Four days after recovering from a COVID-19 infection, President Joe Biden has tested positive again. When he first got sick, Biden—like more than one-third of the Americans who have tested positive for COVID-19 this summer, according to the U.S. government’s public records—was prescribed Paxlovid, an antiviral pill treatment made by Pfizer. Like many Paxlovid takers, he soon tested negative and resumed his normal activities. And then, like many Paxlovid takers, his infection came right back. (Biden does not currently have symptoms, according to his physician.) With more than 40,000 prescriptions being handed out a day, we’re taking Paxlovid at about the same rate that we’re taking oxycodone. When Biden got sick last week, he started taking the pills before the day was out. When Anthony Fauci had COVID in June, he took two courses. That enthusiasm is in line with the government’s messaging around the drug. The Biden administration has consistently hailed Paxlovid as an effective tool in the fight against SARS-CoV-2. “For the most part, Paxlovid is doing what you’re asking it to do,” Fauci told me recently. Many researchers and physicians agree. Ann Woolley, the associate clinical director of transplant infectious diseases at Brigham and Women’s Hospital, told me that she feels “very fortunate” to be able to offer Paxlovid to her patients, even if it’s not a COVID panacea. But some providers are prescribing the drug with a bit less enthusiasm, particularly when it comes to vaccinated patients (such as Biden and Fauci). Reshma Ramachandran, a family-medicine doctor and researcher at Yale, told me that she’s feeling a sense of “resignation” about Paxlovid. Though it’s one of the few COVID treatments she can offer, she can’t say with confidence that the pills will help someone who’s been immunized. Bob Wachter, the chair of medicine at UC San Francisco, called assessing the value of Paxlovid for these patients a “massively complicated three-dimensional chess game.” Anyone who might want to take the drug should discuss with their doctor whether and when they’ve been infected before, how many vaccine doses they’ve had (and when they had them), their age, and other risk factors—all in light of the limited clinical data that are now available. Patients will surely struggle to make sense of all these variables. Their doctors might, too. “I can barely decide whether I want it, and I do this for a living,” Wachter said. A person could have easily forgiven such confusion when Paxlovid was first being rolled out on a large scale, following an emergency authorization last winter. But now, eight months later? More than 3 million people have taken it. Pfizer has announced two sets of results from its clinical trial and submitted data to the FDA for full approval. Dozens of independent studies of the drug have been published or released as preprints. And yet, doctors remain unsure of: who might benefit from Paxlovid and in what ways; who really needs it; why and how often rebound infections such as Biden’s and Fauci’s occur; whether the drug reduces patients’ risk of developing long COVID; and whether the virus will slowly develop resistance to the drug. [Read: Rebound COVID is just the start of Paxlovid’s mysteries] These questions remain unanswered (or incompletely answered) thanks to corporate secrecy, the minutiae of drug testing, and the necessary care with which human trials are conducted. But in a more fundamental way, the persistent fog around Paxlovid comes from the disease that it’s meant to alleviate. The pandemic is simply moving too quickly, the virus is evolving too fast, and our responses to it are changing too often for anyone to find unambiguous answers about one specific drug. Before we walk into that fog, let’s get some things settled: Paxlovid is effective at keeping unvaccinated, high-risk people—those who are most likely to require hospitalization if they come down with COVID—alive and out of the hospital. The drug has some side effects, such as a strange and unpleasant taste, but its safety profile is stellar. (It does have some known, dangerous interactions with other common medications.) No one died while taking it in Pfizer’s clinical trials. Got it? Good. Now on to the mysteries. When I spoke with Fauci, he repeatedly emphasized that the point of Paxlovid is “to keep you out of the hospital and prevent you from progressing to severe disease.” But does the drug really have this benefit for young, vaccinated people, who would seem to represent a significant proportion of those taking it? COVID hospitalization rates for those younger than 60 are currently less than two per 100,000. Given those numbers, Paxlovid—or any other drug, for that matter—isn’t likely to provide much benefit. “If your risk of hospitalization is incredibly low, to make that even lower is somewhat improbable,” David Boulware, an infectious-disease physician and a researcher at the University of Minnesota, told me. That might explain why Pfizer’s trial found no statistically significant effect on hospitalization among a group of unvaccinated people at low risk from the disease and vaccinated people at high risk. An Israeli study conducted this winter similarly showed that Paxlovid did not significantly affect hospitalization rates in vaccinated, high-risk patients younger than 65. A study from Hong Kong did find that vaccinated Paxlovid takers were only about two-thirds as likely as non-takers to be hospitalized; but these data were not broken down by age, and the most popular vaccine choice among older Hong Kongers, Sinovac, is less effective than the mRNA-based vaccines that have dominated in the United States. A study that Woolley co-authored in Massachusetts found that Paxlovid reduced the risk of hospitalization for vaccinated people of all ages by 28 percent; and if their last shot was more than 20 weeks old, the protection offered by the pills nearly doubled. With the exception of Pfizer’s clinical trial, these studies are not placebo-controlled experiments, which makes them vulnerable to confounding factors. Woolley acknowledged the limitations of her own research, and told me that the benefit she found was “incremental.” Still, thanks to the paper, “I do feel like I have, now, significant data and experience to be able to have a well-informed discussion with my patients,” she said. “I’m not worried that we are giving placebo.” [Read: Paxlovid mouth is real—and gross] Other experts aren’t yet convinced. “I think we’re still left with a little bit of head-scratching about the utility of the drug in younger people or in people who are fully vaccinated and boosted,” Wachter told me. Boulware said he’s eager to see Pfizer’s results separated by vaccination status, which the company has not released. Those numbers wouldn’t necessarily tell us how Paxlovid fares against BA.5, but at least they come from a placebo-controlled trial. The data that have been made public to this point, he said, “suggest that there’s really minimal to no benefit, most likely, for the vast majority of people.” If Paxlovid was shown to have benefits beyond keeping people out of the hospital—if we knew that it made symptoms less intense, for example, or go away sooner—then the case for using it in young, vaccinated people might be stronger. But so far, those data have been lacking too. Pfizer’s own trials found that the drug did not reduce the duration of COVID patients’ symptoms or work to prevent infection when taken as a prophylactic. According to a CDC advisory, people who take Paxlovid for a COVID-19 bout could experience a resurgence of the infection—a Paxlovid rebound—between 2 and 8 days after their initial recovery. Biden’s four-day boomerang, then, is fairly typical. How common are these rebounds, and why do they occur? Even now, no one really knows. The Biden administration and researchers have maintained that rebound cases are not severe in general. But no definitive evidence has emerged to indicate how often they occur, who’s most likely to get them, or whether they’re related to Paxlovid at all. “It remains one of the most confusing things I can recall during the pandemic,” Wachter said. The few studies that have quantitatively assessed the rate of rebound have returned a range of numbers, centered at something less than 10 percent. Pfizer told me this spring that just 2 percent of their unvaccinated, high-risk Paxlovid takers rebounded during clinical trials. In June, a Mayo Clinic study of 483 patients logged a symptom-rebound rate of less than 1 percent, while one from Case Western Reserve University and the National Institutes of Health found that 5.4 percent of Paxlovid patients tested positive again within 30 days, and 5.9 percent had a recurrence of symptoms. (Similar numbers rebounded after taking molnupiravir.) Yet some clinicians told me that they don’t yet buy these numbers. Wachter said he suspects the real rebound rate is more like 10 or 15 percent. Ramachandran’s experience with her patients, family, and friends makes her think it’s even higher, perhaps 25 or 50 percent. (She stressed that this estimate is purely based on anecdote.) Woolley didn’t want to pick a number, but said that a rate higher than 2 percent and much lower than 20 seems plausible to her. Even Fauci was willing to entertain the notion that 2 percent simply isn’t right. “I want to be humble and modest enough to say I don’t know,” he said. Daniel Griffin, an infectious-disease expert, believes that fewer than 10 percent of people who take Paxlovid end up rebounding, but he also thinks those rebounds have nothing to do with the drug. “We’ve always seen this,” he told me. According to Griffin, physicians who have been taking care of COVID patients since 2020 were already seeing a pattern of disease, especially in high-risk patients, that entailed two weeks of worsening symptoms. He suspects Paxlovid suppresses the first half of the illness; when that suppression stops, you get the “rebound.” Some experts have hypothesized that the way we’re using Paxlovid may be causing rebound. Wachter raised the possibility that taking Paxlovid too early in your course of illness could be one factor. The idea is plausible, Woolley told me, but “it goes against what we know also to be the case: The earlier you treat with an antiviral, the more effective it is.” (The FDA has only authorized Paxlovid to be distributed within the first five days of a patient’s having COVID symptoms.) Do rebound cases suggest that the virus can evolve, within a patient, to make itself Paxlovid-proof? Again, the research seems to point in two directions. A group of researchers at UC San Diego studied one rebound case very carefully, and ruled out antiviral resistance as the cause. But even if resistance isn’t driving rebound, subsequent research has shown that SARS-CoV-2 is capable of developing resistance to Paxlovid, at least in a lab setting. “Any time you’re treating a disease caused by an RNA virus with a single drug, it’s not optimal, just because their capacity for change is great,” Timothy Sheahan, a virologist at the University of North Carolina at Chapel Hill, told me. He described the way he studies antiviral resistance in the lab. Step one: Grow a virus. Step two: Add some antiviral medicine, but not enough to completely suppress viral replication. Step three: Introduce that virus to a new host. Repeat. It sure sounds a lot like a COVID patient taking Paxlovid, rebounding, not realizing that they're contagious again, and giving the virus to somebody else. To ward off the possibility of resistance, Sheahan said, we need other drugs. “My hope, taking a page from the HIV-therapy playbook, is that there will and should be a multidrug cocktail to treat this disease, at the very minimum containing a few direct-acting antivirals,” he said. He’s also keen to find out whether such a cocktail would eliminate rebound. Other researchers, including the ones from UC San Diego, suspect that prescribing a longer Paxlovid course might do the trick. Pfizer is planning to test whether a 10- or 15-day course of the drug might lead to better results, including lower rebound rates, among immunocompromised patients. “I think it’s really important to determine what the real duration of treatment should be,” Fauci told me. Maybe, he said, it’s “going to have an impact not only on rebound, but also on whether a person gets long COVID or not.” But Ramachandran and Wachter both said they fear that hypothetical connection could go both ways: Perhaps rebound could raise a person’s chances of getting long COVID. To be clear, there is no empirical evidence as yet that supports this possibility—just physicians’ feelings of uncertainty around Paxlovid, plus some anecdotes. A few months ago, Wachter’s wife had COVID, took Paxlovid, and rebounded. Now, he said, she gets tired much more easily than she did before. Don’t expect this fog to lift anytime soon. For one thing, Pfizer has not yet made full data on the use of Paxlovid by vaccinated people available to researchers or anyone else. The Biden administration has not made any public efforts to pressure the company into doing so. More research groups are, of course, working to find answers. Several experts told me they’re eagerly awaiting the results of the RECOVERY trial in the U.K., which will rigorously test Paxlovid in hospitalized patients. Woolley and her colleagues plan to study the risk profiles of patients who request a second course of Paxlovid because they experience a rebound. At UNC, Sheahan is part of a group working on a rebound-related study. Fauci said, “We are making steps and planning studies and doing concept sheets for studies” regarding rebound rates and the appropriate duration of treatment. All of that research is going to take time. A spokesperson for the RECOVERY trial told me that fewer than 100 participants had been recruited as of July 25, and that the researchers need “at least several thousand” to draw conclusions. “It is likely to be many months yet before the trial can generate a result for Paxlovid,” they wrote in an email. Pfizer’s trial in immunocompromised patients, which will specifically investigate rebound and treatment duration, is listed as “not yet recruiting” on clinicaltrials.gov. Sheahan and his colleagues began planning their study around the turn of the new year, and only received approval from their institutional research board this month. They haven’t yet begun enrolling participants. When I asked Sheahan when he expected results, he said, “Hopefully several months.” By the time this work gets peer-reviewed and published, it will be a little out of date. Months from now, America’s immune landscape will be different thanks to new infections, waning immunity, and newly formulated vaccines. We might be facing a new variant or subvariant that causes more or less severe disease, or replicates differently in the body, or simply responds differently to antivirals. The pandemic has been in an accelerating state of all-over-the-place since last year; research on Paxlovid can only lag behind. In the meantime, patients and providers are muddling through. All of the doctors I spoke with said that they’re still erring on the side of prescribing Paxlovid, thanks to its lack of debilitating side effects. Sheahan, though not a medical doctor, was recently a Paxlovid patient when he came down with COVID after traveling. “I ended up on the medication within 48 hours after the onset of symptoms and was antigen negative in nine days. And it never came back,” he said when we spoke last week. Five days later, he emailed me to say that he had tested positive again. from https://ift.tt/ekr8sJG Check out http://natthash.tumblr.com
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When the monkeypox outbreak was first detected in the United States, it seemed, as far as infectious-disease epidemics go, like one this country should be able to handle. Tests and antivirals for the virus already existed; the government had stockpiled vaccines. Unlike SARS-CoV-2, monkeypox was a known entity, a relative softball on the pathogenic field. It wasn’t hypertransmissible, moving mainly through intimate contact during the disease’s symptomatic phase; previous epidemics had, with few interventions, rather quickly burned themselves out. The playbook was clear: Marshal U.S. resources and ensure they go to those most at risk, send aid abroad, and knock it out of the park. “If there was one virus that would lend itself to containment,” says Boghuma Kabisen Titanji, a virologist and infectious-disease physician at Emory University, this should have been it. Two months later, global counts have crested above 21,000 confirmed cases, nearly a fourth of which are in the United States, which now ranks first among countries keeping track. Infections, most among men who have sex with men, have been documented in 46 states, D.C., and Puerto Rico; New York State and San Francisco have declared states of emergency, as has the World Health Organization, on a global scale. Controlling the virus isn’t yet out of reach, says Jay Varma, the director of the Cornell Center for Pandemic Prevention and Response. But as the outbreak grows, so, too, does the challenge of combating it. “It didn’t have to be this hard,” Varma told me. Years of similar snafus surrounding SARS-CoV-2—a far, far more difficult virus to fight—should have taught the U.S. something about its own weak points. Instead, the lackluster response to monkeypox is making clear that the country’s capacity to deal with infectious disease may be even worse than it was at the start of 2020. Monkeypox, the country’s second infectious crisis in three years, isn’t just an unfortunate fumble. It’s confirmation that, although the U.S. might have once seemed like one of nations best equipped to stop and prevent outbreaks, it is, in actuality, one of the best at squandering its potential instead. For years, the warning signs about monkeypox have been there. Decades of sporadic outbreaks in Central and West Africa had made the virus’s toll clear: It can cause a painful, debilitating sickness, with bouts of fevers and rashes, and in numerous cases leaves permanent scars behind; on occasion, certain strains of the pathogen can even kill. And though in many places the virus has infected indiscriminately, striking communities in close physical proximity to wildlife, a 2017 outbreak among young men in Nigeria hinted that sex could pose a particular risk. So when case numbers began to erupt in several parts of Europe in May, indicating that the epidemic was already widespread, “it should have been obvious” that the epidemic had massive potential to expand, Varma told me. Multiple nations were already involved; the upcoming summer travel season posed a high risk. Infections were also concentrating in communities of men who have sex with men—networks that sexual-health experts know to be “dense, and where infectious diseases propagate very fast,” he said. And still, amid ringing alarm bells, the United States “underreacted,” Varma said, again and again. [Read: We should have seen monkeypox coming] Through much of May and June, monkeypox tests remained siloed within the CDC and its network of public-health labs, already stretched by the pandemic response. Health-care providers had to shuttle specimens to these centers for diagnosis, leaving patients on tenterhooks for days, even weeks, and delaying treatment, vaccination, and contact tracing. Even now, after testing capacity has climbed with the help of commercial labs, typical result turnaround times are stretching long. In Missouri, for instance, “they’re still telling us three to four days” at best, Hilary Reno, the medical director of the St. Louis County Sexual Health Clinic, told me. Shots, too, have been troublingly scarce. America’s strategic national stockpile has millions of doses of smallpox vaccine (which also works against monkeypox), but most are ACAM2000, an inoculation that’s been linked to rare but serious side effects and shouldn’t be taken by certain vulnerable groups, including people living with HIV. Another shot, branded as Jynneos in the U.S., is safer, though, as a two-doser, may be trickier to administer post-exposure. Since spring, manufacturers of this shot have been turning the crank on assembly lines to bolster supply. But American officials hemmed and hawed for weeks before flying in much-needed doses from abroad, and then only in spurts. The issue at hand certainly isn’t about vaccine demand. “Evey gay man I know is very ready for this vaccine and is willing to stand in line to get it,” says Steven Thrasher, a journalist and the author of The Viral Underclass, which examines the intersection of infectious disease and social inequality. Even though more vaccine doses are headed out, however, as cases balloon, the country still might not have enough. And with testing still strained, it won’t necessarily send doses to the right places. In Missouri, for instance, only a handful of cases has been reported so far, Reno told me. But with plenty of transmission likely going undetected, the state’s original order of shots might not cover its true needs. The country dawdled so long at the start line that even the relatively slow-moving monkeypox took its chance to race ahead—leaving the gap more and more difficult to close. Early shortages in testing and care have also made the scope of the American outbreak difficult to estimate, or communicate—another parallel to the botched COVID response. A lack of tests means a lack of accurate numbers, which can make a devastating epidemic look deceptively contained. “That amplifies the cycle of neglect,” Varma told me, a pattern to which the U.S. has been particularly prone. Piling on to the problem is the ongoing dearth of funds for America’s sexual-health services, coincident with a recent rise in STIs. People with genital symptoms have struggled to reach providers, opening up even more cryptic channels for the virus to spread through. Monkeypox is also a particularly challenging outbreak to be grappling with in the U.S., where sex is still a polarizing taboo, and men who have sex with men remain a marginalized community. And this is an especially charged time to be discussing the LGBTQ community in America, as the recent rolling back of abortion protections has stoked anxiety that other federal civil liberties may soon be on the chopping block. “We’re at this profoundly anti-gay, anti-trans moment,” Thrasher told me, at a time when those communities need more protection, not less. Experts have praised some of the CDC’s efforts to avoid stigmatizing at-risk groups, which, at this juncture, remains essential. Monkeypox certainly doesn’t need sex to spread, Ina Park, a sexual-health expert at UC San Francisco, told me. Kissing, cuddling, and other situations that put bodies in close proximity for prolonged periods can also transmit the virus. So can contact with clothing or bed linens, because monkeypox can persist on unsanitized surfaces for days. Which does mean that men who have sex with men are definitely not the only ones in danger. At the same time, some people have been so fearful of casting monkeypox as an exclusively “gay disease” that sex has almost been censored from discussions, “giving people a misperception of the different risks that populations are facing right now,” Thrasher said. Especially while supplies remain so limited, we need to be “vaccinating people where the virus is moving.” Which means “we need to give both messages simultaneously,” Park said, “that this is not something that only affects gay men” while nodding to the fact that monkeypox is still “primarily affecting certain communities,” a trend that should influence the distribution of shots. Calls for the mass vaccination of “children or cis-het suburban moms,” Titanji told me, are “not where you’re going to get the most impact.” [Read: U.S. messaging on monkeypox is deeply flawed]
As long as the virus continues to move predominantly through networks of men who have sex with men, the U.S. still has the opportunity to swiftly intervene, track transmission, and dole out resources in a targeted way, Varma told me. But monkeypox’s current pattern may not hold. Already, the virus has begun to hop across genders and age groups, leveraging other, nonsexual forms of close contact. Infections in young children, who likely contracted the infection in their households, and among people incarcerated in prisons, where contagion is particularly difficult to quash, are starting to appear. And across geographies, familiar inequities in access to tests, vaccines, and treatments have begun to appear. Monkeypox’s overlapping tenure with SARS-CoV-2 has aggravated matters as well. “This virus could not have picked a worse time to make its grand entrance to the global scene,” Titanji said. Still reeling from one outbreak, people are weary, and have “very little appetite for taking on another,” Thrasher told me. Numbed by COVID’s persistent toll, the public has also latched onto comforting comparisons that, although based in kernels of truth, have been warped into misleading extremes: Monkeypox might be less transmissible and less deadly than the coronavirus, but it is not an ignorable nuisance that’s guaranteed to dissipate. The larger the swath of society that’s affected, Titanji told me, the unwieldier the outbreak gets. The top priority now, experts told me, should be funneling funds toward distributing vaccines and scaling up testing. Health workers and patients need continued guidance on the disease’s often-subtle symptoms and the possibility of silent transmission, as well as the resources to administer speedy care. Paid sick leave and housing support would also help ease the burden of monkeypox isolation, which, given the lengthy course of symptoms, can last for weeks. Should such efforts fall short, as they clearly have with SARS-CoV-2, monkeypox could become the second virus to set up permanent residence in the U.S. in the span of three years—giving it all the more opportunity to find new ways to spread, shape-shift, and propagate disease. Preventing that means acting decisively now, to make up for the time we’ve already lost. from https://ift.tt/FiUQC12 Check out http://natthash.tumblr.com When the original Omicron variant swept across the country this winter, it launched America into a new COVID era, one in which nearly everyone--95 percent of adults, according to one CDC estimate—has some immunity to the virus through vaccines, infection, or both. Since then, however, Omicron subvariants have still managed to cause big waves of infection. They’ve accomplished this by eroding our existing immunity. This will keep happening. “There’s not a lot of things I’m confident about in SARS-CoV-2 evolution, but I think I’m extremely confident we’ll keep seeing new variants that are progressively eroding antibody neutralization,” says Jesse Bloom, an evolutionary virologist at the Fred Hutchinson Cancer Center. Experts are cautiously optimistic that the pace of variant emergence will eventually slow, and for many people, reinfections are already milder and hospitals are not overwhelmed. But as the virus keeps changing, the only real guarantee is that it will be different—and that its changes won’t necessarily affect everyone uniformly. SARS-CoV-2’s evolution follows a well-understood dynamic: When a variant sweeps around the world, it leaves behind a lot of immunity against itself. This puts intense evolutionary pressure on the virus to change things up; any subsequent variant has to somehow evade immunity to previous variants to keep finding new hosts. There are no limits to how long the coronavirus can keep doing this. Long-established respiratory viruses that cause the flu and common cold are still evolving to keep reinfecting us again and again. But immune escape isn’t an intrinsic property of any new variant. SARS-CoV-2 is not ascending a ladder with each variant, becoming more and more immune escape-y over time. Rather, think of the coronavirus as an indefatigable rabbit being chased by our immune system, an equally indefatigable dog. The rabbit is always running away from the dog, and the dog is always trying to catch up to the rabbit. The space in which they have to chase each other is so big that it might as well be infinite on human timescales. As Bloom told me previously, the number of possible mutations in SARS-CoV-2 far, far exceeds the number of atoms in the known universe. [Read: You are going to get COVID again … and again … and again.] Occasionally, the rabbit might make a dramatic Omicron-like leap and shoot out ahead for a while until our immunity catches up. How often this will happen is difficult to predict. “It probably depends on how much of a black-swan event Omicron was,” says Adam Lauring, a virologist at the University of Michigan. Omicron was so different and so unusual compared with everything that had come before. “Could it happen again? Most people think probably not but … you don’t want to be burned twice.” Whether an Omicron-like event happens every two or 20 or 200 years can mean different trajectories for COVID’s future. But at this point, we have only two and a half years of data to go on, so prognosticate at your own risk. More predictably, though, SARS-CoV-2 is likely to make smaller gains over time, accumulating mutations that make it incrementally better at reinfection. Virologists call this “antigenic evolution.” (Antigenic refers to the parts of a pathogen recognized by our immune system. For SARS-CoV-2, this is predominantly the spike protein.) Different viruses do seem capable of different rates of antigenic evolution. Of the four seasonal coronaviruses that cause common colds, for example, OC43 and 229E are evolving at a rate of 0.3 to 0.5 adaptive mutations in their spike proteins each year. But a third, NL63, doesn’t seem to be changing much at all, says Kathryn Kistler, a virologist also at Fred Hutch who has studied the evolution of the seasonal coronaviruses. She is currently trying to confirm this with blood-serum samples collected in the ’80s and ’90s. And there are so few samples of the fourth coronavirus, HKU1, that we don’t have enough to discern any trend. Influenza is much better studied, and different types of flu also exhibit different rates of evolution from one another. Of the most common ones, influenza B is the slowest, roughly on par with the coronaviruses OC43 and 229E. H1N1 flu is faster, and H3N2, the predominant flu strain in the world right now, is the fastest. The differences may, at least in part, come down to the shape of the antigen that our immune system recognizes. The spike protein in coronaviruses, for example, needs to change enough so it fools the immune system, but not so much that it stops functioning altogether. H3N2 can get away with a smaller change in its spike-protein analogue: “It’s often one single mutation—sometimes two—[that] can give the virus a huge advantage,” Kistler told me. Contrast that with measles, a virus that has barely evolved over decades. Our antibodies recognize multiple parts of its key protein. A recent study found that at least five out of eight key sites of that protein need to change at once to erode our immune defenses. A mutation in only one or two of these sites doesn’t confer much of an advantage, but gaining all five at once is very unlikely. So any potential new variants fizzle out, and the dominant measles variant stays quite stable. [Read: Is BA.5 the ‘reinfection wave’?] SARS-CoV-2, though, has been evolving antigenically faster than any of these viruses, even faster than H3N2. This could come down to the uniqueness of its spike protein, but some of this unusually fast pace over the past two years probably also has to do with the virus being novel. When a new strain of H1N1 “swine flu” hit in 2009, Kistler pointed out, it, too, had an initial burst before slowing down. The coronavirus’s Alpha and Delta variants emerged during a time with many immunologically naive people to infect, and the earliest variants mostly succeeded by becoming more intrinsically transmissible. The virus can only increase its transmissibility by so much, Bloom says, so SARS-CoV-2 is going to have less and less room to improve. However, it can keep finding new ways to get around immunity, as the Omicron subvariants have been doing. The immunity landscape that SARS-CoV-2 is evolving against is also changing, though. Right now, some people have immunity against the original coronavirus or Alpha or Delta, others have immunity against the Omicron family, and yet others have both. As more variants emerge, our individual exposure history is going to be even more heterogeneous; depending on our previous immunity, some of us might be more susceptible than others to a new variant. The impact will be less uniform. We’ve already seen this with the Omicron subvariants, where countries with smaller previous waves are experiencing bigger BA.5 waves. Some people will also experience more waning immunity than others; older people, for example, tend to mount less durable immune responses to SARS-CoV-2, which is why this group is always prioritized for boosters. Aggressive vaccine updates and booster campaigns would help everyone’s immune system keep up. Instead of always trying to catch up to the virus though, could we broaden our immunity and get ahead of it? Our current vaccines, while still very good at protecting against severe disease, are not capable of this. The White House is now promoting—though not really funding--next-generation vaccines that could potentially do better: pan-coronavirus vaccines that scientists hope will elicit antibodies against parts of the spike protein that do not change very much, or nasal vaccines to elicit antibodies in the nose and mouth where the virus first replicates, perhaps stopping an infection altogether. But these ideas are not new to SARS-CoV-2—researchers have been trying these approaches to flu for many years. A universal flu vaccine is still elusive. A nasal flu vaccine, FluMist, does exist, but its effectiveness is quite mixed: It was originally thought to be more effective than the shot, then believed to be less effective—so much so that the CDC pulled the vaccine from 2016 to 2018—until it was reformulated. In any case, it’s clear that FluMist doesn’t come close to preventing all mild flu infections. Barring any major innovations in vaccine technology, our immune systems may be the dog chasing the coronavirus rabbit for a long time still. from https://ift.tt/vdr4Deo Check out http://natthash.tumblr.com Last Christmas, as the Omicron variant was ricocheting around the United States, Mary Carrington unknowingly found herself at a superspreader event—an indoor party, packed with more than 20 people, at least one of whom ended up transmitting the virus to most of the gathering’s guests. After two years of avoiding the coronavirus, Carrington felt sure that her time had come: She’d been holding her great-niece, who tested positive soon after, “and she was giving me kisses,” Carrington told me. But she never caught the bug. “And I just thought, Wow, I might really be resistant here.” She wasn’t thinking about immunity, which she had thanks to multiple doses of a COVID vaccine. Rather, perhaps via some inborn genetic quirk, her cells had found a way to naturally repel the pathogen’s assaults instead. Carrington, of all people, understood what that would mean. An expert in immunogenetics at the National Cancer Institute, she was one of several scientists who, beginning in the 1990s, helped uncover a mutation that makes it impossible for most strains of HIV to enter human cells, rendering certain people essentially impervious to the pathogen’s effects. Maybe something analogous could be safeguarding some rare individuals from SARS-CoV-2 as well. [Read: America is running out of ‘COVID virgins’] The idea of coronaviral resistance is beguiling enough that scientists around the world are now scouring people’s genomes for any hint that it exists. If it does, they could use that knowledge to understand whom the virus most affects, or leverage it to develop better COVID-taming drugs. For individuals who have yet to catch the contagion--a fast-dwindling proportion of the population—resistance dangles “like a superpower” that people can’t help but think they must have, says Paula Cannon, a geneticist and virologist at the University of Southern California. Like any superpower, though, bona fide resistance to SARS-CoV-2 infection would likely “be very rare,” says Helen Su, an immunologist at the National Institutes of Allergy and Infectious Disease. Carrington’s original hunch, for one, eventually proved wrong: She recently returned from a trip to Switzerland and found herself entwined with the virus at last. Like most people who remained unscathed until recently, Carrington had done so for two and a half years through a probable combination of vaccination, cautious behavior, socioeconomic privilege, and luck. It’s entirely possible that inborn coronavirus resistance may not even exist—or that it may come with such enormous costs that it’s not worth the protection it theoretically affords. Of the 1,400 or so viruses, bacteria, parasites, and fungi known to cause disease in humans, Jean-Laurent Casanova, a geneticist and an immunologist at Rockefeller University, is certain of only three that can be shut out by bodies with one-off genetic tweaks: HIV, norovirus, and a malaria parasite. The HIV-blocking mutation is maybe the most famous. About three decades ago, researchers, Carrington among them, began looking into a small number of people who “we felt almost certainly had been exposed to the virus multiple times, and almost certainly should have been infected,” and yet had not, she told me. Their superpower was simple: They lacked functional copies of a gene called CCR5, which builds a cell-surface protein that HIV needs in order to hack its way into T cells, the virus’s preferred human prey. Just 1 percent of people of European descent harbor this mutation, called CCR5-Δ32, in two copies; in other populations, the trait is rarer still. Even so, researchers have leveraged its discovery to cook up a powerful class of antiretroviral drugs, and purged the virus from two people with the help of Δ32-based bone-marrow transplants—the closest that medicine has come to developing a functional HIV cure. The stories with those two other pathogens are similar. Genetic errors in a gene called FUT2, which pastes sugars onto the outsides of gut cells, can render people resistant to norovirus; a genomic tweak erases a protein called Duffy from the walls of red blood cells, stopping Plasmodium vivax, one of several parasites that causes malaria, from wresting its way inside. The Duffy mutation, which affects a gene called DARC/ACKR1, is so common in parts of sub-Saharan Africa that those regions have driven rates of P. vivax infection way down. In recent years, as genetic technologies have advanced, researchers have begun to investigate a handful of other infection-resistance mutations against other pathogens, among them hepatitis B virus and rotavirus. But the links are tough to definitively nail down, thanks to the number of people these sorts of studies must enroll, and to the thorniness of defining and detecting infection at all; the case with SARS-CoV-2 will likely be the same. For months, Casanova and a global team of collaborators have been in contact with thousands of people from around the world who believe they harbor resistance to the coronavirus in their genes. The best candidates have had intense exposures to the virus—say, via a symptomatic person in their home—and continuously tested negative for both the pathogen and immune responses to it. But respiratory transmission is often muddied by pure chance; the coronavirus can infiltrate people silently, and doesn’t always leave antibodies behind. (The team will be testing for less fickle T-cell responses as well.) People without clear-cut symptoms may not test at all, or may not test properly. And all on its own, the immune system can guard people against infection, especially in the period shortly after vaccination or illness. With HIV, a virus that causes chronic infections, lacks a vaccine, and spreads through clear-cut routes in concentrated social networks, “it was easier to identify those individuals” whom the virus had visited but not put down permanent roots within, says Ravindra Gupta, a virologist at the University of Cambridge. SARS-CoV-2 won’t afford science the same ease of study. [Read: Is BA.5 the ‘reinfection wave?’] A full analogue to the HIV, malaria, and norovirus stories may not be possible. Genuine resistance can manifest in only so many ways, and tends to be born out of mutations that block a pathogen’s ability to force its way inside a cell, or xerox itself once it’s inside. CCR5, Duffy, and the sugars dropped by FUT2, for instance, all act as microbial landing pads; mutations rob the bugs of those perches. If an equivalent mutation exists to counteract SARS-CoV-2, it might logically be found in, say, ACE2, the receptor that the coronavirus needs in order to break into cells, or TMPRSS2, a scissors-like protein that, for at least some variants, speeds the invasive process along. Already, researchers have found that certain genetic variations can dial down ACE2’s presence on cells, or pump out junkier versions of TMPRSS2—hints that there could be tweaks that further strip away the molecules. But “ACE2 is very important” to blood-pressure regulation and the maintenance of lung-tissue health, said Su, of NIAID, who’s one of many scientists collaborating with Casanova to find SARS-CoV-2 resistance genes. A mutation that keeps the coronavirus out might very well “muck around with other aspects of a person’s physiology.” That could make the genetic tweak vanishingly rare, debilitating, or even, as Gupta put it, “not compatible with life.” People with the CCR5-Δ32 mutation, which halts HIV, “are basically completely normal,” Cannon told me, which means “HIV kind of messed up in ‘choosing’ CCR5.” The coronavirus, by contrast, has figured out how to exploit something vital to its host—an ingenious invasive move. The superpowers of genetic resistance can have other forms of kryptonite. A few strains of HIV have figured out a way to skirt around CCR5, and glom on to another molecule, called CXCR4; against this version of the virus, even people with the Δ32 mutation are not safe. A similar situation has arisen with Plasmodium vivax, which “we do see in some Duffy-negative individuals,” suggesting that the parasite has found a back door, says Dyann Wirth, a malaria researcher at Harvard’s School of Public Health. Evolution is a powerful strategy—and with SARS-CoV-2 spewing out variants at such a blistering clip, “I wouldn’t necessarily expect resistance to be a checkmate move,” Cannon told me. BA.1, for instance, conjured mutations that made it less dependent on TMPRSS2 than Delta was. [Read: The BA.5 wave is what COVID normal looks like] Still, protection doesn’t have to be all or nothing to be a perk. Partial genetic resistance, too, can reshape someone’s course of disease. With HIV, researchers have pinpointed changes in groups of so-called HLA genes that, through their impact on assassin-like T cells, can ratchet down people’s risk of progressing to AIDS. And a whole menagerie of mutations that affect red-blood-cell function can mostly keep malaria-causing parasites at bay—though many of these changes come with “a huge human cost,” Wirth told me, saddling people with serious clotting disorders that can sometimes turn lethal themselves. With COVID-19, too, researchers have started to home in on some trends. Casanova, at Rockefeller, is one of several scientists who has led efforts unveiling the importance of an alarm-like immune molecule called interferon in early control of infection. People who rapidly pump out gobs of the protein in the hours after infection often fare just fine against the virus. But those whose interferon responses are weak or laggy are more prone to getting seriously sick; the same goes for people whose bodies manufacture maladaptive antibodies that attack interferon as it passes messages between cells. Other factors could toggle the risk of severe disease up or down as well: cells’ ability to sense the virus early on; the amount of coordination between different branches of defense; the brakes the immune system puts on itself, so it does not put the host’s own tissues at risk. Casanova and his colleagues are also on the hunt for mutations that might alter people’s risk of developing long COVID and other coronaviral consequences. None of these searches will be easy. But they should be at least simpler than the one for resistance to infection, Casanova told me, because the outcomes they’re measuring—serious and chronic forms of disease—are that much more straightforward to detect. If resistance doesn’t pan out, that doesn’t have to be a letdown. People don’t need total blockades to triumph over microbes—just a defense that’s good enough. And the protection we’re born with isn’t all the leverage we’ve got. Unlike genetics, immunity can be easily built, modified, and strengthened over time, particularly with the aid of vaccines. Those DIY defenses are probably what kept Carrington’s case of COVID down to “a mild course,” she told me. Immune protection is also a far surer bet than putting a wager on what we may or may not inherit at birth. Better to count on the protections we know we can cook up ourselves, now that the coronavirus is clearly with us for good. from https://ift.tt/YtI4jWU Check out http://natthash.tumblr.com I am on a mission to preserve the most valuable item in my home: my fiancé, who has never had COVID. Through sheer luck and a healthy dose of terror, he made it through the first pandemic year without getting sick. Shielded by the J&J vaccine and a Moderna booster, he dodged infection when I fell ill last November and coughed up the coronavirus all over our cramped New York City apartment. Somehow, he ducked the Omicron wave over the winter, when it seemed as though everyone was getting sick. And in the past few months, he has emerged unscathed from crowded weddings, indoor dinners, and flights across the country. At this point, I worry about how much longer it’s going to last. People like him—I think of them as “COVID virgins”—are becoming a rare breed. Just yesterday, President Joe Biden thinned their ranks by one more person. The Institute of Health Metrics and Evaluation suggests that as of earlier this month, 82 percent of Americans have been infected with the coronavirus at least once. Some of those people might still think they’re never had the virus: Asymptomatic infections happen, and mild symptoms are sometimes brushed off as allergies or a cold. Now that we’re battling BA.5, the most contagious and vaccine-dodging Omicron offshoot yet, many people are facing their second, third, or even fourth infections. That reality can make it feel like the stragglers who have evaded infection for two and a half years are destined to fall sick sooner rather than later. At this point, are COVID virgins nothing more than sitting ducks? [Read: Of course Biden has COVID] The basic math admittedly doesn’t look promising. Most of the people getting infected right now seem to be coming down with the illness for the first time, even though they are a distinct minority. Nationally, we don’t have good data on who is getting COVID, though in New York, first infections seem to be happening at five times the rate of reinfections. Part of why those who haven’t gotten COVID seem to be at a higher risk of infection is that taking into account all other factors—vaccination, age, behaviors—they lack the immunity bump conferred by a bout with the virus, no matter how fleeting that bump may be. On its own, this would suggest that these people are in fact sitting ducks who can’t avoid infection short of hunkering down in total isolation. The experts I talked with agreed that the risk of infection is currently high. “We are finding now that with the more transmissible variants, it’s becoming more and more difficult to avoid infections,” Robert Kim-Farley, an epidemiologist at UCLA, told me. “However, it’s not inevitable.” Richard Bright, the CEO of the Rockefeller Foundation’s Pandemic Prevention Institute, was less certain. “Honestly, it might be inevitable, the way the virus has continued to change,” he said. Still, they reiterated that we still don’t quite know just how at risk those who haven’t had COVID are—especially when BA.5 seems to be reinfecting so many people. “I don’t know if I would call them sitting ducks, necessarily,” Bright said, “but I would say every one of us is more vulnerable.” The unvaccinated are still the most vulnerable by far, especially to more severe outcomes. But even this far into the pandemic, it’s hard to know exactly why some vaccinated and boosted people have gotten sick while others haven’t—good pandemic behaviors might come into play, along with luck. Scientists are still investigating the role of other factors, including whether genetics might be protecting the immune systems of people who haven’t gotten COVID. [Read: Is BA.5 the ‘reinfection wave’?] Nevertheless, all of the experts argued that COVID virgins should still try to avoid infection. Above all, they should get up-to-date on vaccination and boosters. Once those layers of protection are in place, they should continue to be prudent—especially in crowded, indoor settings—but unless they are medically vulnerable, they don’t have to take more precautions than anyone else, Kim-Farley said. The guidance for this group is the same as it is for everybody else largely because immunity by infection is protective, but only to an extent. BA.5, for one, seems to be able to reinfect people who were previously sick, sometimes even those who just a few months ago had an earlier version of Omicron. At this point, an infection from a year ago, let alone two, might not mean much immunologically. “People shouldn’t rely on prior infection, because it just is not as effective as prior vaccination,” Kim-Farley said. And though “hybrid immunity”—which results when a person gets sick and is then vaccinated, or vice versa—is thought to confer a good amount of protection, “that kind of assertion may be challenged” now that so many reinfections are occurring, the Yale epidemiologist Albert Ko told me. The ultimate problem with people viewing themselves as sitting ducks is that this is the exact attitude epidemiologists do not want us to have. It can foster a “why bother?” demeanor, negating all public-health efforts to stop transmission and discouraging personal efforts to protect oneself. In other words, it promotes COVID fatalism, which is appealing because it offers relief from the daily anxiety and behavioral compromises of pandemic life by assuming that an infection is a question of when, not if. This notion can be liberating for those who have never gotten infected—and presumably it is part of the reason so few are left: Many people have already adopted a “meh” attitude toward COVID, not letting the fear of an infection get in the way of living their lives. Even this late in the game, you should really try to avoid getting COVID if you can. Having to take precautions can be frustrating after so many months of pandemic life, but getting sick can be extremely unpleasant, even if you are vaccinated and boosted. There’s the risk of long COVID, yes, but those who escape it can still feel terrible for several days, if not weeks, Bright said. These infections don’t usually lead to hospitalization or death, but they’re no walk in the park either, especially for the elderly and the immunocompromised. And as COVID continues to mutate, you definitely want to forestall a second infection, or a third down the line. The consequences of repeated infections and their potential to cause long COVID or other health issues are not yet known. And, of course, the tenets of COVID 101 are still true: Even if your infection is mild, you can still spread it to someone who could have it much worse. The grim reality is that as long as the virus shows no signs of abating, the number of COVID virgins will continue to shrink. Grappling with this reality will be a lot less stressful if we reframe the way we talk about getting COVID. Instead of fretting about the virus as something that could come for you, focus on what to do when it does. Those who are vaccinated and boosted may still be ducks sitting in the crosshairs of infection, but in all likelihood they won’t die or get severely ill, especially if they are young and healthy. “That’s what we care most about,” Ko said. The people who haven’t gotten sick should remember that they have already won—vaccines, in tandem with the treatments that are now available, means that it’s far better to get sick now than it was a year or two ago. When I told my fiancé that he would probably get COVID but should definitely still try not to get COVID, he described the situation as “Kafkaesque.” Indeed, these are absurd and illogical times. But at the very least, focusing on what is within our control can help us regain a modicum of sense. Short of total isolation, people may not be able to do much to avoid the coronavirus forever, but there’s still plenty they can do to escape the worst when it does come for them. from https://ift.tt/k1AoQRr Check out http://natthash.tumblr.com And there it is: President Joe Biden has tested positive for the coronavirus, the White House announced Thursday morning, and is dosing up with Paxlovid to keep his so-far “very mild symptoms” from turning severe. In some ways, this is one of the cases the entire world has been waiting for—not sadistically, necessarily, but simply because, like so many other infections as of late, it has felt inevitable. Once, it might have seemed possible to avoid this virus; now most Americans have had it. SARS-CoV-2 has been spewing out variants and subvariants at an absolutely blistering clip, and wave after wave of infections has slammed the nation, collapsing case peaks into a never-ending plateau. Vice President Kamala Harris caught the coronavirus in April; Anthony Fauci got it in June. Perhaps the most notable aspect of these high-profile cases is not that they happened, but when. Though certainly on the front lines of the country’s COVID response, these officials have enjoyed the privilege of protection throughout the pandemic, with access to masks, tests, vaccines, and, most recently, antivirals; the comfort and security of jobs that can be done while in isolation; the socioeconomic means to separate themselves from colleagues and loved ones, and even alert them to transmission risks. They, as much as anyone feasibly could, “have had access to all the available tools” the country has to fight the coronavirus, says Anne Sosin, a public-health researcher at Dartmouth College, so much so that they’ve even had the liberty to get a bit avant-garde. Fauci, for instance, received two courses of Paxlovid when his symptoms vanished and then reappeared—a nonconventional use of the drug that sparked some criticism from infectious-disease experts who thought the move unwarranted and potentially baffling for a public unsure of who should be taking the drug and how. Avoiding the virus, or at least a known, test-confirmed infection, up until this point of the pandemic does have real value. In the U.S., our collective capability to evade any serious outcome is much higher than it was in, say, October 2020, when then-President Donald Trump tested positive. Trump’s tussle with the virus unfurled at a time before shots were available, and his doctors treated his illness as a pressing medical emergency, rushing him to the hospital for observation and treatment. At the time, all COVID therapies had to be administered by a trained health-care professional, typically in a medical setting; like Biden, Trump got the best care that was available at the time, but in the first year of the crisis, that entailed a trifecta of treatments with remdesivir, steroids, and still-experimental monoclonal antibodies, which Trump later touted, misleadingly, as a “cure.” Most monoclonal-antibody treatments, including the specific cocktail Trump received, have since fallen out of use because they’re less effective against the variants circulating today. Today, President Biden may not need anything beyond Paxlovid, which the FDA greenlit late last year and can be taken as a pill at home. “We know so much more now,” says Taison Bell, a critical-care and infectious-disease physician at UVA Health. “We understand what treatments work, what treatments don’t.” Although Biden is 79—an age that puts him at high risk of severe outcomes from the virus—he’s quadruply vaccinated, having received his second booster in late March. And clinical trials have shown Paxlovid to be nearly 90 percent effective at slashing the risk of COVID hospitalizations or deaths (though those data were gleaned from an entirely unvaccinated population; real-world estimates of the drug’s performance have been far more mixed). Kevin O’Connor, the president’s physician, wrote in a letter today that “I anticipate that he will respond favorably, as most maximally protected patients do.” In the third year of the pandemic, just as unsurprising as Biden’s illness is the pressure for the White House to leverage it as a statement on the right approach to COVID control. In 2020, Trump alarmed experts by peeling off his mask and walking into the White House just after being discharged from the hospital that treated him for COVID. Nearly two years later, Biden, to begin with, is apparently modeling some version of business as usual: The White House has already announced that he “continues to carry out the full duties of the office while in isolation” … which somehow involves the country’s chief decision maker tweeting out maskless photos (taken by someone else, presumably) of him doing paperwork at his desk. But, like Trump’s, Biden’s experience—including any performative professional displays—is still an exception among exceptions. “The president, as we would want, has access to therapies,” says Utibe Essien, a physician and health-equity researcher at the University of Pittsburgh. “We would hope that everyone should.” They do not. Although the White House has made plenty of noise about the need for funding to keep the country awash in tests, treatments, and vaccines, Congress has not provided those resources, and the administration has not marshaled the political will to change that situation. Nor has it sparked the enthusiasm necessary to reignite America’s pandemic response where it has flagged. Cases remain undercounted; tests remain underused. Vaccination rates—especially boosting rates—remain worrisomely low. Effective treatments have been collecting dust on shelves amid enormous disparities in access. And gathering restrictions and masks are now mostly mitigation measures of the past, even though the CDC’s loosened guidelines currently recommend that people in more than a third the country’s counties should be covering their face to control the coronavirus’s spread. At the beginning of this month, in a Fourth of July celebration, the president crowed that the country was “closer than ever to declaring our independence from a deadly virus”; weeks later, he is playing host to that same foe. And although he might have had access to the tools needed to combat it, “that doesn’t mean they’re going into the hands of the people who need them,” Essien told me. That the president’s infection happened now, during the nation’s roiling, months-long, multi-subvariant wave, speaks to the bad cycle that the country has found itself in. The current surge shows few signs of slowing; more iterations of the virus are undoubtedly on their way. And yet little is being done in response to the danger, let alone as a preventive to keep the situation from going further off the rails. The U.S. has defaulted to acceptance, Sosin told me, of the status quo: uncontrolled transmission, viral evolution on loop.
from https://ift.tt/Ucms3xJ Check out http://natthash.tumblr.com In early July, Sebastian Kohn, a 39-year-old nonprofit professional in Brooklyn, woke up with a fever, a sore back, and swelling in the lymph nodes of his throat and groin. He took a COVID test, which was negative. But Kohn had some clue as to what might be going on. Pride celebrations had taken place a week earlier, and a newly infamous disease was circulating largely in the gay community: monkeypox. Suspicious that he might have the viral illness, Kohn immediately isolated. Two days later, a painful, itchy rash appeared in an intimate location. He knew then that he was in for a ride. Kohn found an urgent-care center where a doctor was able to swab his skin lesions and send them off to a lab, where technicians searched for signs of the virus’s genetic material. Then he waited, alone, in his home. More than 15,000 monkeypox cases have been confirmed around the world since the outbreak began in May, but the condition, which spreads through close contact with the rash or body fluids of an infected individual, has been difficult to diagnose because of a lack of available testing. New York City was at one point able to test only 10 patients a day. When Kohn got sick, the system was still running at significant delays. While an analogous COVID test can be turned around by the next day in many cases, Kohn’s positive result for monkeypox took four days to arrive—all while a blistering rash spread out across his body. (Six days after that, Kohn received a phone call from a contact tracer working for the local department of health. He may have been exposed to monkeypox, the person warned.) [Read: Gay men need a specific warning about monkeypox] In terms of sheer numbers, the nation’s monkeypox-testing capacity has increased dramatically since Kohn’s run-in with the system. On Monday, the Centers for Disease Control and Prevention announced that the U.S. is now capable of evaluating 80,000 cases a week, up from 6,000 initially. But another, more important bottleneck remains stubbornly in place: The CDC’s official guidance recommends that labs test for monkeypox using only samples of a patient’s skin, taken at the site of a visible rash. As a result, people like Kohn, whose fever and swollen lymph nodes come on a few days before their lesions, must let the illness grow before it can be diagnosed. Others may develop hidden sores in their mouth or anus, and not realize that they can be tested. And many more without symptoms will be left to wait and wonder, after an exposure, whether they might have been infected. As the outbreak spreads—with more than 2,000 cases in the U.S., by the latest count—public-health authorities have doubled down on this restriction: Testing for the virus must make use of swabs taken from a lesion, according to a “Safety Communication” issued by the Food and Drug Administration last Friday. “The FDA is not aware of clinical data supporting the use of other sample types, such as blood or saliva, for monkeypox virus testing,” the communication said, and testing of these other types “may lead to false test results.” This alarming messaging, delivered at a crucial moment in the virus’s spread, will have a profound effect on how quickly new monkeypox infections can be identified, isolated, and treated. With this disease, like many others, early detection is invaluable as a means of promoting early treatment. Vaccination shortly after exposure can prevent monkeypox from occurring in many cases, and inoculation during the early phase of illness may reduce the severity of symptoms or curtail the contagious period. Although no medications have been approved specifically for monkeypox, several antivirals originally meant for smallpox are thought to help. As we have seen with the COVID antivirals Paxlovid and remdesivir, these types of therapies tend to work best when given as early as possible. It may be just as important to identify those infected asymptomatically. An intriguing study out of Belgium, posted earlier this month but not yet peer-reviewed, examined swabs taken from the mouth and anus of 224 men in May. Samples had originally been collected to look for gonorrhea and chlamydia, but the scientists found monkeypox DNA in three of them. None of those men reported any symptoms of disease before or after testing, nor did any of their close contacts. Nevertheless, the study’s authors believe that these and other potential asymptomatic carriers could well be contagious. (Guidance from the CDC, last updated at the end of June, says that spreading can happen only after symptoms start.) In the meantime, other studies, conducted in Europe and Africa, have shown that monkeypox DNA is in many cases detectable in saliva, blood, urine, and rectal samples, even before a rash appears. [Read: The U.S. is underreacting to monkeypox] Matt Ford, a 30-year-old actor and video producer who lives in Los Angeles and New York, told me that he suspects he passed the virus on during the very early phase of his infection. He caught monkeypox last month, and was subsequently placed under public-health isolation. But in the week between his exposure and when he first noticed skin spots, he said, he spent an evening with a guy he was seeing. That guy would later come down with the disease himself. In retrospect, Ford had been a little tired during that time, but he had not felt unwell enough to pay it any mind. If people really are passing on the virus with few to no symptoms—and we don’t know for sure—then an early-detection test collected by mouth, vein, or rectal swab might prevent this onward spread. Yet last week’s warning from the FDA was very specific: Unless you have an active rash, don’t bother to get tested. When I asked the agency what specific data it was relying on for its safety communication, an FDA spokesperson repeated only that the organization is “not aware of clinical data supporting asymptomatic testing or testing samples other than those taken directly from a suspect lesion.” CDC Director Rochelle Walensky also confirmed to reporters last week that a skin lesion is required for testing from her organization’s perspective, though she said that the CDC is exploring the possibility of saliva, throat, and blood tests. This “absence of evidence” maneuver by authorities should be quite familiar at this point. In December 2019 and January 2020, the Chinese government publicly stated that there was no clear evidence of human-to-human transmission of the new coronavirus, and the World Health Organization repeated the claim. Three months later, in April, officials from the WHO cited “no evidence” that wearing masks prevented COVID transmission in a wider community setting. In the case of monkeypox testing, such conservatism is particularly self-defeating. When public-health authorities warn of a lack of clinical data for the effectiveness of blood and saliva tests, they are not only ignoring a small but growing list of published studies; they are also making it that much harder for researchers to collect more clinical data. The FDA and the CDC should be encouraging labs to run and evaluate new tests, Jay Varma, a public-health physician and professor at Cornell, told me. Instead the agencies are telling labs to stay away from them. The FDA is correct that any new test for monkeypox would almost certainly produce some false results. (Even the gold-standard skin tests for monkeypox can misclassify cases.) But the advantages of having an early diagnostic for monkeypox are beyond dispute: Most people would take precautions to reduce their chance of exposing others if they knew they were infected, and contact tracers could hunt down additional cases far more quickly. Ideally, one could imagine integrating monkeypox testing into the sexual-health infrastructure that is already in place. Many members of the gay community are used to receiving regular screening for HIV and other sexually transmitted diseases, according to Joseph Osmundson, a clinical assistant professor of biology at NYU. “There is a real desire in the community for scale testing” for monkeypox, too, he told me. Throat and rectal swabs collected for gonorrhea and chlamydia, for example, could also be tested for the virus. Varma suggests checking participants at any event where casual sex is expected to occur. As things stand, physicians, patients, and laboratories would have to defy the explicit advice of U.S. public-health authorities in order to make this happen. Labs are legally permitted to create their own monkeypox diagnostics, even in the face of the FDA’s official warnings. Indeed, some organizations have already begun doing so. (If the U.S. government were to formally declare monkeypox a public-health emergency—as some politicians are calling for—then, ironically, this regulatory flexibility could be revoked.) Benjamin Pinsky, the medical director of the clinical-virology lab at Stanford, has overseen the testing of more than 70 patients for monkeypox, using samples from the nose, mouth, rectum, and bladder, as well as traditional skin scrapings. The newer methods have already picked up a few cases, he told me, but developing those tests without the cooperation of the government has been difficult. Pinsky said that public-health labs initially refused to provide him with real patient samples to confirm the validity of his approach. Many less-experienced lab directors will be dissuaded entirely from setting up their own protocols, because designing a diagnostic from scratch is far more complicated than using an off-the-shelf tool provided by the government. Also, no lab director would be eager to explain to hospital administrators why he or she is openly flouting an official safety warning. One need only look back at the COVID testing snafus of 2020 to get a sense of what can happen when the government works against, rather than with, the medical community. At the start of the pandemic, the FDA prohibited labs from developing their own COVID-detection methods without first completing an arduous authorization process. Hospitals were encouraged to rely on the CDC’s official test, just as they are now for monkeypox. The government COVID test turned out to have a serious manufacturing defect, which thankfully hasn’t been repeated during the monkeypox outbreak. But excess caution remains a problem, and has once again left the country dangerously short of diagnostic capacity. U.S. hesitation also puts the country out of step with the international community. The WHO, parts of Canada, and the United Kingdom, for instance, all recommend analyzing a throat swab in some circumstances. It’s not that the FDA’s concerns are unfounded. A monkeypox-testing bonanza, in which anyone and everyone can start to market their own services with limited oversight, could have undesirable consequences. Once the rules were loosened for COVID tests, small and inexperienced laboratory outfits served up diagnostic errors on occasion, or engaged in exploitative practices. But most labs follow proper quality-control procedures, and the Centers for Medicare and Medicaid Services still provides routine supervision. Any risk of false results in such an environment must be weighed against the more serious consequence of missing cases entirely. Less testing for monkeypox this summer will inevitably lead to more people suffering from ulcerating rashes, drenching night sweats, malodorous rectal discharge, and expansive onward spread. Members of the gay community want easier and earlier testing for monkeypox. Public-health experts want the same thing. Aggressive case-finding may be the only way to get the current outbreak under control, and most large labs have the ability to detect the presence of monkeypox DNA in a variety of body fluids. We don’t yet know the real-world performance of a monkeypox-screening program based on all these fluids, but doctors could and should be coordinating with one another and with public-health agencies to find out. “We want the best diagnostics, the best vaccines, the best treatment protocols, and the best science in the world,” Osmundson told me. “But we are also in an emergency, and people are getting sick, and they are not able to access the care they need.” from https://ift.tt/1CGucXt Check out http://natthash.tumblr.com Jacob Bor has been thinking about a parallel universe. He envisions a world in which America has health on par with that of other wealthy nations, and is not an embarrassing outlier that, despite spending more on health care than any other country, has shorter life spans, higher rates of chronic disease and maternal mortality, and fewer doctors per capita than its peers. Bor, an epidemiologist at Boston University School of Public Health, imagines the people who are still alive in that other world but who died in ours. He calls such people “missing Americans.” And he calculates that in 2021 alone, there were 1.1 million of them. Bor and his colleagues arrived at that number by using data from an international mortality database and the CDC. For every year from 1933 to 2021, they compared America’s mortality rates with the average of Canada, Japan, and 16 Western European nations (adjusting for age and population). They showed that from the 1980s onward, the U.S. started falling behind its peers. By 2019, the number of missing Americans had grown to 626,000. After COVID arrived, that statistic ballooned even further—to 992,000 in 2020, and to 1.1 million in 2021. Were the U.S. “just average compared to other wealthy countries, not even the best performer, fully a third of all deaths last year would have been prevented,” Bor told me. That includes half of all deaths among working-age adults. “Think of two people you might know under 65 who died last year: One of them might still be alive,” he said. “It raises the hairs on the back of my neck.” These counterfactuals puncture two common myths about America’s pandemic experience: that the U.S. was just one unremarkable victim of a crisis that spared no nation and that COVID disrupted a status quo that was strong and worth restoring wholesale. In fact, as one expert predicted in March 2020, the U.S. had the worst outbreak in the industrialized world—not just because of what the Trump and Biden administrations did, but also because of the country’s rotten rootstock. COVID simply did more of what life in America has excelled at for decades: killing Americans in unusually large numbers, and at unusually young ages. “I don’t think people in the United States actually have any awareness of just how poorly we do as a country at letting people live to old age,” Elizabeth Wrigley-Field, a sociologist at the University of Minnesota, told me. Although Bor’s study has yet to be formally reviewed, Wrigley-Field and five other independent researchers vouched for its quality to me. “The paper is extremely important, and the researchers who produced this know what they’re doing,” Steven Woolf, a population-health expert at Virginia Commonwealth University, told me. “It builds on, and considerably expands, what we’ve already known.” Several studies, for example, have shown that America’s life expectancy has tailed behind other comparable countries since the 1970s. By 2010, that gap was already 1.9 years. By the end of 2021, it had grown to 5.3. And although many countries took a longevity hit because of COVID, America was once again exceptional: Among its peers, it experienced the largest life-expectancy decline in 2020 and, unlike its peers, continued declining in 2021. But Bor says that people often misinterpret life-expectancy declines, as if they simply represent a few years shaved off the end of a life. Someone might reasonably ask: What’s the big deal if I die at 76 versus 78? But in fact, life expectancy is falling behind other wealthy nations in large part because a lot of Americans are dying very young—in their 40s and 50s, rather than their 70s and 80s. The country is experiencing what Bor and his colleagues call “a crisis of early death”—a long-simmering tragedy that COVID took to a furious boil. In every country, the coronavirus wrought greater damage upon the bodies of the elderly than the young. But this well-known trend hides a less obvious one: During the pandemic, half of the U.S.’s excess deaths—the missing Americans—were under 65 years old. Even though working-age Americans were less likely to die of COVID than older Americans, they fared considerably worse than similarly aged people in other countries. From 2019 to 2021, the number of working-age Americans who died increased by 233,000—and nine in 10 of those deaths wouldn’t have happened if the U.S. had mortality rates on par with its peers. “This is a damning finding,” Oni Blackstock, the founder and executive director of Health Justice, told me. [Read: How did this many deaths become normal?] The crisis of early death was evident well before COVID. As many studies and reports have shown, since the turn of the 21st century, “midlife ages are where health and survival in the U.S. really go off the rails,” Wrigley-Field told me. “The U.S. actually does well at keeping people alive once they’re really old,” she said, but it struggles to get its citizens to that point. They might die because of gun violence, car accidents, or heart disease and other metabolic disorders, or drug overdoses, suicides, and other deaths of despair. In all of these, the U.S. does worse than most equivalent countries, both by failing to address these problems directly and by leaving people more vulnerable to them to begin with. Consider how many years the missing Americans would have collectively enjoyed had they survived—all the birthdays and anniversaries that never happened. In other rich countries, the total “years of life lost” have flatlined for the past five decades. In the U.S., they have soared: In 2021 alone, the 1.1 million missing Americans lost 25 million years of life among them. That number doesn’t account for the events that preceded many of these deaths—the “years of disability, illness, and loss of human potential, creativity, and dignity,” Laudan Aron, a health-policy researcher at the Urban Institute, told me. And, especially in the case of middle-aged deaths, they left behind young dependents, whose own health might suffer as a result. The sheer number of missing Americans, and the “profound ripple effects” of their absence, are “really hard to wrap one’s head around,” Aron said. [Read: The final pandemic betrayal] These staggering numbers also help contextualize COVID’s toll. The coronavirus caused the largest single-year rise in mortality since World War II, becoming the third leading cause of death in the U.S., after only heart disease and cancer. But this enormous tragedy unfolded against an already tragic backdrop: The number of missing Americans from 2019 is larger than the number of people who were killed by COVID in 2020 or 2021. This isn’t to minimize COVID’s impact; it simply shows that in the Before Times, America had “very successfully normalized to an extremely high level of death on the scale of what we experienced in the pandemic,” Justin Feldman, a social epidemiologist at Harvard, told me. And when COVID drove those levels skyward, America proved that “we’ll accept even more deaths compared to our already poor historical norms,” Feldman said. Such deaths, though obvious on a graph, are hidden from Americans with social privilege. In the summer of 2020, Bor remembers having an outdoor BBQ with a friend who grew up in a low-income housing project. “At that point, six months in, he knew six people in his close circle who had been killed by COVID,” Bor told me. “I still don’t.” The fact that half of the working-age Americans who died last year should still be alive “isn’t visceral if you haven’t lost anyone,” he said. The current mortality crisis was long in the making. In terms of mortality, America’s peer countries—many of which had been hammered by World War II and its aftermath—began catching up with it in the mid-1970s before overtaking in the early 1980s. That was a pivotal era, when globalization, automation, and a growing service industry led to huge losses in mining, manufacturing, and other blue-collar sectors. The U.S. profoundly failed to protect its citizens from these changes. Its social safety net—state assistance for parents, or people facing job, food, or housing insecurity—was meager; its public-health system was languishing after decades of underinvestment; and unlike every other wealthy country, it lacked universal health care. These factors “privatized risk,” Bor and his colleagues wrote in their paper, “tying health more closely to personal wealth and employment.” As labor unions declined and minimum wages stagnated, more Americans had fewer resources to lean on if their health declined. Poorer Americans already lived, on average, shorter lives than rich ones, and that gulf started to widen. Other particularly American choices exacerbated the stresses on the health of the country’s citizens, again weighing more heavily on less wealthy people. A growing mass-incarceration industry punished them. A deregulatory agenda that began with Ronald Reagan’s administration left them vulnerable to unhealthy foods, workplace hazards, environmental pollutants, guns, and opioids. “America basically says: If you’re poor, you don’t have access to safe choices,” Bor told me. Factors like social inequalities and frayed social safety nets are the fundamental weaknesses of American society, which more specific problems like opioids, metabolic disorders, and COVID exploit. During the pandemic, for example, poor and minority groups were more likely to be infected because they lived in crowded housing, distrusted medical leaders, and couldn’t work from home or take time off when sick. And instead of addressing these foundational problems, policy makers instead focused on personal responsibility. America’s drastic underperformance in health also stems from its history of segregation and discrimination. Racist policies have obviously harmed the health of minorities. But as the policy expert Heather McGhee and the physician Jonathan Metzl have independently argued, elites have long marshaled the racial resentment of poor white Americans to undermine support for public goods that would benefit everyone, such as universal health care. Per Frederick Douglass and other Black leaders, “They divided both to conquer each.” [Read: How public health took part in its own downfall] COVID, for example, disproportionately killed Black, Latino, and Indigenous Americans—a trend that, when highlighted to white people, reduces their concern about the pandemic and their support for safety measures. But in 2021, young white Americans still died at three times the rate of the average resident of other peer nations, while young Black and Indigenous Americans died at rates five- and eightfold higher, respectively. “There are thousands of racial-disparity studies that compare Black people to white people—but white Americans are a terrible counterfactual,” Bor told me. They’re frogs in the same pot, boiling more slowly but boiling nonetheless. By using them as a baseline, we ignore how “everyone is harmed by the status quo in the U.S.,” Blackstock told me, while also underestimating how dire things really are for people of color. (The same problem applies to income inequality: White Americans living in the richest 1 percent of counties still have higher rates of maternal and infant mortality than the average residents of wealthy countries.) So, “what happens now?” Bor asked me. “Are we going to have 1 million missing Americans a year, every year, going forward? Or more?” His study doesn’t suggest a reason for optimism, but it does provide a defense against nihilism. The entire concept of missing Americans is rooted in a comparison with other countries, which shows that these early deaths aren’t inevitable. The U.S. could at least start moving in the direction of its peers by adopting policies that work elsewhere, such as universal health care, minimum-wage increases, federally required paid sick leave, and better unemployment insurance. But “the inability of our politics to generate policies that manage health threats is grim,” Bor said. None of the weaknesses that COVID exposed have been addressed; some, like the chasm-sized health gaps between rich and poor or white and Black, have been widened. Vaccines significantly reduce the risk of dying from COVID, but their power is blunted by low uptake, new variants, the lifting of almost all infection-thwarting protections, and the looming loss of COVID funding. Reactionary laws that hamstring what public-health departments can do in emergencies will make the U.S. vulnerable to the new viruses that will inevitably assault it in future years. America’s already underperforming health-care system has been badly battered by the pandemic, and weakened by waves of health-care-worker resignations. In recent months, the Supreme Court has constrained both gun and carbon-emission regulations, while clearing the road for states to restrict or ban abortions—a move that could easily boost America’s already sky-high maternal mortality rates. The climate is still changing rapidly, exposing people who have no choice but to work outside to the ravages of heat. As much of the country returns to normal, Bor’s study makes plain what normal actually meant—and, as I wrote in 2020, that normal led to this. “A lot of Americans may be under the impression that we had a bad go of it during COVID, and once the pandemic is over, they can go back to having the best health in the world,” Woolf told me. “That is a gross misconception.” from https://ift.tt/k49ds5L Check out http://natthash.tumblr.com My time on Delta Airlines 5308, seat 17B, sent my cortisol levels through the roof. Because of “bad weather” and “air traffic,” the departure time got pushed back … and again … and again. As we sat on the JFK tarmac for a solid two hours, a maskless woman directly in front of me didn’t stop coughing. They were sputtering, throaty noises like nothing I have heard before: Less your usual ack and more like huh-khleagggghhh. Since getting vaccinated, I haven’t exactly built my life around avoiding COVID—but still, I’d rather not get sick. And this flight, scheduled for a Wednesday evening in early June, felt more stressful than it had to be. I did not end up getting COVID, though perhaps I got lucky. Mask wearing is no longer required by major airlines in the U.S., and as anyone who has flown recently can tell you, even in a month of crowded summer travel and the rapid spread of BA.5, Americans are done with masks. “Since the mask mandate ended, I’ve flown to Europe, I’ve flown to New York, I’ve flown to Dallas–Fort Worth, and I’ve flown to a couple more places,” Henry Harteveldt, an airline-industry analyst, told me last month. “Depending on the destination, as little as 20 percent of passengers are wearing masks.” [Read: Is BA.5 the reinfection wave?] I get it. Masking up for many hours on a flight is, to use a technical term, a pain. Enduring the discomfort of wearing a mask for the sake of lowering your risk, and everybody else’s, is a tough ask, especially when the risk of getting COVID seems unlikely to abate anytime soon. But what if I told you that there’s a third option here—a way to split the difference between going bare-faced on a plane and never taking off that N95? And that this strategy lets you nearly max out your COVID protection with just a tiny fraction of the annoyance? Here’s the cheat code: Instead of masking up for your whole flight, just cover up at the start and end of it. Those crucial few minutes—first when you’re boarding the plane, and then after you’ve landed—account for only a sliver of your travel time, but they are by far the riskiest for breathing in viral particles. Everyone already knows to switch off cellphone service when their flight is about to leave the gate, and then to turn it on the second they’ve landed. Something like the same principle could work for masking, too. Call it “airplane mode” for your face: Keep your mask in place until your plane is in the air, and then put it on again after you land. Otherwise, you’re free to breathe about the cabin. A commercial flight might seem like the scariest possible setup for super-spreading COVID: Hundreds of strangers who have been God-knows-where over the past few days cram into a metal tube for hours on end. In such quarters, and given current infection rates, you’re very likely to have at least one sick person on board. Indeed, people have caught the virus while on planes, especially on flights without mask mandates. On one trip from London to Hanoi in early March 2020, a sick passenger in business class wound up spreading COVID to 14 travelers and one crew member. But your chances of getting sick don’t stay the same during the course of the flight, Joseph Allen, a Harvard public-health professor who studies ventilation, told me. When the plane is at cruising altitude, the risk will be at its lowest. That’s because planes are equipped with virus-zapping ventilation systems that put schools, restaurants, and other places to shame. About half of the stale, germ-laden air gets flushed out of the plane as the engines suck in more air from outside, and the other half gets recycled through HEPA filters. No other indoor spot that people typically frequent rivals that level of ventilation: In a home, the air gets refreshed every three hours. In a bank, it’s every 45 minutes. In a hospital operating room, it’s at least every five minutes. On airplanes, that cycle takes as little as two minutes. But these primo ventilation systems aren’t always on, and they’re not always operating at full blast. To cut down on fuel costs and exhaust emissions—at least before the pandemic—pilots often shut off the ventilation system while planes are at the gate, Dan Freeman, a safety-management systems expert at Boeing, told me. A passenger can sometimes feel that difference in real time: Maybe it’s a bit hot and muggy when you first get on board; then the lights flicker for a second and you hear the engine come to life, followed by a rush of cool air from the AC vent above you. To make matters worse, passengers jam together in the aisles during the hot and muggy phase, huffing and puffing out aerosols as they strain to lift their bags into overhead bins. Even on the ground, with a plane’s jet engines offline, pilots can use other methods to power ventilation systems. And in the early days of COVID, airlines claimed that they were making the most of them. In July 2020, for example, United vowed to “maximize air flow volume and recirculation of cabin air for passengers from the moment they step onboard.” But it’s not clear whether such measures are here to stay. Representatives for Delta, United, American, and Southwest all told me that, yes, they’re still piping in fresh air while their planes are on the ground. (Spirit did not respond to a request for comment.) Anecdotal evidence is not as promising. In recent months, passengers armed with pocket-size monitors that gauge ventilation have tweeted out images of readings during boarding and disembarking that might indicate the presence of stale air. When a Bloomberg reporter ferried around one of these monitors for several weeks’ worth of travel in April, she found that some of the highest readings of carbon dioxide occurred on airplanes, specifically as she was boarding. (The benefits of HEPA filters would not show up on these monitors.) “It seems wildly variable,” Allen told me. “I don’t think we know what airlines are doing or not doing and why it varies from one plane to the next and one airport to the next.” So we shouldn’t think about airplane masking as an all-or-nothing binary, where you’re either sucking fabric for eight hours straight or giving up on masking altogether. Covering up for the minutes at the very start and very end of a flight makes a big, big difference. When the plane is stopped, definitely put that mask on; in the air, it’s okay to peel it off. “Wearing your mask during those critical periods is a way to drop the risk of flying,” Allen said, making it “lower than any other part of your trip.” Let me show you how to put your face in airplane mode. The first step is making sure that you have an N95 or something equivalent. (A baggy cloth mask that’s two years old does not cut it.) Then, keep that mask in place at the very least until your plane leaves the gate. “We’ll get the most bang for our buck with mask wearing if we do it during boarding and deplaning,” Linsey Marr, an environmental engineer at Virginia Tech, told me. You can also choose to wait a little while longer before you take it off, just to make sure that the ventilation system has time to cycle out every bit of standing air. Five to 10 extra minutes should do the trick, Marr said. Or, if you can stand it, keep the mask on until your flight hits cruising altitude. That’s when the plane’s ventilation reaches peak performance, Joshua Santarpia, an aerosol expert at the University of Nebraska Medical Center, told me. He said that when you’re safe to use your laptop, you’re safe to unmask. Putting your face in airplane mode won’t make sense for everyone. If the guy sitting next to you makes a stray comment about how he can’t smell anything today, even fully active cabin ventilation may not prevent contagion. And if you’re unvaccinated, elderly, or immunocompromised, any number of hours of prolonged masking might be more than worth the inconvenience. But for Americans who are burned out on endless masking, this approach has the upside of being eminently doable. Let’s crunch the numbers: The average domestic flight distance in the U.S. is 905 miles, and usually takes at least two hours. Boarding and deplaning together take about 50 minutes, on average, Harteveldt said. If you’re masking only then, you’ll be free and clear for more than 70 percent of your trip. Naturally, the math gets even better for international, long-haul flights. On a trip from New York to Singapore, one of the longest commercial flights in the world, you might spend 17 hours—or 93 percent percent of the journey—unmasked, with just a marginal increase to your risk of getting sick. Ideally, this could be an official airline rule. Maybe Delta gate attendants would hand you a cute Keep Climbing–stamped N95 when they scanned your ticket, and then you’d see a little mask logo above your cabin row, next to the seat-belt sign that dings when turbulence hits. I asked Airlines for America, the industry’s trade group, if it would consider supporting a very limited masking policy of this kind. “We are pleased that the CDC has lifted pandemic-era restrictions—including mask and pre-departure testing requirements—in accordance with science and research,” a spokesperson told me in an email. For now, airplane mode is a choice, but it’s an easy one to make. The practice will be useful in this summer of BA.5, but also in the future when COVID case rates are much lower. SARS-CoV-2 is not the only airborne virus, of course, and though we don’t go into full lockdown over the flu or common colds, a few basic precautionary measures may still be worth the cost. In 1977, an Alaska Airlines flight sat on the tarmac in Homer, Alaska, for three hours to sort out an engine problem. Within three days, 72 percent of the passengers had come down with the flu. Maybe if people’s faces had been in airplane mode that day in Homer, a super-spreader event would have been avoided. “Do I enjoy wearing a mask in public? Yeah, not even a little bit. But I hate being sick,” Santarpia said. “So if it’s flu season, am I going to wear a mask on the airplane? Yeah, you’re damn right I’m going to.” from https://ift.tt/RAfsXu5 Check out http://natthash.tumblr.com Not so long ago, America’s next COVID fall looked almost tidy. Sure, cases might rise as the weather chills and dries, and people flock indoors. But Pfizer and Moderna were already cooking up America’s very first retooled COVID vaccines, better matched to Omicron and its offshoots, and a new inoculation campaign was brewing. Instead of needing to dose up three, four, even five times within short order, perhaps Americans could get just one COVID shot each year, matched roughly to the season’s circulating strains. Fall 2022 seemed “the first opportunity to routinize COVID vaccines,” says Nirav Shah, the director of the Maine Center for Disease Control and Prevention, and simultaneously recharge the country’s waning enthusiasm for shots. [Read: This fall will be a vaccination reboot] Now that fall is [checks notes] officially 10 weeks away, that once-sunny forecast is looking cloudier. The Biden administration could soon offer second booster shots to all adults—an amuse bouche, apparently, for fall’s Omicron-focused vaccines, which may not debut until October at the earliest, by which time BA.5 may be long gone, and potentially too late to forestall a cold-weather surge. In April, the FDA’s leaders seemed ready to rally around a fall reboot; in a statement last month, Peter Marks, the director of the agency’s Center for Biologics Evaluation and Research, struck a more dispirited tone. The coming autumn would be just a “transitional period,” he said. Which checks out, given the nation’s current timetable. “I see this fall shaping up to be more incremental,” says Jason Schwartz, a vaccine-policy expert at Yale, “rather than that fresh start of let’s begin again.” This, perhaps, is not where experts thought we’d be a year and a half ago, when the vaccines were fresh and in absurdly high demand. Since then, the tale of the U.S.’s COVID immunity has taken on a tragicomic twist: First we needed a vaccine; then we needed more people to take it. Now the problem is both. Yes, fall’s vaccine recipe seems set. But much more needs to happen before the nation can be served a full immunization entrée. “It’s July, and we just heard that the FDA would like to see a bivalent vaccine,” with the spike of BA.4 and BA.5 mixed with that of the OG SARS-CoV-2, Schwartz told me. When, exactly, will the updated shots be ready? How effective will they be? How many doses will be available? We just started prepping for this new inoculation course, and are somehow already behind. Then, once shots are nigh, what will be the plan? Who will be allowed to get one, and how many people actually will? Right now, America’s appetite for more shots is low, which could herald yet another round of lackluster uptake. There’s little time to address these issues. Fall “is, like, tomorrow,” says Jacinda Abdul-Mutakabbir, an infectious-disease pharmacist at Loma Linda University, in California. Autumn, the season of viral illnesses and packed hospitals, already puts infectious-disease experts on edge. “We dread fall and winter season here,” says Yvonne Maldonado, a pediatric-infectious-disease specialist at Stanford University. The system has little slack for more logistical mayhem. The world’s third COVID autumn, far from a stable picture of viral control, is starting to resemble a barely better sequel to the uncoordinated messes of 2020 and 2021. The coming rollout may be one of America’s most difficult yet—because instead of dealing with this country’s vaccination problems, we’re playing our failures on loop. In an ideal version of this fall, revamped COVID vaccines might have been doled out alongside flu shots, starting as early as August or September, to prelude a probable end-of-year surge. But that notion may have always been doomed. At an FDA advisory meeting in early April, Marks told experts that the fall vaccine’s composition should be decided no later than June. The agency didn’t announce the new ingredients until the final day of last month. And it chose to include BA.4 and BA.5, the reigning Omicron subvariant—rather than the long-gone BA.1, which Pfizer and Moderna had been working with. That decision may further delay the shots’ premiere, punting the delivery of some doses into November, December, or even later, depending on how the coming months go. If the goal is preventing a spate of seasonal sickness, that’s “cutting it quite close,” says Wilbur Chen, an infectious-disease physician and vaccine expert at the University of Maryland. Whenever the shots do appear, they could once again be hard to keep in stock. Coronavirus funds are still (still!) stalled in congressional purgatory, and may never make it out. Although the Biden administration has agreed to purchase more than 100 million doses of Pfizer’s revamped Omicron vaccine for the months ahead, federal officials remain worried that, as Ashish Jha, the nation’s top COVID-response coordinator, has said, “we’re not going to have enough vaccines for every adult who wants one” this fall. Meanwhile, state and local leaders are awaiting marching orders on how much vaccine they’ll be getting, and who will be eligible for boosters—intel they may not receive until after the updated shots are authorized. With a year and a half of experience under their belts, health workers know how to roll out COVID shots, says Chrissie Juliano, the executive director of the Big Cities Health Coalition. But distribution could still get tangled if “we’re back to a situation of scarcity,” she told me. The government may allocate shots based on states’ populations. Or it could opt to dole out more doses to the regions with the highest vaccination rates, wasting fewer shots, perhaps, but widening gaps in protection. More than two years into the pandemic, with the health-care system under constant strain and staff exhausted or frequently out sick, local communities across the nation may not have enough capacity to deploy fall shots en masse. In particular, pharmacies, a vaccination mainstay, will need to handle a simultaneous surge in demand for flu and COVID shots amid “a serious nationwide staffing shortage,” Michael Hogue, the dean of Loma Linda University’s pharmacy school, told me. A lack of funding only compounds these problems, by making it harder, for instance, to get doses to people who aren’t insured. For that reason alone, “some of the contractors we’ve used in the past have not been able to keep up the same services,” including vaccination drive-throughs, Phil Huang, the director of Dallas County Health and Human Services, told me. In Douglas County, Nebraska, pop-up vaccination sites are closing because not enough nurses can staff them. How do you get people vaccinated, Lindsay Huse, the county’s health director, asked me, “when nobody wants to work for what you’re paying, or they’re just burned out?” Even if more resources free up, greater shot availability may not translate to greater protection: Less than half of eligible vaccinated Americans, and less than a third of all Americans, have received a first booster dose, a pattern of attrition that experts don’t expect to massively improve. And just how much of an immunity boost the updated shot will offer is still unclear. When the FDA recommended including BA.4/5’s spike, it had limited data on the proposed recipe, collected in mice by Pfizer’s scientists. And Pfizer and Moderna won’t have time to generate rock-solid efficacy data in humans before the shots are authorized, then roll out in the fall. “So when we get these vaccines cranking off the assembly line, the case public-health officials may be able to make will be tempered,” Schwartz told me. That these doses will offer big improvements on their predecessors is a decent bet. But believing that will, for the public, require a small leap of faith—at a time when Americans’ trust in public health is already low. America has had its share of COVID-vaccination victories. Hundreds of millions of people have gotten at least one dose. Distribution and administration have been streamlined. Communities have come together to bring shots to people in all sorts of venues. The local experts I spoke with felt confident that they’d rise to the challenge of this autumn, too. But if the shots themselves are not in demand, an infusion of supply-side resources alone won’t be enough. [Read: America created its own booster problems] With two years of data on COVID vaccines’ safety and efficacy, the case for dosing up has only strengthened, scientifically. But the public’s interest and trust in the shots has fallen off as recommendations have shifted, often chaotically, and the number of necessary shots has ballooned. Even Americans who lined up for their first doses are now over the idea of rolling up their sleeves again. Abdul-Mutakabbir hears often: “I got the two doses; that’s what you told me I needed to do. I’m not doing anything else.” In Camden County, New Jersey, a team led by Paschal Nwako, the region’s health officer, has “knocked on doors, given out freebies and gift cards, visited people in all areas: grocery stores, shops, restaurants, schools, churches, shows,” he told me. “We have exhausted all the playbooks.” Still, people have refused. The shifting culture around COVID in the U.S. has undoubtedly played a role. “We don’t have the same sense of desperation that we did in December of 2020,” Maldonado, of Stanford, told me. Americans are eager to put the pandemic behind them. And boosters are a tough sell in a nation that has dispensed with nearly all other COVID-prevention measures, and where political leaders are triumphantly declaring victory. “We start talking about COVID, and people’s eyes glaze over,” says Nathan Chomilo, a pediatrician and health-equity advocate in Minnesota. “The messaging will have to be fundamentally different, even, than last year’s conversation about boosters.” [Read: Don’t wait to get your kid vaccinated] When the vaccines were fresh, the popular narratives were tantalizing: The shots could permanently stop transmission in its tracks. But that was probably never going to pan out, says Luciana Borio, the FDA’s former acting chief scientist. “Everybody that worked in the vaccine space,” she told me, knew that the safeguards against infection “were not going to last. Their voices did not get listened to.” Instead, the more appealing story took root, setting “expectations that could not be sustained.” Disappointment ensued, fracturing public faith; mis- and disinformation seeped into the cracks. And no one, including the nation’s leaders, was able to offer a compelling enough counternarrative to put the matter to rest. An upgraded shot could be enticing to some pandemic-weary folks. “I know a lot of people, including my family members, who say, ‘If it’s the same vaccine, why would I have to get it?’” Nwako told me. “They want something different.” Chomilo suggested that it may also be wise to stop counting how many shots people have gotten: “I hope no one 15 years from now is saying, I’m on my 15th booster.” But nothing about these new vaccines promises to unify Americans around the why of COVID vaccines. At April’s advisory meeting, Marks said the FDA knew that the U.S.’s current vaccination strategy couldn’t go on forever. “We simply can’t be boosting people as frequently as we are,” he said. And yet, the nation’s leaders now seem keen on okaying another round of original-recipe shots for adults under 50—without emphasizing other tactics to lower transmission rates. Getting COVID shots, too, can be a chore. With so many brands, doses, schedules, and eligibility requirements in the matrix, it’s “the most complex vaccine we have,” says Erik Hernandez, the system director of clinical-pharmacy services at the University of Pittsburgh Medical Center. The fall will introduce even more snarls: Boosters are switching to an Omicron blend, but, contrary to what the FDA had initially planned, primary-series shots will be sticking with the original recipe. “That has massive operational implications,” Maine CDC’s Shah said, and could “increase the risk of errors.” Nor have federal officials offered clarity on how long people getting shots now will have to wait before they’re eligible for yet another this autumn. And Loma Linda University’s Hogue thinks that it’s very unlikely that children, especially the youngest ones, will be greenlit for bespoke Omicron doses this fall—another caveat to juggle. Some experts also worry that different states will once again select different rules on who can sign up for shots first. “You almost have to have a computer algorithm” to figure out what shots you need, Chen, of the University of Maryland, told me. Recommending an updated dose for everyone at once could be less confusing, but if shots are truly scarce, broad eligibility could simply put the privileged at the front of the queue. [Read: Vaccines are still mostly blocking severe disease] Less funding already means less community outreach, and less support for the people most vulnerable to COVID’s worst. The country could easily default back to many of the failures of equity it’s rehearsed before. Abdul-Mutakabbir, who’s the lead clinician and pharmacist for the COVID-19 Equitable Mobile Vaccination Clinics, serving Black and Latino communities in San Bernardino County, says she’s “very nervous” that large swaths of the country will once again “end up in this place where people of minority groups are going to be those that suffer, and people of lower socioeconomic status are going to be those that suffer.” An infusion of dollars would allow the government to purchase more vaccines; it would furnish states with the funds to hire more workers, expand their community clinics, and reach people who might otherwise never get their shots. But the underlying issue remains: The U.S. does not have a strong, coordinated vaccination plan. Experts still can’t agree on how many shots people need, how often we’ll need to update them, even what the purpose of a COVID vaccination should be: stopping just severe disease and death? Blocking as much infection as possible? “We don’t really have a grand unified theory of what we’re doing when we vaccinate,” Shah told me, at least not one that’s been properly messaged—a deficit that will keep hamstringing the country’s immunization efforts.
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