Keeping an infant fed is a precarious task in the best of circumstances, and for many American parents, the circumstances have become quite bad. Nutritional formulas are currently in very short supply across the United States, and in some markets, more than half of all products are out of stock. For babies with medical conditions, as well as older kids and adults whose lives similarly depend on access to specialty nutritional formulas, the situation is nearing catastrophe. Because it can take weeks for increased production to show up on store shelves—and because most factories were already functioning near capacity—the shortage is likely to get worse before it gets better. In an acute sense, this chaos was caused by the February shutdown of a large Abbott Nutrition manufacturing plant in Michigan and an associated product recall, following the deaths of at least two infants, which the FDA believes were connected to tainted Similac formula. The loss of this particular plant’s manufacturing capacity would have caused supply issues no matter when it happened, but it came at a very delicate moment: Nutritional formula is among the many consumer products that have been periodically scarce throughout the pandemic, leaving the market ill-equipped to deal with the sudden, extended closure of one of the country’s biggest formula plants—and, in the case of some specialty formulas, one of the country’s only plants. (A representative for Abbott did not respond to a list of specific inquiries about the plant closure, but did provide a statement arguing that the FDA had not provided conclusive evidence that its products were tainted.) The chronic problem, though, began long before the pandemic. Parents affected by recent shocks to the nation’s formula supply were already in a delicate position, thanks to a threadbare social safety net and a history of commercial consolidation. Infant formula is a lifeline for millions of families, but the industry that creates it has shown evidence of rot for decades. In the past, if you encountered a news story about infant formula, it was probably because people were stealing it in bulk. Law enforcement and retail organizations frequently overstate the risks posed to the general public by “shoplifting rings” and organized theft, but a thriving black market does exist for secondhand baby formula. Buying through these channels is genuinely dangerous—fudged expiration dates and improper storage can turn the product into a health hazard. That parents nonetheless resort to feeding their babies formula sourced on Craigslist or Facebook Marketplace suggests a long-standing and considerable desperation. [Read: The great shoplifting freak-out] In a perfect world, parents wouldn’t need formula at all, because they would be able to follow the common advice to breastfeed exclusively for six months and in tandem with other appropriate foods for at least a year. But breastfeeding cannot—and never has—fully addressed the nutritional needs of every baby. Some newborns latch poorly or have allergies; some mothers find nursing physically or psychologically difficult; some babies are adopted. But one of the biggest obstacles that new American parents encounter when trying to follow breastfeeding advice is man-made: In 2021, less than a quarter of U.S. workers had any access to paid family leave through their employer, and relatively few employers offer other kinds of support for lactating mothers. “The shock of having to go back to work six weeks after delivering a new baby is terribly disruptive to breastfeeding access,” Steven Abrams, a professor of pediatrics at the University of Texas’s Dell Medical School, told me. The results of these policies show up in predictable ways in statistics about infant nutrition: The babies of richer families are more likely to be breastfed exclusively, and they are breastfed for longer on average. For families that need to go to work and keep their kids fed, the primary safety net is maintained by private-sector food and pharmaceutical conglomerates. The Special Supplemental Nutrition Program for Women, Infants, and Children, or WIC, provides about half of all American newborns with nutritional aid through a federal program, but is administered by the states, which sign individual deals with manufacturers for the exclusive rights to provide formula to a state’s benefit recipients. This program has been very effective at getting formula to low-income families, but it also exacerbates problems within the formula market. Because of WIC’s scale, its exclusive statewide contracts encourage consolidation, according to Brian Dittmeier, the senior director of public policy at the National WIC Association, an organization that advocates on behalf of WIC recipients and the program’s workers. Manufacturers struggle to compete in markets where they don’t have a WIC contract, even for products that are not covered by the program’s rebates. A recent analysis of retailer sales data from 2006 to 2015 found that when a manufacturer won a new WIC contract, its sales of eligible formula shot up more than 300 percent in that state. And the researchers found what they called a “spillover” effect—sales of the manufacturer’s non-rebated products also jumped significantly. Over time, these exclusive contracts have been won by a shrinking number of ever larger manufacturers. In 2015, Abbott, the company whose plant closure triggered current shortages, held WIC contracts in 23 states. Now the number is at least 31. “There are only a few manufacturing plants in the country, and there are four infant-formula companies that control about 90 percent of the supply in the United States,” Dittmeier told me. “It’s a highly concentrated market with a highly concentrated production capacity, so that when one plant is taken offline for just a period of weeks, you see these ripple effects throughout the entire sector.” Formula manufacturers, like any other for-profit companies, tend to do what’s best for their balance sheets. Snapping up as many exclusive statewide contracts as possible helps to muscle out competition. Running fewer, larger manufacturing plants is more cost-efficient than having more, smaller plants around the country, even if that redundancy would reduce the risk of catastrophic shortages. Extreme consolidation of the country’s infant-nutrition industry affects everyone, not just WIC recipients. “You have to consider whether there are implications to both the availability and the price of [the] product, if such a large customer base is limited to a specific brand,” Dittmeier said. According to a 2004 study from the Department of Agriculture, when a manufacturer wins an exclusive WIC contract, it raises prices on all of its products within that state. American parents’ current plight could have been mitigated or prevented in many different ways. A host of federal policy changes could decrease demand for formula or ameliorate the market’s brittleness: Guaranteed paid parental leave—something all other rich countries provide—would make it possible for more mothers to breastfeed exclusively, if they’re so inclined. Universal prenatal care would better prepare low-income mothers to solve common problems that preclude breastfeeding. Regulators could crack down on formula marketers, who have a long history of employing tactics that a United Nations report recently described as “pervasive, misleading, and aggressive”—and of using these tactics to pursue low-income Black moms in particular. The federal government could take a more active role in ensuring that reserves of vital goods are always available, or require manufacturers that win public contracts to guarantee certain types of redundancy in their supply chains. And reforming WIC contracts to allow multiple manufacturers to supply rebated formula within a state would encourage a healthier, more stable nutritional-formula industry. But even among people who have dedicated their professional lives to addressing the country’s infant-nutrition and family-safety-net problems, what has transpired over the past few weeks has been a shock. “I think everyone was taken aback, especially by the sudden collapse of the whole system,” Steven Abrams told me. “Nobody predicted that.” from https://ift.tt/arOXLnc Check out http://natthash.tumblr.com
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Last October, a young girl with severe and unusual liver failure was admitted to a hospital in Birmingham, Alabama. Her symptoms were typical: skin and eyes yellow with jaundice, markers of liver damage off the charts. But she tested negative for all the usual suspects behind liver disease. Her only positive test was, surprisingly, for adenovirus—a common virus best known for causing mild colds, pink eye, or stomach flu. In rare cases, it’s linked to hepatitis, or inflammation of the liver, in immunocompromised patients. But this girl had been healthy. Then it happened again. A second kid came in, about the same age, with all the same symptoms, and again positive for adenovirus. “One patient is a fluke; two is a pattern,” says Markus Buchfellner, a pediatric infectious-diseases doctor at the University of Alabama at Birmingham (UAB). Two quickly became three and then four. Alarmed, the hospital’s doctors alerted local health authorities and the CDC, whose investigation ultimately found nine such cases of unusual hepatitis in kids in Alabama. Two needed liver transplants. Buchfellner originally thought that whatever was happening was local to Alabama. But this spring, investigators in the U.K. began independently puzzling over their own mysterious uptick in hepatitis among kids. They have since identified more than 150 such cases in the U.K. This prompted the CDC to cast a wider net, bringing the number of suspected cases across the U.S. to 109. Fifteen of the kids have needed liver transplants, and five have died. Worldwide, probable cases now total 348 spread across 20 countries. The early evidence continues to point to a link with adenovirus—an unexpected correlation that is too strong to dismiss and not strong enough to close the case. Seventy percent of the probable cases globally have tested positive for adenovirus, according to the World Health Organization. But although biopsies have been conducted in a small fraction of those cases, they have failed to find adenovirus in the kids’ livers. At the same time, we definitely know that a different virus infected a massive number of kids recently: SARS-CoV-2, of course. Yet the correlation here is even less clear; only 18 percent of the probable cases tested positive for COVID. Adenovirus and coronavirus aren’t necessarily mutually exclusive explanations. The leading hypotheses now suggest an interaction between adenovirus and the pandemic—either because social distancing changed the patterns of adenovirus immunity, allowing for more severe or simply more adenovirus infections, or because previous infection or co-infection with the coronavirus triggers an unusual response to adenovirus. Alternatively, did the adenovirus itself recently change, evolving to more readily damage the liver? Severe liver failure in kids is very rare, says Helena Gutierrez, the medical director for pediatric liver transplants at UAB and Children’s of Alabama. But when it does happen, a significant proportion of cases even in normal times remains entirely mysterious. No identifiable cause is ever found in almost half of kids with liver failure so severe that they might need a transplant. Ultimately, understanding the recent pattern of unexplained liver-failure cases in kids may shed light on previously mysterious cases that were once too infrequent to attract much attention. [Read: A human liver can be cooled to -4 degrees C and survive] But why is there an increase right now? The only culprit that can be conclusively ruled out is COVID vaccines, because kids under 5, who make up the bulk of the hepatitis cases, cannot yet be vaccinated. In the weeks ahead, experts will be looking at three key pieces of data to parse the remaining hypotheses. The first and perhaps most obvious set of data to gather is: Have these kids had COVID before? The overwhelming majority of the kids with hepatitis tested negative for the coronavirus, but investigators are now collecting antibody data to see if any of them had COVID in the past. “I don’t think it’s directly related to the virus itself,” says Buchfellner, but perhaps a COVID infection could have predisposed a kid to liver failure once something else—say, an adenovirus infection—came along. And although multisystem inflammatory syndrome, or MIS-C, following coronavirus infection can affect the liver, the hepatitis patients did not exhibit the other hallmark signs of that condition, such as high inflammatory markers and heart damage. When the COVID antibody data do come out, a lot of the kids will be positive—simply because a lot of kids in general have had COVID recently. Experts will want to go one step further to determine whether the coronavirus is really playing a role. If so, they’d expect that kids with hepatitis are more likely to have COVID antibodies than a control group of kids who did not have hepatitis. [Read: COVID-19’s effect on kids is even stranger than we thought] A second key piece of data is about the adenovirus itself. Adenoviruses are very common, so could all the positive tests simply reflect incidental infections unrelated to liver failure? Here, too, investigators will want to see if kids hospitalized with hepatitis are more likely to test positive for adenovirus than those hospitalized for other reasons. If they are, the link to adenovirus becomes stronger. The U.K. is analyzing these exact data and is expected to have results in the next week. Exactly how many kids test positive for adenovirus sounds like a simple statistic, but it can be messy early on, when investigators are dealing with mostly retrospective data. Different doctors in different hospitals might think to order different tests. UAB happened to test for adenovirus, but it’s so low on the list of hepatitis culprits that the test is not necessarily routine. And how tests are done can affect whether they come back positive, says Benjamin Lee, a pediatric infectious-diseases doctor at the University of Vermont. “Is the virus able to be detected in the blood at the time the patient presents for care? Are there other sites that need to be tested?” he asks. What about the nose and throat? Or stool? And indeed, U.K. investigators have had to make sense of a mélange of blood, stool, and respiratory samples, with varying positivity rates. A third prong of the investigation will focus on the adenoviruses found in these samples. Sequencing their genomes can determine whether the viruses recently acquired new mutations that can explain the link to liver failure. Adenovirus variants have popped up before, and this type of virus is especially apt at reshuffling its genome. Whole genome sequencing is in the works, though scientists in the U.K. originally had trouble getting enough virus out of early samples. And scientists don’t have a big database of old adenovirus samples of this kind to compare with the new ones. “We take that for granted out with SARS-CoV-2,” says James Platts-Mills, an infectious-diseases doctor at the University of Virginia. So the initial progress may be slow. Partial sequencing of the viral genome, though, has already pinpointed one particular type of adenovirus that predominates in the hepatitis cases: adenovirus 41, also known as 41F. (There are more than 100 types of adenovirus. F refers to the species, the number reflects the order in which the types were discovered.) Adenovirus 41 infects the GI tract. Platts-Mills has studied adenovirus 41 in developing countries, where it is a leading cause of hospitalizations for diarrhea in children. It circulates in wealthy countries, too, but in the U.S. it doesn’t cause enough trouble to justify active surveillance. Potentially, Platts-Mills says, the hepatitis cases are only the “tip of the iceberg” of a large number of undocumented mild adenovirus 41 cases. The invisible surge, if there is one, could be due to either new viral mutations or many young children getting infected at once, with COVID restrictions relaxing. Still, it’s surprising to see adenovirus 41 specifically as a suspect in these hepatitis cases, adenovirus experts told me. Although adenovirus has been linked to severe liver failure, it’s not been adenovirus 41 but types 1, 2, 3, 5, and 7. Plus, these cases almost always happen in patients with suppressed immune systems. “In those immunocompromised kids, you could see it in the liver. When we made slides, you could see the viral particles,” says Kurt Schaberg, a pathologist at UC Davis who has studied adenovirus hepatitis. The dark centers of the infected liver cells become big and swollen. It’s all quite obvious. Biopsies didn’t find any of these patterns in the livers of the non-immunocompromised kids. If adenovirus plays a role, it is probably more indirect. Perhaps it somehow triggers the immune system to start attacking the liver, either by itself or in combination with another virus, toxin, or environmental factor. And this might continue even after the virus itself is cleared, so tests for adenovirus could turn up negative. All of this means that figuring out the answer to these hepatitis cases in kids won’t be straightforward. “If we found virus in the liver, we would be done,” says Buchfellner, in Alabama. “The fact we can’t find that means it’s much harder to prove.” Instead of a single direct cause, investigators are probably looking for an indirect one or multiple indirect ones. In the weeks ahead, nailing down three key questions—whether these kids have also been infected with COVID, whether their adenovirus infections are incidental, and whether their viruses have mutated—will at least narrow down the list of plausible hypotheses. Meanwhile, the nine kids in Alabama are all recovering. Whatever the cause, doctors stressed to me, the risk of severe hepatitis for healthy kids is still very, very small. from https://ift.tt/ePQr8LB Check out http://natthash.tumblr.com Up here in the Northern Hemisphere, the spring weather’s just barely warming, but regulators in the United States are already wringing their hands over a tricksy fall brew: the contents of the COVID shot that vaccine makers are prepping for autumn, when all eligible Americans may be asked to dose up yet again (if, that is, Congress coughs up the money to actually buy the vaccines). In a recent advisory meeting convened by the FDA, Peter Marks, the director of the agency’s Center of Biologics Evaluation and Research, acknowledged the “very compressed time frame” in which experts will need to finalize the inoculation’s ingredients—probably, he said, by the end of June. Which is, for the record, right around the corner. A big choice is looming. And whatever version of the virus that scientists select for America’s next jab is “probably going to be the wrong one,” says Allie Greaney, who studies the push and pull between viruses and the immune system at the University of Washington and the Fred Hutchinson Cancer Center. Unavoidably, several months will separate the selection of this autumn’s vaccine and the deployment of said shot. That’s eons in coronavirus time. Half a year ago, we were all still living in Delta’s world; now a whole gaggle of Omicrons are running the show. Any decision that scientists make in June will have to involve assumptions about how SARS-CoV-2 will shape-shift in the future, which exactly no one is eager to make. “We keep getting burned,” says Adam Lauring, a virologist at the University of Michigan. Perhaps the virus will stay on its Omicron bender, making an Omicron vaccine—a favorite for the fall’s jab jubilee—sound like a no-brainer. Or perhaps by the time summer’s through, it will have moved on to a Rho, Sigma, or Chi that sproings out from somewhere totally unexpected and undermines that Omicron shot. With so many people around the world harboring some degree of immunity, the virus is being forced to continually reinvent itself, and no one knows what new costumes it might try on next. [Read: We might not need annual COVID shots] Our choice of fall shot, then, is inevitably going to be a gamble and a guess. But with the clock ticking down, most of the experts I’ve been talking with think an ingredient swap is wise, and probably inevitable. “We should be updating the vaccines now or yesterday,” said Jonathan Abraham, a physician and immunologist at Harvard Medical School. Modeled on the version of the virus that kick-started the crisis more than two years ago, our current crop of immunizations is still guarding against severe illness and death. But that OG variant has long since fizzled out—leaving our shots, in this one sense, frozen in the past, while the real SARS-CoV-2 continues to race ahead. A 2022 revamp might finally give our vaccines a chance to close some of that gap. The decision that regulators make in early summer won’t just be about a boost. In the recent advisory meeting, Marks emphasized that any vaccine updates would be expected to be comprehensive, replacing old formulations as both boosters and primary-series doses; after the changeover, people who haven’t gotten their first doses—who number in the tens of millions in the U.S. alone, and would include future generations of kids—might not be able to nab an original-recipe shot. “We would not be going backwards,” Marks told the committee. “It would be too confusing and potentially dangerous to have different regimens.” The same system shuffles the populace through a new flu-shot formulation year after year, and it usually works just fine. Those viruses have been twining themselves into the human population for centuries; host and pathogen have settled into an uneasy rhythm, with a more or less set flu season playing out in most parts of the world each year. Last year’s successful flu strains tend to give rise to this year’s, which then sire next year’s—a phenomenon scientists call “ladder-like evolution,” because of its soothing stepwise shape. To concoct the forthcoming season’s flu shot, “we do surveillance; we figure out what to be prepared for,” Lauring told me. With SARS-CoV-2, however, “the dynamics are still so wacky.” Waves of infection crest and crash in different countries every few months; the virus is still sloshing out new variants and subvariants at breakneck speed. The emergence of coronavirus iterations has also been less ladder-ish and more radial, like spokes erupting out of the center of a bicycle wheel: Alpha did not beget Delta, which did not birth Omicron. In recent months, though, the virus appears to have taken a different tack. Since the end of 2021, nearly everything’s been coming up Omicron. From BA.1 (a.k.a. Omicron classic) to BA.2, and now the rising BA.2.12.1, BA.4, and BA.5, the last few viral successions have all occurred within the Omicron clan. So our next move might seem obvious: counter with an Omicron-centric vaccine, a switch some experts have been favoring for months. On that front, Moderna and Pfizer might soon deliver. The two vaccine makers have each been testing, among other options, bespoke BA.1 versions of their shots that they say could be ready within the next few months, just in time for a pre-winter inoculation push. “We plan to have a data readout soon,” Jerica Pitts, a spokesperson for Pfizer, wrote in an email. [Read: Why can’t we just call BA.2 Omicron?] By numbers alone, there is a pretty strong likelihood that more BA-whatever subvariants will come down the pike. And as a booster, especially, an Omicron shot could have clear perks, shoring up the defenses laid down by previous doses while also, ideally, pushing a new batch of immune cells to wise up to the variant’s unique and never-before-seen quirks, says Marion Pepper, an immunologist at the University of Washington. The hope is that Pfizer’s and Moderna’s data will back that notion up and show that people boosted with Omicron’s spike are better at duking it out with most of the BA fam than those who are injected with the original recipe again. But there’s also a chance that the evidence won’t bear this out. A smattering of recent studies, some in animals, hint that chasing an original-recipe shot with something Omicron-y might not push the body to develop a ton of Omicron-specific defenses, at least not at first; studied head-to-head, a BA.1 booster and an OG booster performed about the same. Pepper still has faith that a lesson on Omicron’s spike will pay dividends—the effects just might take more time to unspool. Taia Wang, an immunologist at Stanford, agrees. “Boosting with Omicron will almost certainly provide more immunity against currently circulating strains,” she told me. Currently could quickly become previously, though, if another variant elbows in. Although the virus’s evolution might look sort of, kind of, more stepwise right now, “we’ve seen the different lineages pass the baton back and forth,” Siobain Duffy, a virologist at Rutgers University, told me. “There’s absolutely nothing stopping a similar large jump in SARS-CoV-2 evolution from happening again.” Perhaps the bigger worry is whether BA.1 will end up being a terrible teacher when deployed as an unvaccinated person’s starter shot. The variant’s bizarro-looking spike, so unlike any that came before it, is such an outlier that it may fail to show an unsavvy immune system how to recognize other morphs of SARS-CoV-2. That’s not a problem if the future of the virus stays hooked on Omicron. But should it be booted by another variant more resembling Alpha, Delta, or something else, bodies schooled on BA.1 alone might be ill-prepared. Pfizer, which is testing a triple-Omicron series in a group of previously unjabbed people, could produce data to the contrary. Absent those, a premature pivot to Omicron might bias immune systems toward the wrong track. [Read: Should we go all in on Omicron vaccines?] If an Omicron-only vaccine is starting to sound like a possible lose-lose situation, maybe it’s no surprise that the experts I spoke with ran the entire gamut of opinions about it. “If I could get an Omicron booster now, I definitely would,” Wang told me. Harvard’s Abraham said that he’s in the same boat. Meanwhile, John Wherry, an immunologist at the University of Pennsylvania, was one of several scientists who said that option’s a “nope”—safer, they said, to keep something with OG. The most common refrain, though, was, I’m not sure, and I’m glad I’m not the one deciding. There could still be a quasi-compromise: a dose that includes two spike variations, maybe more, in the same shot. So-called bi- and multivalent vaccines are already in the works; both Moderna and Pfizer are slurrying together spikes from BA.1 and the OG coronavirus variant, a recipe that Moderna executives have repeatedly described as their “lead candidate for fall 2022.” That tactic could simultaneously enhance and focus the body’s defenses, says Lexi Walls, a biochemist and vaccine developer at the University of Washington. Such combo shots are the wary vaccinologist’s hedge: They might offer both a reminder of a version of the virus that most immune systems have already seen, as well as a preview of what might still be to come. Cramming several spikes together isn’t a perfect solution. A recipe that’s half BA.1 and half OG won’t necessarily yield an immune response that splits the difference. Such a concoction also doesn’t fully solve the problems of an Omicron-only vaccine. The pesky delay between design and deployment always puts the humans behind: BA.1 may no longer be the most relevant form of Omicron to use, because it’s rapidly being ousted by speedier siblings. And a body trained on BA.1 might have some trouble tussling with some of its more irksome kin, which appear to circumvent some of the antibodies their predecessor lays down. The BA subvariants, for now, share the name Omicron, but in reality, some of them are “just as divergent as some of the variants of concern that have their own Greek letter,” says Jemma Geoghegan, a virologist at the University of Otago, in New Zealand. Several experts, including UW’s Greaney and Michigan’s Lauring, told me that, in an ideal world, they would have liked to see BA.2’s spike slotted into the next shot instead. That’s not necessarily a reason to forgo an upgrade to BA.1, though, because that could still better familiarize bodies with other Omicron offshoots than if they were left none the wiser. Strain-vaccine mismatches happen all the time with flu shots, Geogeghan points out, and even so, those vaccines “are still really good at protecting against severe disease and death.” Experts won’t know for sure how bivalent vaccines will fare until Moderna and Pfizer publish data from their ongoing trials. Omicron-only shots might outperform them; original-recipe boosters might still trounce them all; none of those data will have clear bearing on the next theoretical variant to rise. Abraham, for one, isn’t quite sold on the idea of a bivalent vaccine. “We don’t know what the second-best antigen would be” after Omicron’s spike, he told me; pick the wrong one, and it may just end up wasting space in shots. He’d prefer to lean into Omicron’s ongoing monopoly, he said, and model the next shot on only that. (Moderna is also trialing a Beta-OG bivalent shot—remember Beta?—that the company says is performing well, even against BA.1.) Vaccines may not always need to lag variants this much. Geogeghan expects that the pace at which new, antibody-dodging variants sprout off the coronavirus family tree will eventually slow down. And researchers such as Walls, at UW, are working on universal vaccines that may be able to guard against a whole menagerie of coronavirus iterations—perhaps even ones that haven’t yet been detected—so that the game of variant whack-a-mole can end. Until then, experts are working with limited options, based on limited data—and there is yet another option that may feel like the easiest of all: Do nothing, and stick with the vaccines we have. They are, after all, still performing extraordinarily well, especially when delivered in full rounds of at least three doses; it’s what’s known, and maybe, what feels safe. Among the dozen-plus experts I spoke with for this piece, there wasn’t consensus on what our next vaccine’s main ingredients should be. Still, most agreed on this: The worst thing to do would be to stay stagnant with our shots—to miss an opportunity to move our understanding forward when the virus has already gained so much ground. “We’re always playing catch-up,” says Karthik Gangavarapu, a computational biologist at UCLA. “But if we don’t do anything, we’re for sure not going to be able to win the race.” from https://ift.tt/pK3ChAF Check out http://natthash.tumblr.com In this, the season of Bill Gates’s atonement, the billionaire is willing to acknowledge that things don’t always turn out as they should have, and that—at least in some cases—that’s on him. There was the high-profile divorce from his wife of 27 years, Melinda French Gates (“definitely a sad thing,” he said); allegations of an affair and inappropriate flirting at work (“false, recycled rumors,” a spokesperson insisted); and his association with the convicted sex offender Jeffrey Epstein (a “big mistake” on a whole list of them). But Gates is not one to dwell on the painful past, particularly when that past conflicts with his arduously cultivated image as the world’s preeminent techno-savior. Bill Gates is a doer. And a fixer. And the thing he’s most focused on now is how he can help save the world from the next pandemic. After all, he’s seen for himself that no one man—not even a president, not even an innovator, not even a billionaire—was able to stave off this one. I recently met with Gates, whose foundation has long preoccupied itself with global public-health initiatives, to talk about what he might do differently next time, and what we can learn from the hell of the past two years. His obsession with the subject is honorable, but I had to notice that his approach felt a little, well, predictable. Gates bets big on futuristic biotech—a library stocked with millions of antiviral drugs, for example, and machines that can test 150,000 samples a day for multiple pathogens. But the major building blocks for his plan are decades old: He wants better disease surveillance; more drugs to treat the infected; and enough shots to vaccinate as many people as possible, as quickly as possible. How should we prevent the next pandemic? By doing the things we try to do already—only better. Much of the world’s response to the coronavirus—and America’s response in particular—has been, to put it lightly, a mess. It’s telling of our sorry situation that Gates’s grandest ambitions are simply to do the most basic things right—to have a real plan and stick to it. But while one big lesson of the pandemic has been how badly plans are needed, another has been how easily even the best ones fail. I spoke with Gates at the Washington, D.C. Four Seasons hotel, in a windowless basement conference room at a table lined with empty chairs and unopened water bottles. Gates was on a multicity promotional tour for How to Prevent the Next Pandemic, a book that lays out in 215 pages his vision for avoiding future catastrophic global illness. A few notable points: Governments should encourage innovation, cut red tape, and agree to manufacture game-changing global-health tools. Everyone in the world should have access to good primary health care. One chapter focuses on organization; each country should appoint a pandemic czar, it says, while the whole world creates a full-time pandemic-prevention organization called “the GERM (Global Epidemic Response and Mobilization) team.” The next chapter focuses on improving disease surveillance, another on practicing the world’s response through simulated outbreaks, and so on. The book is in fact Gates’s second about averting an existential global crisis in just as many years. His first world-saving manifesto, How to Avoid a Climate Disaster, came out in February 2021. Although saving all of humanity is indeed a grand mission, Gates’s choice to do so by way of a $19 hardcover is somewhat quaint, if not outright confusing. He is one of the world’s richest human beings. He takes private meetings with prime ministers and presidents, and pours money into projects that tackle—among other things—education, tobacco control, nutrition, maternal health, and a slate of diseases. (Disclosure: The Bill & Melinda Gates Foundation also has supported some Atlantic events and projects.) What good does a book do? Gates sipped from a can of Diet Coke while he listened to this question. Then he failed to answer me at great length, instead going on an extended jag about the good his foundation and wealth have done. With How to Prevent the Next Pandemic, he said finally, “I thought I had an opportunity to be somewhat educational and frame in a fairly straightforward way what things would make it very, very different next time.” He told me that he hoped his writing would help readers understand complicated issues in a nonpartisan way. (A book, it’s worth noting, is also one way to attempt to shift public focus from questions about your failed marriage, or alleged impropriety at work, or friendship with a sexual predator.) I asked Gates whether many parts of his pandemic-prevention scheme weren’t already embedded in preexisting plans. He didn’t deny it, but argued that new inventions and research would pave an easier path to success this time around. We have mRNA vaccines, he told me; we have Gavi, the Vaccine Alliance, which helps poor countries buy immunizations (and has received more than $4 billion from the Gates Foundation); and crucially, “we have a much better understanding of why people die.” Gates is, in this way, an optimist. To believe that you need only a plan rests on an assumption that humans are rational creatures who have roughly the same values and priorities as you do, and—even more improbable—that humans are inclined to follow plans of any kind. After all, when Gates laid out a strategy for solving climate change last year, he was boldly going where world leaders had gone many, many times before without success. The United Nations has held no fewer than 26 annual climate-change conferences. The world committed to the Kyoto Protocol in 1997, but failed to meet its goals. The Paris Agreement is seven years old, and the UN itself says we’re falling short. But Gates told me that the plan he offered in How to Avoid a Climate Disaster has already done some good for the planet. “I feel like the book played a strong role in getting the dialogue onto the only way to square the circle, which is through innovation,” he said. In the meantime, Gates is pursuing a billionaire’s more traditional channels of persuasion: access to other people in power. “I have an ongoing conversation with Joe Manchin about climate-related things,” he told me. “You know, the tax credits that may or may not make it into some reconciliation bill.” Like the world’s unmet climate goals, the graveyard of unfollowed pandemic plans is dispiriting. Gates’s new book cites a report published by the International Health Regulations Review Committee after the 2009 swine-flu outbreak, which “prophetically” concluded that the world was not ready for a pandemic—but its advice went unheeded. By March 2020, the Trump administration was lagging severely behind on many steps of a 2016 pandemic plan from the National Security Council and utterly flouting others. Before Joe Biden took office, he released yet another pandemic plan that included a promise to “ensure equity throughout the vaccination process” and make shots widely available for free; in reality, Black and Hispanic Americans didn’t receive vaccines as quickly as their white peers, and uninsured people might need to pay out of pocket for future doses. Gates assured me that this time, the plans would be followed. “I don’t think either party is for pandemic death” in the U.S., he said, and global health is much cheaper than other world-saving projects. Gates writes in his book that the GERM team could run on a cool $1 billion a year, while the improvements the team would recommend to individual governments would cost a total of $15 billion to $20 billion a year over a decade, for the whole world. Compare that with the Green New Deal, which would probably cost Americans between $10 trillion and $93 trillion. After so much death and suffering over the past two-plus years, Gates told me, “it would be so weird, so—you know—irrational, not to fund something.” The choice seemed so obvious, he said, that he’d been worried, while writing the book, that people would tell him, “Well, Bill, of course, we all know that. You didn’t need to write that down.” He figured that by the time the book came out, his plan, or something like it, would already be in motion. Now he’s less confident, especially since Russia began its war on Ukraine. If fuel and fertilizer become harder to find, and inflation continues, and national budgets become too bloated with defense spending, and powerful people become distracted, then “that creates the risk, along with the polarization we’ve got, that maybe we won’t fund pandemics, which is stunning,” he said. “I’m mostly optimistic, but governments doing the right things is, you know—it’s a challenge. And the level of discussion about preparing for the next pandemic is less than I would have expected.” But like any master planner, Gates has a contingency. The last chapter of How to Prevent the Next Pandemic, a book that is effectively a giant plan with lots of context, is called “Make—and fund—a plan for preventing pandemics.” A plan for making a plan: Now, who wouldn’t get on board with that? from https://ift.tt/gWqKAOE Check out http://natthash.tumblr.com In the two years since she caught the coronavirus, 38-year-old Jessica McGovern has cycled through “well over 100 drugs, supplements, and therapies” to try to keep her long-COVID symptoms at bay. In almost all cases, she told me, the interventions were to no avail: Exhaustion, weakness, and aches still lashed her to the couch; she still felt suffocating chest pain that worsened when she inhaled; her upper body was still haunted by a sharp, staticky sensation that reminded her of running hot water over frozen hands. McGovern would fall asleep in agony, then dream of more agony. Then, around the start of April, she began a five-day course of Paxlovid, Pfizer’s antiviral pill. By her second day on the drug, McGovern “could feel the messaging in my body shifting.” Four weeks later, her fatigue, aches, and labored breathing remain. But the screaming, nerves-on-fire pain that gripped her body for two dozen months “is basically gone,” she told me. She’s recovered some mobility. She’s spending more time with her three young kids. A flutist for nearly three decades, she’s playing her instrument again after a two-year hiatus, “which feels incredible,” like reclaiming a shade of her former self. To date, no established treatments exist for long COVID. But in recent weeks, a smattering of long-haulers—McGovern among them—have been surprised to feel their sicknesses subside after taking Pfizer’s new drug. The case for treating long COVID with antivirals is far from open-and-shut. But should these anecdotal reports augur a flood of similar data, Paxlovid might offer a surprisingly straightforward fix to one of the pandemic’s biggest puzzles. Long COVID is so ranging, so diverse, so capable of wreaking havoc on a multitude of tissues that treatment, for many, will undoubtedly require the rehabilitation of many bodily systems at once. Maybe, though, for a subset of long-haulers, a few days of antiviral pills could be all it takes to rev the healing process into gear. [Read: The pandemic after the pandemic] That Paxlovid may quench anyone’s long-COVID symptoms is itself a bit mysterious: The drug works best when delivered fast and early, futzing with the virus’s ability to xerox itself inside human cells and making it easier for the immune system to jettison the bug. But long COVID can take weeks or months to manifest, and hasn’t been proven to have a persistent viral source. Experts still don’t know how common, or lasting, post-pill reprieves might be; they can’t say with confidence why the drug could have palliative effects, or—if said effects are substantiated—which long-haulers stand to benefit most. Even in the rosiest scenario, Paxlovid won’t be a panacea. But if it has a chance of doing something, even for just a fraction of long-haulers, “we have to at least try,” says Jeanne Marrazzo, the director of the division of infectious diseases at the University of Alabama at Birmingham School of Medicine, “because we have nothing else.” Millions of people in the United States alone are estimated to have developed long COVID’s harrowing symptoms since the pandemic’s start; their numbers grow with each additional wave. “This is an intervention that should [have been] under clinical trial yesterday,” says David Putrino, a neuroscientist and rehabilitation specialist at Mount Sinai. And yet there are, to date, no well-designed studies investigating Paxlovid’s potential as a long-COVID drug, and none publicly poised to begin. The search for long-COVID therapies has been stymied, in part, by the nature of long COVID. The condition, like cancer, appears to be not a single disease but a category of related-but-distinct syndromes, each of which could manifest with its own set of symptoms, require its own treatments, and stem from a slightly different cause. In some proportion of long-haulers, maybe the majority, the virus is believed to have come and gone, leaving behind physiological devastation—battered tissues, raging inflammation, self-attacking antibodies, discombobulated nerves, a freckling of blood clots. In these cases, experts told me, Paxlovid probably won’t do diddly-squat. But perhaps the drug could help another group of long-haulers, who are thought to harbor hard-to-reach reservoirs of virus that regularly rile the body up. The snarl is that no one has yet provided slam-dunk evidence of these hidden viral caches. Many scientists, including Yale’s Akiko Iwasaki, one of the world’s top long-COVID researchers, argue that strong hints are there: SARS-CoV-2 certainly can stick around in certain people’s bodies for months, and can also mosey out of the airway to colonize other tissues, including ones that certain immune fighters can’t easily access. Researchers have seen traces of the virus’s genetic material and proteins in a mélange of organs, sometimes months after infections begin. But while those fragments could represent active virus, they could also be bits of stray microbial trash. To help clinch the case, researchers would have to recruit tons of long-haulers, guess where the virus might be lurking, and see if they could extract enough of the microbe from that tissue to infect new cells in the lab—studies that are invasive, “long and slow and painful” to get just right, and couldn’t even prove that the virus was causing the symptoms at hand, says Catherine Blish, an immunologist at Stanford. Still, Vineet Menachery, a coronavirus expert at the University of Texas Medical Branch, believes long-term infection is probably “more common than we think,” he told me. People’s lived experiences support that too. Some long-haulers have reported feeling a massive, unexpected upswing in well-being after receiving COVID vaccines—a trend several experts attribute to the shots galvanizing immune cells into finally, finally kicking out remnant virus. The handful of post-Paxlovid improvement stories now emerging echo what other long-haulers felt with the vaccines. A group of Stanford researchers, led by the physician Linda Geng, recently reported that a 47-year-old woman’s long-COVID symptoms—among them, fatigue, insomnia, body aches, cognitive issues, and a racing heartbeat—evaporated after she took Paxlovid for a possible reinfection. “She was able to go back to work, and started exercising again,” Geng told me. A couple of long-haulers being treated at a clinic at UCSF may be on a similar trajectory. Lavanya Visvabharathy, a 37-year-old immunologist at Northwestern University, experienced a bounceback as well. After months of headaches, fatigue, and disturbed sleep, she nabbed Paxlovid at the end of March, and “all my symptoms went away,” she told me. Visvabharathy, who takes immunosuppressive drugs to manage her rheumatoid arthritis, had been repeatedly testing antigen-positive. But after she finished Pfizer’s pills, she saw a negative for the first time since she was infected, in December. Anecdotes and case studies alone won’t be enough. So far, the reports of post-Paxlovid improvements have been too inconsistent, too scant “to gauge what’s really happening,” Angela Meriquez Vázquez, who runs Body Politic, an advocacy group that offers support to people with long COVID, told me. Many long-haulers do not qualify to take Paxlovid, because they haven’t recently tested positive and are not considered at “high risk” of developing severe COVID. Long COVID’s symptoms can also naturally wax and wane, making it difficult to tie relief to a definitive cause. To show with any real clarity whether Paxlovid’s doing what many long-haulers hope, someone needs to test the theory with rigorous clinical trials, ideally with the help of the company that’s manufacturing the drug. Pfizer doesn’t seem actively opposed. The company is “considering how we would potentially study it,” Kit Longley, a spokesperson for Pfizer, wrote in an email, but declined to clarify why the company has no study under way. That frustrates Putrino, of Mount Sinai, who thinks Pfizer will need to spearhead many of these efforts; it’s Pfizer’s drug, after all, and the company has the best data on it, and the means to move it forward. The NIH, whose RECOVER initiative has a budget of more than $1 billion to study long COVID, recently sought proposals for clinical trials of new long-COVID therapies, including, potentially, antivirals—a promising step, Stanford’s Geng told me. But the agency has been sharply criticized for dillydallying in the year-plus since the program launched, and for de-emphasizing treatment-focused trials. And there’s no guarantee that Paxlovid will be among the treatments tested. When asked to elaborate on Paxlovid’s experimental status, Lindsay Gorby, an agency spokesperson, said only that “NIH is very interested in long term viral activity as a potential cause of PASC (long COVID), and antivirals such as Paxlovid are in the class of treatments being considered for the clinical trials.” In all fairness, a Paxlovid–long-COVID trial would be tough. Researchers still haven’t reached a consensus on how to define or diagnose long COVID, or what it means for patients to markedly improve. Drugs against severe disease have an ultra-clear readout: “You count the number of people who end up in the hospital,” says Steven Deeks, a long-COVID researcher at UCSF. Long COVID’s sprawling scope, however, means no single ruler can measure the drug’s potential impact. Many of the experts I spoke with felt a bit daunted by the idea of trying to quantify the disease’s qualitative symptoms pre- and post-Paxlovid. That challenge, they said, could be a stumbling block for any research effort. But JD Davids, the co-founder of the Strategies for High Impact and its National Network for Long COVID Justice, who has long COVID, told me scientists don’t have to look far for inspiration. Researchers have already developed metrics for another chronic illness, ME/CFS (which Davids also has) to rate, for instance, the severity of fatigue, mobility limitations, and pain. “You just have to believe that people can tell you how they are feeling,” Davids said. [Read: Long-haulers are fighting for their future] Then there’s the question of whom to enroll, and how many of them. If only a small fraction of long-haulers are duking it out with persistent virus, “you might not see the benefit” in trials, unless they’re gargantuan in size, says Daniel Griffin, an infectious-disease physician at Columbia. Researchers could hedge their bets by selectively recruiting long-haulers who continually shed bits of virus genetic material in their feces, say, or who only recently developed long-COVID symptoms and might be more likely to have SARS-CoV-2 still inside them. But select the wrong subset, and a trial could tank. Iwasaki, of Yale, wants to explicitly study the drug’s effects in a wide range of people. “The goal is not to cure everyone but understand who benefits,” she told me—and when. In some people, long COVID could evolve from a viral problem into an autoimmune one, making early intervention essential. Paxlovid has baggage too. In recent weeks, some people taking the five-day pill course for new infections have reported a rebound in symptoms and test positivity—a likely indication, UTMB’s Menachery told me, that the pills aren’t sweeping all the SARS-CoV-2 out. It’s still unclear how common the relapses are, and the problem may be cropping up with long COVID too. Alisa Valdes, a 53-year-old writer who has battled more than 220 long-COVID symptoms, “felt normal for the first time in 25 months” after taking Paxlovid in April. “I was skipping, I was jumping,” she told me. “I thought, This is a miracle.” But within a day of the drugs running out, her body was once again aching, feverish, and inflamed; angry red rashes that had disappeared came roaring right back. Visvabharathy, the Northwestern immunologist, told me that a few weeks after taking Paxlovid, she felt some symptoms creeping back as well. A test she took at the end of April also came up positive. Perhaps Paxlovid’s five-day regimen for acute COVID will need to be lengthened in some newly infected patients; long-haulers may require something more extended still. Such a tweak could prompt a slew of safety questions. The original clinical trials turned up side effects--occasional bouts of diarrhea, a nasty sour tang in the mouth—that did not raise huge concerns, but after months of unabating illness, long-haulers’ bodies may not react in the same way to the drugs, especially when dosed on an extra-long course. Paxlovid also interferes with a hefty list of other medications, some of which can’t be paused for extended periods. [Read: Paxlovid mouth is real—and gross] Right now, long-haulers are gambling with all of those question marks as they seek the drug out—some of them through loopholes in the health-care system, with the help of providers sympathetic to their cause. With so few options on the table, people are “itching for any type of treatment,” Body Politic’s Vázquez told me, and some are willing to stomach a bit of risk. But in the absence of real data and rigorous research, and with so many unable to access the drug at all, others are hesitant and confused—and afraid of being once again let down. From the start of the pandemic, skepticism has dogged long COVID and the people who live with it. McGovern, the flutist, spent much of 2020 being repeatedly told that her symptoms were just anxiety, or that she was feeling off because she was allergic to her pet parrots. (She is not.) Attitudes have improved in the years since—but some doctors, once unsure of long COVID’s existence, now struggle to wrap their head around the prospect of out-of-the-box treatments. At one point, I asked McGovern which of the many therapies she’s tried actually helped. “Aside from my family and close friends, you’re the first person to ask me that,” she told me. “I’ve never had a physician ask me ‘What has worked for you?’” This skepticism can extend to research too. Benjamin tenOever, a virologist at NYU, told me that he recently had NIH funding pulled from a project that would have investigated whether antivirals could combat long-COVID symptoms in a hamster model. His contact at the agency said the study had “no merit,” tenOever told me. “They were like, This doesn’t make sense, because why would Paxlovid ever help long COVID? The virus is long gone.” (I reached out to the NIH about tenOever’s study, and they told me they were looking into it.) Others posited that the possible benefit of antivirals for long-haulers might not feel worth the effort required to prove it: Even if viral persistence plays a role, it may be quite uncommon. Yale’s Iwasaki dismisses this. “Say it’s only 10 percent of patients that respond positively,” she told me. That’s still potentially millions of people in the U.S. alone. America’s neglectful posture on long COVID is choreographed into just about every aspect of what’s left of the country’s pandemic response. Vaccines can’t totally block long COVID, but are being billed, via boosters, as one of the only interventions people need; the CDC’s newest guidelines on masks almost entirely elide the condition’s existence, as it’s not classically considered to be clinically “severe.” Researchers aren’t even sure if early-acting treatments such as antivirals slash people’s chances of getting long COVID, though Iwasaki is hopeful that they do. With so few protections against long COVID available or in use, its burden only stands to grow. Therapies, at least, could finally construct an exit ramp.
from https://ift.tt/KeHSY0q Check out http://natthash.tumblr.com In the foreword to her book A Distant Mirror: The Calamitous 14th Century, the historian Barbara W. Tuchman offered a warning to people with simplistic ideas about what life was like in the medieval world, and what that might say about humanity as a whole: You think you know, but you have no idea. The period, which spans roughly 500 to 1500, presents some problems for people trying to craft uncomplicated stories. “No age is tidy or made of whole cloth, and none is a more checkered fabric than the Middle Ages,” Tuchman wrote. Historians, she noted, have disagreed mightily on basic facts of the era: how many people there were in various parts of Europe, what they ate, how much money they had, and whether war deaths meant society was overpopulated with women, or childbirth deaths meant it was overpopulated with men. What’s even more complicated is determining the nature of life—how well different kinds of people lived, the quality of familial bonds, what people did to occupy their time and amuse themselves, how they thought about their lives. Draw broad, confident conclusions at your own peril. Tuchman’s warning was prescient, if not especially well heeded. Her book was published in 1978 and won the National Book Award for History, but in the nearly half century since, the Middle Ages have been a common hobbyhorse for people of all political persuasions who suspect modernity might be leading us down the primrose path, especially as the internet has become a more central and inescapable element of daily life. Our ancestors of the distant past can be invoked in conversations about nearly anything: They supposedly worked less, relaxed more, slept better, had better sex, and enjoyed better diets, among other things. Their purported habits are used as proof of recent folly, but also of future possibility. Things could be better; after all, they have been before. The problem is that these assertions about our glorious history usually don’t quite check out—they tend to be based on misunderstandings, disputed or outdated scholarship, or outright fabrications long ago passed off as historical record. But that doesn’t stop people from regularly revisiting the idea, counterintuitive though it may be, that some parts of life were meaningfully better for people who didn’t have antibiotics or refrigeration or little iPhone games to play to stave off boredom. What, exactly, is so irresistible about a return to the Middle Ages? To untangle exactly what is going on here, let’s use a recent example of the phenomenon. A few weeks ago, an oft-cited historical trope made the rounds once again, primarily on Twitter. The upshot: Medieval peasants worked less, had more free time, and were guaranteed more holidays with their family than you. The tweet, from the writer Azie Dungey, was hugely popular—it racked up 127,000 likes—and she followed it up with an explanation of her intent: “We give a lot more labor to increase someone else’s wealth than in times past. We generally work much longer hours. We have far fewer holidays and times of community festivity,” she wrote. “The idea that this is normal is completely wrong and frankly outrageous.” Dungey went on to cite her source: The Overworked American, a 1991 book by the sociologist Juliet Schor. Schor’s book, a best seller and classic of its genre, may very well be the origin story for how so many people otherwise uninvolved in medieval history came to know and share this particular factoid. In it, she cites a then-recent estimate by Gregory Clark, a medievalist and economic historian at UC Davis, who pegged the average number of workdays per year in medieval England at about 150. Modern Americans work more—about 250 days a year, if you work five days a week and get federal holidays off. This kind of historical citation makes for a very compelling device: The circumstances of modern labor can feel inflexible and alienating, and that’s because, for many workers, they are. If even medieval peasants—most of whom performed forced labor as feudal serfs—worked fewer hours and got more vacation days than you do, then maybe you shouldn’t settle for whatever your boss thinks you deserve. Schor, an enormously well-regarded scholar, used this idea in much the same way that progressives on social media now tend to—not to assert that medieval life overall was paradise for the lower classes, but to highlight a modern absurdity through juxtaposition with an era that people tend to think of as unambiguously miserable. The thing about history, though, is that much of our understanding of the past isn’t settled fact. Clark no longer believes that his estimate of 150 days, made early in his career, is accurate. “There’s a reasonable controversy going on in medieval economic history,” Clark told me. He now thinks that English peasants in the late Middle Ages may have worked closer to 300 days a year. He reached that conclusion by inspecting the chemical composition of fossilized human remains, as well as through evidence of the kinds of goods that urban peasants in particular had access to. These factors suggest that they may have lived more materially luxurious lives—eaten much more meat and other animal products, specifically—than usually estimated, suggesting that they had higher incomes than would be possible at the era’s common daily pay rates if they didn’t work most days of the year.. Across the world and throughout human history, poor populations rarely consume much meat and dairy. That’s not to say that the vision of history on which Schor’s, and in turn Dungey’s, point relies is conclusively false. Clark and his colleagues have revised their estimates upward, but the school of thought his previous numbers belonged to still has many academic supporters, who generally base their estimates of how much peasants worked on records of per-day pay rates and annual incomes. “This other view is that they were quite poor, but they were poor kind of voluntarily, because they didn’t like work and didn’t want to do a lot of work,” he told me. Perhaps these groups of long-dead people were poor and lazy and happier for it. Or the discrepancies may have another explanation. It’s possible, for example, that peasants were commonly paid part of their wages in something besides hard currency, which may explain where all that meat in their diets came from. Right now, no one really knows. You can dedicate your life to figuring out a problem, uncover troves of new information, and still not end up with any easy answers. None of this makes for an especially good tweet, but it’s a stumbling block that you hit again and again when trying to tease out pop-historical beliefs about medieval life. The era resists surety: During that time in Europe—and these references are almost always made to Europe—the majority of people, including virtually all peasants, were illiterate. Detailed records plotted the lives of royalty, nobility, and important religious figures, but there are relatively few primary sources that describe the day-to-day existences of regular working stiffs. If you can’t read or write, you can’t even keep a diary that someone might find 1,000 years later. This, Clark said, means that historians have to do far more subjective interpretation of medieval life than is required for post-Enlightenment eras of history. The necessity of interpretation is convenient for anyone trawling for a good historical anecdote to prove a point—you can shop around and probably find something that suits whatever opinion you’ve already formed. The medieval period’s enormous messiness aids in this grab-bag dynamic, according to Eleanor Janega, a medieval historian at the London School of Economics. Because there was no one dominating empire that overwhelmed everything around it, as had been the case during previous periods of Greek and Roman domination, European life varied mightily from region to region and across the age’s 1,000-year span. That level of heterogeneity makes the period hard to teach and hard to learn; it’s a void in most people’s understanding of humanity, waiting to be filled. “It allows people to make their own medieval mythology and cling to that,” Janega told me. “They’re just kind of navigating on vibes.” People also tend to bring plenty of modern biases to the table, even when they’re not seeking expedience. This is particularly important when trying to discuss medieval work, Janega said. The clear delineations that people assume between work and personal life just aren’t particularly tidy for peasants doing agrarian labor. “They’re thinking of these people as having, like, a 9-to-5 job, like you’re a contracted employee with a salary and you get vacation days,” she told me. “The thing about having a day off is like, well, the cows ain't gonna milk themselves.” So while people are correct that European peasants celebrated many more communal holidays than modern Americans, in many cases, that just meant they weren’t expected to do a particular set of tasks for their lord. Minding the animals, crops, and themselves never really stopped. Their vacations weren’t exactly a long weekend in Miami—after all, they didn’t really have weekends. There were, of course, some other obvious downsides to medieval life. A huge chunk of the population died before the age of 5, and for people who made it out of childhood, the odds of seeing your 60th birthday weren’t great. There wasn’t any running water or electricity, and there was a very real possibility that mercenaries might one day show up and kill you because your feudal lord was beefing with some other lord. Although the desire to rebalance work and life is generally categorized by modern Americans as a progressive goal, similar historical devices are frequently used to reactionary (and, at times, similarly viral) ends. If a grand yearning for a glorious and mostly imaginary past feels tad familiar, it might be because right-wingers tend to deploy cherry-picked factoids about the Middle Ages—and, to be fair, basically every other era of history—as an argument to Make Western Civilization Great Again. Some people think the distant past seems ideal not because they’re sick of their commute, but because they’re sick of pluralistic society and want to be more enthusiastically venerated as white Christians. This kind of historical hang-up doesn’t fit neatly onto any one part of the American political spectrum—or into any one part of history. Modern people might have seized on the Middle Ages in particular in the past few years, but Janega pointed out that the mindset of wanting to return to better days is in fact quite medieval itself. In Europe, people’s lives were ordered by the Church, and Christianity is a linear religion. “The way they thought about the world is that we’re in a constant process of getting further and further away from the Garden of Eden, when everything was ‘natural’ and fine and good,” she said. American life is less religious, but it’s no less obsessed with how things change over time, and especially between generations. And lots of modern people have perfectly rational reasons to question the nature of progress—whether the internet does more harm than good, whether corporations have accumulated too much power, whether climate change can be halted before it immiserates us all. “There’s this amazing impulse to think maybe we’re all on the wrong track,” Clark said. He and Janega are both sympathetic to those prone to rooting around in the historical record in search of better ways to imagine the future—you probably won’t find many historians who think that the past has nothing to offer in our pursuit to understand ourselves. The trope endures primarily because it’s useful. People have a hard time believing that something is possible if they can’t see proof of concept. Medieval history, with its 1,000-year span and huge variety, is full of concepts. If you’re looking for a vision of history where people were generally peaceful and contented, though, you might want to check in with societies outside of the Middle Ages. Perhaps look for a group of people not perpetually engaged in siege warfare. “Medieval peasants are a weird one to go to, because, you know, they were rebelling constantly,” Janega noted. “Why are they storming London and burning down the Savoy Palace, if this is a group of happy-go-lucky, simple folk who really love the way things are?” from https://ift.tt/yO51qXm Check out http://natthash.tumblr.com More than two years into this pandemic, we finally have an antiviral treatment that works pretty darn well. Paxlovid cuts a vulnerable adult’s chances of hospitalization or death from COVID by nearly 90 percent if taken in the first few days of an infection. For adults without risk-heightening factors, it reduces that likelihood by 70 percent. Also, it might make your mouth taste like absolute garbage the whole time you’re taking the pills. In Pfizer’s clinical trials, about 5.6 percent of patients reported an “altered sense of taste,” called dysgeusia in the medical literature. A Pfizer spokesperson assured me that “most events were mild” and “very few patients discontinued study as a result”; the outer packaging of the drug doesn’t mention it at all, and the patient fact sheet breezes past it. But Paxlovid-takers told me it’s absolutely dysgeusting. The bad taste may come on shortly after people take their first set of pills. (If prescribed Paxlovid, you’re supposed to take three pills, twice daily, for five days.) For a 36-year-old dog walker in Washington, D.C., named sangam 'alopeke (who styles their name without capital letters), the effect emerged within about an hour of the first dose. Lindsay Wright, a 40-year-old creative director in Winnipeg, Canada, said she noticed it after 90 minutes. Sheila Borkar, a 30-year-old transportation engineer who also lives in Washington, took a pill before bed and woke up to the taste. “I imagine this is what grapefruit juice mixed with soap would taste like,” Anna Valdez, a nursing professor in Sonoma Valley, California, told me. (We communicated over Twitter direct messages because Valdez had lost her voice from COVID.) “It is horrible and does not go away.” Borkar was reminded of acid reflux. “This didn’t taste like food,” she said. “It didn’t quite taste poisonous, but it definitely tasted like something that should not be consumed.” Her friend Jeffrey Holliday, a 33-year-old business analyst, told me, “It tasted like I chewed a bunch of vitamins.” “I heard that for some people, it’s a metallic taste, and I’m a little jealous,” Wright said. “I’m describing it as, like, bitter, burnt grapefruit, but mixed with—you know that taste when you try to swallow Tylenol and it doesn’t go down the first time? It’s a little bit of that failed-Tylenol-swallow mixed in.” While dysgeusia is listed as a side effect of many drugs, including antibiotics, chemotherapeutics, and antihistamines, the specific experience varies. In many cases, patients report a bitter or metallic taste, Steven Munger, the director of the University of Florida’s Center for Smell and Taste, told me. That might be because human mouths are more primed to detect bitterness, in all its subtleties, than other flavors. According to Munger, humans have one kind of taste receptor for sweetness, one for umami, one for salt, two for sourness, and a whopping 25 for bitterness. That makes evolutionary sense, he said: Many toxic substances are bitter, so it’s more important that we taste them. “If the sweet receptor misses something, okay, well, maybe there’s more food coming along. That’s not going to be a life-or-death situation. But ingesting something that’s toxic could kill you.” [Read: The paradox of sour food] Munger told me that Paxlovid Mouth might result from chemesthesis, a chemical-sensing process that we often conflate with taste. (We sense both the chill of menthol and the heat of chiles through chemesthesis, not taste.) Or it could just be plain old taste, or a combination of the two. If taste is the culprit, one bitter-taste receptor in particular might be to blame: TAS2R7. Danielle Reed, of the nonprofit Monell Chemical Senses Center, told me that the receptor has a “metallic, bitter vibe to it.” TAS2R7 isn’t activated very often in our daily lives, Reed said, because the compounds that bind to it are not in our foods, because—again—they taste awful. That might explain why those with Paxlovid Mouth have had trouble naming exactly what they’re going through, and why it feels so strange. “I’m a pretty adventurous eater normally. I’m usually the one that likes flavors other people don’t like. But this was over the line,” Borkar said. TAS2R7 can be activated by metal salts, including magnesium sulfate, a.k.a. Epsom salt. You’re not supposed to eat it, but Reed told me if I tasted it and spat it out, I’d probably be fine. All I had at home was lavender-scented Dr. Teal’s Pure Epsom Salt Soaking Solution, but I tried it anyway. When I put a few crystals on the tip of my tongue, I had the sensation of having licked a lamppost. When I tried some farther back on my tongue, the flavor was extremely sour, with hints of dime. I suddenly understood what Wright meant when she said, “I think I might be ruined for grapefruit for the rest of my life.” When I asked Pfizer about the funny taste, a spokesperson said, “Paxlovid is a combination of nirmatrelvir and ritonavir tablets … Both nirmatrelvir and ritonavir are bitter substances, which may contribute to the reports of taste-related side effects.” That clears things up! Of course, most tastes last for about as long as you’re eating something. The same was true for Epsom salt: It activated my TAS2R7 receptor, but then stopped activating it after I’d washed my mouth out with water. But Paxlovid Mouth works differently: “It is constant now,” Valdez told me. “I can taste food for the first bite or two, and then the bitterness takes over.” (Even pine nuts have been associated with a metallic taste that can last for weeks after eating them.) Two possible mechanisms could explain that lingering, Reed said. Some molecules simply stick to our taste buds better than others, even when you try to wash them off by rinsing your mouth or brushing your teeth. (Many people experience this with high-intensity sweeteners, such as the ones in diet sodas.) Other molecules have a way of tickling our taste receptors even after they’re absorbed into the bloodstream; some medications, for example, can be excreted back into the mouth via saliva. [Read: Families are going rogue with rapid tests] The sticking-around-in-the-bloodstream theory makes particular sense given what Pfizer told me about the combination of drugs in Paxlovid: “Nirmatrelvir is a novel molecule designed to inhibit viral replication at a stage known as proteolysis, which occurs before viral RNA replication. Co-administration with a low dose of ritonavir helps slow the metabolism, or breakdown, of nirmatrelvir in order for it to remain active in the body for longer periods of time at higher concentrations to help combat the virus.” So if nirmatrelvir is causing the dysgeusia, ritonavir could be working to extend the effect. The Paxlovid Mouthers have been coping with their lasting flavor in different ways. “I’m, like, constantly with a lozenge or Tic Tacs or mints or like something in my mouth to try and mask it a little bit. But nothing really takes it away,” Wright said. 'alopeke has mostly been eating applesauce, which “doesn’t have a ton of flavor already, but is at least not actively disgusting to mix with the Paxlovid taste.” Still, everyone I spoke with who had experienced Paxlovid Mouth said they’d take the drug again if they were reinfected and had another bout of COVID. “It’s a hell of a lot better than a ventilator,” Wright said. She’s immunocompromised, and has taken her fair share of medicines throughout her life. “It’s not my first encounter with a medication that leaves kind of a taste in your mouth,” she told me. “But I’ve never experienced anything this extreme. This is next-level.” from https://ift.tt/L0dqjZJ Check out http://natthash.tumblr.com On the topographical map of the coronavirus pandemic, it would not be unfair to call America’s recent winter wave an Everest among a series of rolling bunny slopes. At the zenith of the peak, the nation was clocking, scientists estimate, multiple millions of new infections each day; the portion of Americans ever infected by the virus may have doubled in the span of just a few weeks. It was the spike that sent every COVID graph’s y-axis a-reelin’, the trend that rejiggered the nation’s conception of steep. Now that infection rates are trending up again from their early-spring low, it’s hard to put them in perspective. Sure, we’ve once again blown past the mark of 60,000 new documented cases a day (and that’s just the ones we know about), but that’s less than 10 percent of what the CDC was recording in mid-January, when the original version of Omicron, now called BA.1, was at the top of its game. Sure, hospitalizations are headed in the wrong direction, but deaths, so far, are still going down. If BA.1’s horrific blitzkrieg was a wave, what do we call this? A wavelet? A swell? A bump, a ripple, a Hobbit-size hillock? Euphemisms for the recent rise—sharp, but not the sharpest—have been trickling in for weeks. But maybe it’s time to just call a surge a surge. To be fair, terms like surge and wave don’t “really mean anything, scientifically,” says Sam Scarpino, the vice president of pathogen surveillance at the Rockefeller Foundation. Still, two years into the pandemic, many people have gotten an intuitive feel for what those words can imply: a sudden and sustained upwelling in infections that activates our crisis radar. It’s terminology that goes beyond semantics. In detecting and describing surges, we can then react to them—take precautions, enact policy changes, in essence hunker down for a bit until the threat abates. Surges are the upswings we take seriously enough to name, to number, to do something about. [Read: America is staring down its first so what? wave] Calling waves and surges was more straightforward in 2020 and most of 2021. Americans’ conceptions of crisis were well-enough aligned to delineate the country’s first five peaks, which all fell within about an order of magnitude of one another—a range small enough to assess on the screen of a smartphone. Back then, logging 50,000 cases a day was bad; 200,000 felt hellish. Now, though, the scale bar is different, and our collective sense for what constitutes a concerning case jump is totally out of whack. “We’ve developed a new normal,” says Maia Majumder, an infectious-disease modeler at Harvard Medical School and Boston Children’s Hospital, that casts what we endured in January as “the very worst possible thing.” After BA.1’s squeeze, our COVID barometer is broken: Anything that’s better than this winter just feels straight-up good. Perspective isn’t the only problem. Our data, too, are on the fritz. “We are drastically underestimating the number of cases in the community right now,” says Bertha Hidalgo, an epidemiologist at the University of Alabama at Birmingham. Community testing sites have gone dark; many people without medical insurance can no longer access diagnostics for free. Plenty have lost interest in testing at all, and a good number of those still game to swab are performing their nose checks only at home and rarely, if ever, reporting the results. It feels, Hidalgo told me, like the virus has gone “incognito.” Even with the holes in our data stream, the situation doesn’t look great. Recorded cases are already toe-to-toe with where they were around the middle of last July, when Delta was bursting out of the South and into the North, East, and West; hospitalizations, recently at their lowest since the pandemic’s start, have clambered back up to where they were at the beginning of last summer, when only about half of Americans had gotten their first vaccine doses. In states across the Northeast, including Massachusetts and Rhode Island, where vaccination rates are among the nation’s highest, “we have more cases reported per day than during the peak of Delta,” Majumder told me. And in Puerto Rico, new documented infections are at about a third of their January peak. Researchers tracking the levels of coronavirus particles in wastewater—a metric that’s agnostic to how many people are testing and reporting their results—are painting an even gnarlier portrait, showing in several parts of the country “really, really high rates of viral RNA,” Scarpino told me, “way beyond” what diagnostics show. [Read: America is starting to see what COVID immunity really looks like] It’s hard to know how much higher the true infection counts actually are. But experts have for weeks been worried about a confluence of factors. New, antibody-dodging subvariants of Omicron have been sprouting left and right; the country is mask-loose and fancy-free; America’s booster campaign remains a big old bust. And even muddy data can’t fully obscure what people are seeing on the ground. “I feel as though we’re swimming in COVID here right now,” says Anne Sosin, a health-policy researcher at Dartmouth College. In Vermont, where she lives, new hospital admissions are dancing around their Omicron peak. And on the (highly vaccinated) university campus where Sosin works, just across the New Hampshire border, “we had a huge BA.1 outbreak. And now we’re having a huge BA.2 outbreak.” Adding to the murkiness are the messages beamed out from the nation’s leaders. The country’s goals, as determined by the CDC, are now centered less on stanching transmission than on dialing down disease severity; the virus can spread more or less as it pleases, as long as America’s medical infrastructure stays afloat. As things stand, more than 98 percent of American counties are still marked in soothing shades of green and yellow on the CDC’s map of community-level risk, because although cases are rising, hospitals have not yet filled up to precarious levels. How can the nation be in trouble when it still looks like a sun-dappled meadow? The CDC guidance doesn’t just affect perception; it influences behavior too. In green or yellow spots, masks are billed mostly as a matter of personal preference—no need to cover up, because the health-care system’s still supposedly fine. The shift away from a focus on case rates does make sense in some respects, Scarpino said. The average SARS-CoV-2 infection today does not portend what it did a year ago, or even what it did a few months ago, when fewer people were boosted or recently infected and effective antivirals were even harder to get. The one-two punch of immunity and treatment have lowered the likelihood that infections will turn severe or lethal. In terms of infection, Scarpino told me, “the risks are very high right now, pretty much across the whole U.S.” But “if what you care about is how cases translate into hospitalizations or deaths,” he said, “your tolerance for cases is going to be much higher.” Maybe hospitalizations and deaths won’t skyrocket this spring. That, however, is not a guarantee. Just 30 percent of people in the U.S. have nabbed a booster dose; kids younger than 5 remain ineligible for any shots at all. Millions of Americans have health conditions that blunt the protective powers of vaccines. And though most people in this country have been infected at some point in the past two years, the protection those encounters leave behind doesn’t seem to stick well on its own. The proportion of SARS-CoV-2 infections that turn serious is indeed reduced, but a big enough crest in case rates will drag along severe disease. Even if hospitalizations fall short of where they were during BA.1—again, low bar—they will still take a staggering toll. The smallest number of hospital admissions the U.S. has hit during a lull was about 1,500 people a day—a rate that, stretched out over a year, rivals some of the worst flu seasons of the past couple of decades. And America couldn’t even sustain that number for more than a few weeks. Nor has serious illness hit Americans uniformly: High-risk, high-exposure communities, including essential workers, residents of rural regions, and people of color, have borne the pandemic’s brunt since early on—disparities that remain largely unaddressed. COVID’s risk is, on average, lower. It just hasn’t been cleaved away from everyone to an equitable degree. [Read: Have we already ruined our next COVID summer?] Hospitalizations and deaths are also just a sliver of the chaos that COVID can cause. Even initially symptomless infections can unfurl into long COVID, which we “can’t say we care about preventing if we say we’re not concerned about cases,” Sosin told me. And any brush with the virus can pull someone out of work, school, or caregiving for more than a week. Many infections fall outside the tight sphere of “severe disease,” and thus largely outside the purview of the U.S.’s new posture on COVID, which purports to minimize impact on the medical workforce. But nonhospitalized cases, too, “have health-system impacts,” Sosin said. Treatments require diagnoses, prescriptions, and drug delivery, taxing the bandwidth of primary-care physicians, pharmacists, and more. If our crisis compass is off-kilter, maybe it’s time to recalibrate. “We shouldn’t compare to the highest peak we were at,” Theresa Chapple, a Chicago-area epidemiologist, told me last month. Rather, we should set our sights on reaching a sustainable baseline where the most vulnerable among us can feel safe. “Otherwise, people start to feel like they no longer have to contribute to the work of bringing rates down.” This winter, states across the country were pumping the brakes on mitigation well before infection counts had fallen to where they’d been in November, and still about 2,000 Americans were dying each day. The sense of phew took hold, then stubbornly stuck.
from https://ift.tt/pdUt1iP Check out http://natthash.tumblr.com I, as far as I can tell, have not yet been infected by the virus that causes COVID-19. Which, by official counts, makes me an oddball among Americans. Granted, I could be wrong. I’ve never had a known exposure or symptoms, but contact tracing in the United States is crummy and plenty of infections are silent. I’ve taken many coronavirus tests, but not that many coronavirus tests, and it’s always possible that some of their results missed the mark. If I am correct, though, then I’m in the rapidly dwindling fraction of Americans who are still coronavirus-naive. Roughly 60 percent of people in the U.S. have caught SARS-CoV-2, according to the latest CDC estimates, which go through February of this year. And that’s very possibly a serious underestimate. The Institute for Health Metrics and Evaluation, a global health-research center at the University of Washington, puts the tally higher, at 76 percent, as of the beginning of April. And Virginia Pitzer, an epidemiologist at Yale’s School of Public Health, who’s been modeling infections and vaccinations among Americans, told me the true number might even exceed 80 percent. No matter how you calculate it, though, the proportion of Americans who have been infected dwarfs the fraction who are up-to-date on their vaccines. [Read: Are we in the middle of an invisible COVID wave?] Just months ago, when most of the Omicron subvariants bopping around today were but a twinkle in the coronavirus’s eye, the people who’d been infected were still the unusual ones. Now that the pandemic script has flipped, it’d be easy to assume that all those infections have raised a bulwark against future surges—and that everything from here on out could be just fine. Perhaps a shred of that feels fair. Population-level protection against COVID probably is around an all-time high in the U.S., which may be why cases and hospitalizations aren’t rising as much as they could be right now: A smaller proportion of cases are turning very severe. Last week, Anthony Fauci, President Joe Biden’s chief medical adviser, told several news outlets that America had exited “the full-blown explosive pandemic phase,” and was transitioning toward a “more controlled” chapter of the crisis. But if that pivot sounds nice and neat and tidy, it shouldn’t. Cases are still rising, to levels likely undercounted, and are still meeting numbers that the nation hit during the early parts of last summer’s devastating Delta surge. Other countries are also battling gargantuan swells in cases, and new branches of Omicron’s lineage are circumventing the defenses left behind by the last. The pandemic is very much gunning. Not so long ago, the world was clinging to the hope of herd immunity—to the notion that the population would eventually reach some communal level of protection sufficient to quash the outbreak for good. Maybe, experts posited many months back, once 60 to 90 percent of people had been infected or vaccinated or both, the virus would run out of viable hosts, and simply fizzle out. Now it’s clear that “that’s too simplistic,” says Sarah Cobey, an infectious-disease modeler at the University of Chicago. Immunity against the most serious forms of COVID has decent staying power, especially if laid down by vaccines. But our defensive shields aren’t strong or durable enough to block transmission long-term; the virus keeps finding the holes in our blockades. That doesn’t make the protection we do have useless. The types of immunity more relevant to the current pandemic era blunt the frequency and severity of future waves, rather than obliterate them. If classic herd immunity was a silencer, then we’ve had to trade it in for herd immunity lite—a muffler, whose effects accumulate gradually, and can still strengthen with effort and time. There is no pandemic off switch. So we must instead work to maintain incremental gains: In this universe, 60 percent of people infected is mostly meaningful in that 60 is higher than 50, and 40, and anything below. It might translate into some level of heightened population resilience, but it is not a guarantee that the virus’s threat is gone. On our messy pandemic playing field—where immunity against infection can accumulate, then wane, and transmission can be tamped down, but not totally blocked—no clear line will demarcate a post-crisis phase, says Maia Majumder, an infectious-disease modeler at Harvard Medical School and Boston Children’s Hospital. Sixty percent infected—if that’s even accurate—actually isn’t the most relevant metric when it comes to forecasting how rough the road ahead might be. Vaccinations, too, can confer protection. And the fraction of Americans who have been infected or vaccinated is probably above 90 percent. But because immunity against infection and transmission ebbs over time, more than 90 percent exposed doesn’t translate to more than 90 percent “protected” against another viral encounter. There’s quite a “mosaic of immunity,” says Deepta Bhattacharya, an immunologist at the University of Arizona, with plenty of vulnerable cracks and crevices into which the coronavirus will still seep. Some people who have banked multiple and recent exposures—three shots and an Omicron infection, say—are quite far along the spectrum of immune protection. Others very much aren’t, because they still have no experience with the virus or vaccines at all, or have logged those encounters so far in their past that they’re likely quite easy to infect or reinfect. And for some people the safeguards of shots struggle to properly take, or fade faster because of age or underlying health conditions. To make matters more complex still, no one knows exactly where they fall along the spectrum of protection; many people can’t even say for sure whether they’ve had the virus or not, given how disastrous America’s testing infrastructure has been, and how tough it can be to detect virus-elicited antibodies in blood. “We’re in this position where we have a poor understanding of how different levels of immunity map to reductions in infectiousness,” Cobey told me. What’s far more clear, though, is this. Across communities at the local, state, and national level, protection is absolutely not uniform. Which means Americans are trudging along a pandemic path that often meanders—and sometimes doubles back. With protection against serious disease and death stalwart, especially for communities with high vaccination rates, future outbreaks should—broadly speaking—continue to ease in severity. But waves of infection, some big, some small, will keep coursing through the population. [Read: Will Omicron leave most of us immune?] In the absence of perfect immunity, there can be no hard line between people who have been infected in the past and people who will be infected in the future. It is instead a boundary that people will cross constantly, and not always knowingly, as immunity naturally ebbs and flows. Perhaps better vaccines will come along that help anti-infection shields stick around for longer. But even then, another variant—one that’s a massive departure from both Omicron and our current vaccines—could arrive, and reset our immune landscape “like an Etch-a-Sketch,” says Shweta Bansal, an infectious-disease modeler at Georgetown University. Even in the absence of a total makeover, the coronavirus has plenty of tricks to keep spreading. In South Africa, where cases have once again been ticking up, some unvaccinated people who caught BA.1 just months ago may now be vulnerable to a pair of Omicron-family offshoots, BA.4 and BA.5, that seem to hopscotch over infection-induced immunity, and have already been detected in the U.S. From the beginning of the pandemic, it seemed very possible that nearly all Americans would eventually be infected by this coronavirus. In recent months, that reality’s come to feel just about inevitable, and may come to pass sooner than many people hoped. With a virus like this, infection won’t be “a one-and-done situation,” Pitzer told me. The virus’s saturating spread may well continue for generations to come; reinfections and vaccinations throughout a person’s lifetime could become, for most of us, a new pathogenic norm. For perspective, Cobey points out that pretty much everyone ends up infected by a flu virus by the time they’re about 10. SARS-CoV-2 spreads even faster, and experts don’t know whether its pace will eventually slow. “I think if you haven’t gotten it yet, you’re extremely lucky,” Majumder told me. “It reflects privilege,” she said, more than almost anything else: the ability to work from home, access to masks, being up-to-date on vaccines. Majumder and I both check these boxes, likely insulating us against the worst of most exposures; she doesn’t think she’s been infected either. Perhaps there is some biology at play, too. Some people could be genetically less primed to be infected by certain pathogens, even after they’re exposed—a phenomenon well documented with HIV, for instance. Others might be a bit more resilient against contracting the coronavirus because they’re carrying a smidge more immune protection, laid down by the SARS-CoV-2-like pathogens they’ve encountered in their past. But “those are things that affect you on the extreme margins,” Bhattacharya told me, unlikely to account for most of the noncases in the mix. If the weightiness of mostly infected isn’t super scientifically significant, maybe it’s more a psychological shift. Nations decide what level of transmission, disease, and death they’re willing to live with; a virus’s presence becomes a sort of background noise. People start to see infections as common; individual infections, even outbreaks, stop making front-page news. It’s not an inappropriate transition to make when a country truly is ready for it. A lot has changed in the past two years, and scientists have cooked up tools to cushion the coronavirus’s blow. Pitzer, of Yale’s School of Public Health, benefited from several of them when she caught the virus a few weeks ago. She had a relatively easy go of it, safely isolating at home, thanks to her three doses of vaccine and a speedy course of Paxlovid, “dropped off on my doorstep” within a day of receiving a positive test result. But most of America isn’t there yet. Pitzer knows that her case was “by far the exception.” Across the country, people have struggled to find and acquire the antiviral, because they’re unable to test, can’t reach a prescriber or a pharmacy, or don’t even know they’re eligible; many who lack paid leave feel compelled to go to work sick. Until we have more equitable access to COVID accoutrement such as treatments, tests, and boosters, experts told me, pandemic-caliber suffering will persist in vulnerable communities. Our roster of tools also remains incomplete. “We still don’t understand very well what the long-term consequences of milder infections are,” or how to prevent or treat them, Cobey told me. And for some people who struggle to mount immune responses, getting infected may never be low-risk; many of these individuals have had to go to unsustainable extremes over the past two years to have a shot at staying safe. All of this leaves the country in a troubling spot, a time when the coronavirus is still very much on the move. Cases are once again ticking upward nationwide, pulling the sick out of work and school, and straining a health-care system that’s been stretched past breaking for years. [Read: The pandemic after the pandemic]
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