling headaches, or sluggish?’” said Goldberg, who worries about long-term or invisible symptoms going undiagnosed in species. And so animal COVID has lingered unchecked, increasing the chances that it could mean something bad for us. The good news is that the overall risk of getting COVID from animals is considered low, according to the CDC. This is partly explained by evolutionary theory, which predicts that most variants that emerge in an animal population will have adapted to become better at infecting the host animal—not us. But some of them, strictly by chance, “could be highly transmissible or virulent in humans,” Holmes said. “It’s an unpredictable process.” His concern is not that animals will start infecting people en masse—your neighbors are far likelier to do that than raccoons—but that in animals, SARS-CoV-2 could form new variants that can spill over into people. Some scientists believe that Omicron emerged this way in mice, though evidence remains scant. A troubling sign is that there’s already some evidence that COVID has made its way from humans to animals, where it mutated, and then made its way back into humans. Take white-tailed deer, by now a well-known COVID host. Every fall, hunters take to the golden meadows and reddening forests of southwestern Ontario to shoot the deer, giving researchers an opportunity to test some of the hunted animals for COVID. The species has been infected with the same variants circulating widely in humans—a handful of Staten Island deer caught Omicron last winter, for example—which suggests that people are infecting them. How the deer get infected still isn’t clear: Extended face time with humans, nosing around in trash, or slurping up our wastewater are all possibilities. The researchers in Canada found not only that some of the animals tested positive, but also that the variant they carried had never before been seen in humans, indicating that the virus had been spreading and mutating within the population for a long time, Brad Pickering, a research scientist for the Canadian government who studied the deer, told me. In fact, the new variant is among the most evolutionarily divergent ones identified so far. But despite its differences, it appeared to have infected at least one person who had interacted with deer the week before falling ill. “We can’t make a direct link between them,” Pickering said, but the fact that such a highly diverged deer variant was detected in a human is very suggestive of how that person got sick. This research adds to the small but growing body of evidence that the COVID we spread to animals could come back to bite us. Fortunately, this particular spillback does not appear to have had serious consequences for humans; rogue deer variants don’t seem to be circulating in southern Canada. But this is not the sole documented instance of animal-to-human spread: People have been infected by mink in the Netherlands, hamsters in Hong Kong, and a cat in Thailand. Other spillbacks have probably occurred and gone unnoticed. So far, no data show that the animal variants that have spread to humans are more dangerous for us. Even if a potential animal variant isn't the next Omicron, it could still be better at dodging our existing treatments and vaccines, Pickering said. But there is also, frankly, a lack of data. Local wildlife-surveillance efforts led by researchers like Goldberg and Pickering are ongoing, but they do not exist in most countries, Holmes said. An international database of known animal infections, maintained by Complexity Science Hub Vienna, is a promising start. An interactive map shows the locations of previously infected animals, including large hairy armadillos (Argentina), manatees (Brazil), and cats (everywhere). At the very least, with animal COVID, “we need to know what species it’s in, in what abundance, and genetically, what those variants look like,” Holmes said. “It’s absolutely critical to know where [the virus] is going.” Without this, there is no way of knowing how often spillback occurs and whether it puts humans at risk. And we can’t tell whether new COVID variants are also putting animals in danger, Goldberg said; a devastating Omicron-like variant could emerge in their populations too. The steps we need to take to mitigate the animal-COVID problem—and prevent other zoonotic diseases from jumping into humans—are clear, even if they don’t seem to be happening. Eliminating wet markets where wild animals are sold is an obvious preventive measure, but it has been difficult to implement because the livelihoods and diets of many people, especially in the global South, depend on them. As climate change and land development decimate even more habitats, wildlife will be forced into ever-closer quarters with us, fostering an even more efficient exchange of viruses between species. Unlike mask wearing and other straightforward options for curbing the human spread of COVID, preventing its transmission to, from, and among animals will require major upheavals to the way our societies run, likely far greater than we are willing to commit to. Humans tend to act like COVID ends up afflicting us after traveling through a long chain of species. But to think so is like living in the Middle Ages, Holmes said, when the Earth was considered the center of the universe. As we learned then, we are not that important: Humans are but a node in an immense network of species that viruses move through in many directions. Just as animal viruses infect us, human viruses can spread to animals (measles, for example, kills a variety of great apes). There are definitely bigger problems than animal COVID—no one needs to hunker down for fear of sneezing deer—but as long as animals keep getting infected, we can’t overlook what that means for us. Paying attention to animal COVID often starts with a single swab—and a snout to stick it in. from https://ift.tt/wYqAbzh Check out http://natthash.tumblr.com At the start of the coronavirus pandemic, one of the worst things about SARS-CoV-2 was that it was so new: The world lacked immunity, treatments, and vaccines. Tests were hard to come by too, making diagnosis a pain—except when it wasn’t. Sometimes, the symptoms of COVID got so odd, so off-book, that telling SARS-CoV-2 from other viruses became “kind of a slam dunk,” says Summer Chavez, an emergency physician at the University of Houston. Patients would turn up with the standard-issue signs of respiratory illness—fever, coughing, and the like—but also less expected ones, such as rashes, diarrhea, shortness of breath, and loss of taste or smell. A strange new virus was colliding with people’s bodies in such unusual ways that it couldn’t help but stand out. Now, nearly three years into the crisis, the virus is more familiar, and its symptoms are too. Put three sick people in the same room this winter—one with COVID, another with a common cold, and the third with the flu—and “it’s way harder to tell the difference,” Chavez told me. Today’s most common COVID symptoms are mundane: sore throat, runny nose, congestion, sneezing, coughing, headache. And several of the wonkier ones that once hogged headlines have become rare. More people are weathering their infections with their taste and smell intact; many can no longer remember when they last considered the scourge of “COVID toes.” Even fever, a former COVID classic, no longer cracks the top-20 list from the ZOE Health Study, a long-standing symptom-tracking project based in the United Kingdom, according to Tim Spector, an epidemiologist at King’s College London who heads the project. Longer, weirder, more serious illness still manifests, but for most people, SARS-CoV-2’s symptoms are getting “pretty close to other viruses’, and I think that’s reassuring,” Spector told me. “We are moving toward a cold-like illness.” That trajectory has been forecast by many experts since the pandemic’s early days. Growing immunity against the coronavirus, repeatedly reinforced by vaccines and infections, could eventually tame COVID into a sickness as trifling as the common cold or, at worst, one on par with the seasonal flu. The severity of COVID will continue to be tempered by widespread immunity, or so this thinking goes, like a curve bending toward an asymptote of mildness. A glance at the landscape of American immunity suggests that such a plateau could be near: Hundreds of millions of people in the U.S. have been vaccinated multiple times, some even quite recently with a bivalent shot; many have now logged second, third, and fourth infections with the virus. Maybe, just maybe, we’re nearing the level of cumulative exposure at which COVID gets permanently more chill. Then again? Maybe not—and maybe never. [Read: What does it mean to care about COVID anymore?] The recent trajectory of COVID, at least, has been peppered with positive signs. On average, symptoms have migrated higher up the airway, sparing several vulnerable organs below; disease has gotten shorter and milder, and rates of long COVID seem to be falling a bit. Many of these changes roughly coincided with the arrival of Omicron in the fall of 2021, and part of the shift is likely attributable to the virus itself: On the whole, Omicron and its offshoots seem to prefer infecting cells in the nose and throat over those in the lungs. But experts told me the accumulation of immune defenses that preceded and then accompanied that variant’s spread are almost certainly doing more of the work. Vaccination and prior infection can both lay down protections that help corral the virus near the nose and mouth, preventing it from spreading to tissues elsewhere. “Disease is really going to differ based on the compartment that’s primarily infected,” says Stacey Schultz-Cherry, a virologist at St. Jude Children’s Research Hospital. As SARS-CoV-2 has found a tighter anatomical niche, our bodies have become better at cornering it. With the virus largely getting relegated to smaller portions of the body, the pathogen is also purged from the airway faster and may be less likely to be passed to someone else. On the individual level, a sickness that might have once unfurled into pneumonia now gets subdued into barely perceptible sniffles and presents less risk to others; on the population scale, rates of infection, hospitalization, and death go down. This is how things usually go with respiratory viruses. Repeat tussles with RSV tend to get progressively milder; post-vaccination flu is usually less severe. The few people who catch measles after getting their shots are less likely to transmit the virus, and they tend to experience such a trivial course of sickness that their disease is referred to by a different name, “modified” measles, says Diane Griffin, a virologist and an immunologist at Johns Hopkins University. It’s good news that the median case of COVID diminished in severity and duration around the turn of 2022, but it’s a bit more sobering to consider that there hasn’t been a comparably major softening of symptoms in the months since. The full range of disease outcomes—from silent infection all the way to long-term disability, serious disease, and death—remains in play as well, for now and the foreseeable future, Schultz-Cherry told me. Vaccination history and immunocompromising conditions can influence where someone falls on that spectrum. So too can age as well as other factors such as sex, genetics, underlying medical conditions, and even the dose of incoming virus, says Patricia García, a global-health expert at the University of Washington. New antibody-dodging viral variants could still show up to cause more severe disease even among the young and healthy, as occasionally happens with the flu. The BA.2 subvariant of Omicron, which is more immune-evasive than its predecessor BA.1, seemed to accumulate more quickly in the airway, and it sparked more numerous and somewhat gnarlier symptoms. Data on more recent Omicron subvariants are still being gathered, but Shruti Mehta, an epidemiologist at Johns Hopkins, says she’s seen some hints that certain gastrointestinal symptoms, such as vomiting, might be making a small comeback. [Read: Will we get Omicron’d again?] All of this leaves the road ahead rather muddy. If COVID will be tamed one day into a common cold, that future definitely hasn’t been realized yet, says Yonatan Grad, an epidemiologist at Harvard’s School of Public Health. SARS-CoV-2 still seems to spread more efficiently and more quickly than a cold, and it’s more likely to trigger severe disease or long-term illness. Still, previous pandemics could contain clues about what happens next. Each of the past century’s flu pandemics led to a surge in mortality that wobbled back to baseline after about two to seven years, Aubree Gordon, an epidemiologist at the University of Michigan, told me. But SARS-CoV-2 isn’t a flu virus; it won’t necessarily play by the same epidemiological rules or hew to a comparable timeline. Even with flu, there’s no magic number of shots or past infections that’s known to mollify disease—“and I think we know even less about how you build up immunity to coronaviruses,” Gordon said. The timing of when and how those defenses manifest could matter too. Almost everyone has been infected by the flu or at least gotten a flu shot by the time they reach grade school; SARS-CoV-2 and COVID vaccines, meanwhile, arrived so recently that most of the world’s population met them in adulthood, when the immune system might be less malleable. These later-in-life encounters could make it tougher for the global population to reach its severity asymptote. If that’s the case, we’ll be in COVID limbo for another generation or two, until most living humans are those who grew up with this coronavirus in their midst. COVID may yet stabilize at something worse than a nuisance. “I had really thought previously it would be closer to common-cold coronaviruses,” Gordon told me. But severity hasn’t declined quite as dramatically as she’d initially hoped. In Nicaragua, where Gordon has been running studies for years, vaccinated cohorts of people have endured second and third infections with SARS-CoV-2 that have been, to her disappointment, “still more severe than influenza,” she told me. Even if that eventually flips, should the coronavirus continue to transmit this aggressively year-round, it could still end up taking more lives than the flu does—as is the case now. Wherever, whenever a severity plateau is reached, Gordon told me that our arrival to it can be confirmed only in hindsight, “once we look back and say, ‘Oh, yeah, it’s been about the same for the last five years.’” But the data necessary to make that call are getting harder to collect as public interest in the virus craters and research efforts to monitor COVID’s shifting symptoms hit roadblocks. The ZOE Health Study lost its government funding earlier this year, and its COVID-symptom app, which engaged some 2.4 million regular users at its peak, now has just 400,000—some of whom may have signed up to take advantage of newer features for tracking diet, sleep, exercise, and mood. “I think people just said, ‘I need to move on,’” Spector told me. Mehta, the Johns Hopkins epidemiologist, has encountered similar hurdles in her COVID research. At the height of the Omicron wave, when Mehta and her colleagues were trying to find people for their community studies, their rosters would immediately fill up past capacity. “Now we’re out there for weeks” and still not hitting the mark, she told me. Even weekly enrollment for their long-COVID study has declined. Sign-ups do increase when cases rise—but they drop off especially quickly as waves ebb. Perhaps, in the view of some potential study volunteers, COVID has, ironically, become like a common cold, and is thus no longer worth their time. For now, researchers don’t know whether we’re nearing the COVID-severity plateau, and they’re worried it will get only more difficult to tell. Maybe it’s for the best if the mildness asymptote is a ways off. In the U.S. and elsewhere, subvariants are still swirling, bivalent-shot uptake is still stalling, and hospitalizations are once more creeping upward as SARS-CoV-2 plays human musical chairs with RSV and flu. Abroad, inequities in vaccine access and quality—and a zero-COVID policy in China that stuck around too long—have left gaping immunity gaps. To settle into symptom stasis with this many daily deaths, this many off-season waves, this much long COVID, and this pace of viral evolution would be grim. “I don’t think we’re quite there yet,” Gordon told me. “I hope we’re not there yet.” from https://ift.tt/1njw689 Check out http://natthash.tumblr.com When I called the epidemiologist Denis Nash this week to discuss the country’s worsening COVID numbers, he was about to take a rapid test. “I came in on the subway to work this morning, and I got a text from home,” Nash, a professor at the City University of New York, told me. “My daughter tested positive for COVID.” Here we go again: For the first time in several months, another wave seems to be on the horizon in the United States. In the past two weeks, reported cases have increased by 53 percent, and hospitalizations have risen by 31 percent. Virus levels in wastewater, which can provide an advance warning of spread, are following a similar trajectory. After the past two years, a winter surge “was always expected,” Nash said. Respiratory illnesses thrive in colder weather, when people tend to spend more time indoors. Thanksgiving travel and gatherings were likewise predicted to drive cases, Anne Rimoin, an epidemiologist at UCLA, told me. If people were infected then, their illnesses will probably start showing up in the data around now. “We’re going to see a surge [that is] likely going to start really increasing in velocity,” she said. Winter has ushered in some of the pandemic’s worst moments. Last year, Omicron’s unwanted arrival led to a level of mass infection across the country that we had not previously seen. The good news this year is that the current rise will almost certainly not be as bad as last year’s. But beyond that, experts told me, we don’t know much about what will happen next. We could be in for any type of surge—big or small, long or short, national or regional. The only certain thing is that cases and hospitalizations are rising, and that’s not good. The pandemic numbers are ticking upward across the country, but so far the recent increases seem especially sharp in the South and West. The daily average of reported cases in Mississippi, Georgia, Texas, South Carolina, and Alabama has doubled in the past two weeks. Hospitalizations have been slower to rise, but over the same time frame, daily hospitalizations in California have jumped 57 percent and are now higher than anywhere else in the United States. Other areas of the country, such as New York City, have also seen troubling increases. Whether the nationwide spike constitutes the long-predicted winter wave, and not just an intermittent rise in cases, depends on whom you ask. “I think it will continue,” Gregory Poland, a professor of medicine at the Mayo Clinic, told me. “We will pour more gas on the fire with Christmas travel.” Others hesitated to classify the uptick as such, because it has just begun. “It’s hard to know, but the case numbers are moving in the wrong direction,” Rimoin said. Case counts are unreliable as people have turned to at-home testing (or just not testing at all), though hospitalizations and wastewater readings remain reliable, albeit imperfect, metrics. “I’ve not seen a big enough change to call it a wave,” Susan Kline, an infectious-diseases expert at the University of Minnesota Medical School, told me. But what to call the ongoing trend matters less than the fact that it exists. For now, what happens next is anyone’s guess. The dominant variants—the Omicron offshoots BQ.1 and BQ.1.1—are worrying, but they don’t pose the same challenges as what hit us last winter. Omicron drove that wave, taking us and our immune systems by surprise. The emergence of a completely new variant is possible this year—and would change everything—but that is considered unlikely. The lack of data on people’s immune status makes it especially difficult to predict the outcome of the current rise. Widespread vaccination and infection mean we have a stronger wall of immunity now compared with the previous two winters, but that protection inevitably fades with time. The problem is, people fall sick asynchronously and get boosted on their own schedules, so the timing varies for everyone. “We don’t know anything about how long ago people were [vaccinated], and we don’t know anything about hybrid immunity, so it’s impossible to predict” just how bad things could get, Nash said. Still, a confluence of factors has created the ideal conditions for a sustained surge with serious consequences for those who get sick. Fading immunity, frustratingly low booster uptake, and the near-total abandonment of COVID precautions create ideal conditions for the virus to spread. Meanwhile, treatments for those who do get very sick are dwindling. None of the FDA-approved monoclonal antibodies, which are especially useful for the immunocompromised, works against BQ.1 and BQ.1.1., which make up about 68 percent of cases nationwide. Paxlovid is still effective, but it’s underprescribed by providers and, by one medical director’s estimate, refused by 20 to 30 percent of patients. The upside is that few people who get COVID now will get very sick—fewer than in previous winters. Even if cases continue to surge, most infections will not lead to severe illness because the bulk of the population has some level of immunity from vaccination, previous infection, or both. Still, long COVID can be “devastating,” Poland said, and it can develop after mild or even asymptomatic cases. But any sort of wave would in all likelihood lead to an uptick in deaths, too. So far, the death rate has remained stable, but 90 percent of people dying now are 65 and older, and only a third of them have the latest booster. Such low uptake “just drives home the fact that we have not really done a good job of targeting the right people around the country,” Nash said. Even if the winter COVID wave is not ultimately a big one, it will likely be bad news for hospitals, which are already filling up with adults with flu and children with respiratory syncytial virus, or RSV. Many health-care facilities are swamped; the situation will only worsen if there is a big wave. If you need help for severe COVID—or any kind of medical issue—more than likely, “you’re not going to get the same level of care that you would have without these surges,” Poland said. Critically ill kids are routinely turned away from overflowing emergency rooms, my colleague Katherine J. Wu recently reported. We can do little to predict how the ongoing surge might develop other than simply wait. Soon we should have a better sense of whether this is a blip in the pandemic or something more serious, and the trends of winters past can be helpful, Kline said. Last year, the Omicron-fueled surge did not begin in earnest until mid-December. “We haven’t even gotten to January yet, so I really think we’re not going to know [how bad this surge will be] for two months,” Kline said. Until then, “we just have to stay put and watch.” It is maddening that, this far into the pandemic, “stay put and watch” seems to be the only option when cases start to rise. It is not, of course: Plenty of tools—masking, testing, boosters—are within our power to deploy to great effect. They could flatten the wave, if enough people use them. “We have the tools,” said Nash, whose rapid test came out negative, “but the collective will is not really there to do anything about it.” from https://ift.tt/GPpDX5q Check out http://natthash.tumblr.com |
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