One year ago, around the end of March, Carly Taylor received a positive result for two tests in two consecutive weeks. The first was a test for the new coronavirus. The second was a pregnancy test. Her daughter, Ophelia, arrived on December 22, within days of the public debut of the first COVID-19 vaccines in the United States. In the weeks after, Taylor, a 20-year-old former daycare worker who lives in Alabama—a state she describes as “a cesspit of anti-vax rhetoric”—waffled on whether to get her shots. No pregnant or lactating people had been enrolled in the clinical trials run by Moderna or Pfizer-BioNTech; health agencies like the CDC and the World Health Organization were treading carefully, or even discouraging pregnant people from getting certain shots, in their official guidance. Taylor’s social-media feed had been flooded with speculation about the shots’ effects on fertility and infant health. Even her father and stepmother had doubts, citing QAnon conspiracy theories about the vaccine’s dubious contents. “At first,” she told me, “I thought, I don’t know.” Three months later, Taylor’s thinking had changed. On March 21, she received her first dose of the Pfizer vaccine, a decision she made for both herself and her daughter, who has been nursing since she was born. Taylor can’t yet get Ophelia a vaccine. But with breast milk as a conduit, she might be able to offer some of her own immunity instead. Like Taylor, pregnant and lactating people around the country who might once have hesitated to get a vaccine are lining up for their shots. In doing so, they’re helping provide much-needed data on whether vaccines can safely guard them from the virus, and hints that some of that protection might, through the placenta or breast milk, trickle down to their children. Baseless concerns about the vaccines’ risks to fetuses and infants are being replaced with talk of their benefits; the narrative is evolving from “No, I don’t think so, I’ll wait on this, to When is it my turn to receive this vaccine?” Ifeyinwa Asiodu, a nurse and breastfeeding researcher at the University of California, San Francisco, told me. After months in limbo, pregnant and lactating people are now seeking out inoculations not in spite of their children but because of them. [Read: A pandemic pregnancy is a more dangerous pregnancy] The protection that birthing parents pass on to their children through the placenta and breast milk is temporary, “passive” immunity. As caregivers await the arrival of pediatric vaccines, and as collective immunity to the coronavirus mounts, these short-term transfers can function as a sort of immunological bridge. Pandemic babies, born or conceived amid this global crisis, might not need to navigate their earliest days entirely unguarded—one of the few windfalls new parents have gotten this year. There’s good reason to wonder if vaccines will work differently in pregnant and lactating people. To ensure that an embryo—a wad of unfamiliar tissue—will be tolerated, parts of a pregnant person’s immune system must remain muzzled for months, then rebound after the baby is born. Pregnancy also alters how the body metabolizes drugs, some of which can move across the placenta or into breastmilk. Many of the bodily changes that bookend birth remain poorly understood. Despite these questions—and because of them—pregnant and lactating people have largely been left out of trials for COVID-19 treatments and immunizations, allowing misinformation to fill the data void. Conspiracy theorists argued that the shots were part of a plot to render people infertile, trigger miscarriages, or deliver dangerous lab-made toxins to newborns. None of these ideas was based in fact. But by the time the first vaccines were authorized, serious damage had been done. Kelly Nolan, a 35-year-old business owner in San Diego, flip-flopped over the decision to vaccinate while she and her husband were trying to conceive their second child in the fall. “I didn’t have a lot of faith in the last administration when it came to science,” she told me. When a pregnancy test came back positive for Nolan in December, “I thought I wasn’t going to be the first in line to get this vaccine,” she said. But Nolan was soon heartened to see pregnant friends and colleagues signing up for their shots. Among them was Toluwalaṣé Ajayi, a pediatrician and palliative-care physician, who received her first shot of the Pfizer vaccine when she was midway through her third trimester. Ajayi, too, had her worries. “It was pretty nerve-wracking,” she told me. “We didn’t know much about how the vaccine would affect pregnant women.” What Ajayi was certain of, however, was the threat the virus posed to pregnant people, who are more likely to become severely ill after infection—a threat that was likely multiplied by her frequent exposures to the virus as a health-care worker. Fully vaccinated, Ajayi delivered her new daughter, Ayokárí, on March 4; two weeks later, Nolan got her first shot. [Read: Why the coronavirus hits kids and adults so differently] Nolan told me that building evidence of the shots’ safety and effectiveness for pregnant people, shared in a bevy of online support groups, also helped clinch her choice to immunize. Most states are now prioritizing pregnant people for the vaccination queue. As of March 29, more than 69,000 pregnant Americans have reported receiving their shots, according to a CDC registry, and so far, “the data seems to suggest there has not been a safety signal” in this population, Kathryn Gray, an expert in maternal-fetal medicine at Brigham and Women’s Hospital in Boston, told me. In a study published last week, Gray and her colleagues found that the Pfizer and Moderna vaccines did not seem to trigger more side effects in pregnant or lactating people, and still roused an impressively robust immune response, comparable to what’s been seen in other populations. “The risk calculus … is indisputable at this point,” Andrea Edlow, a maternal-fetal-medicine specialist at Massachusetts General Hospital in Boston and a co-author on the study, told me. These results haven’t yet been backed by clear-cut proof from clinical trials, which are now in the works for this population. And certain vaccine side effects, including intense fevers, which can be dangerous during pregnancy, are still important to keep tabs on. But watching the number of safely immunized individuals grow is “incredibly reassuring,” Geeta Swamy, an expert in maternal immunization at Duke University, told me. There’s also nothing to support the notion that certain vaccine ingredients (which have not yet been specifically vetted in clinical trials for infants) might be inadvertently shuttled to a fetus or a nursing newborn. mRNA, the active agent in the Pfizer and Moderna vaccines, is extraordinarily fragile, and would have a hard time traversing the placenta or entering breast milk intact. (Even if a shred or two of the molecule did meander into milk, it would stand no chance of surviving the infant gut.) One very small study, not yet peer reviewed, found no traces of mRNA in samples of breast milk from six lactating individuals who had gotten the Pfizer or Moderna vaccine. “Some people have been told to ‘pump and dump’” in the hours or days after getting their shots, Stephanie Gaw, a UCSF researcher who led the study, told me. “But there is no evidence whatsoever for discarding breast milk after a vaccine.” [Read: Here comes the COVID-19 baby bust] Researchers do, however, expect something else to pass to fetuses and infants after vaccination: antibodies, Y-shaped immune molecules that can block viruses from entering human cells. Gray and Edlow’s team found that antibodies generated in response to the vaccine are detectable in umbilical-cord blood and breastmilk—a strong sign that they’re being transported to fetuses and infants, potentially raising a temporary neonatal shield against the coronavirus. Immunity is one of the first heirlooms that kids inherit from their parents. Antibodies naturally cross the placenta into the fetus, then persist throughout the first six or so months of the baby’s life, as the infant’s own immune system begins to churn out homemade batches of microbe-vanquishing molecules. Some vaccines, like those that work against whooping cough, leverage antibodies’ wayfaring tendencies and are recommended for all pregnant people specifically to keep newborns safe. But researchers still don’t know the amount or type of antibody necessary to reliably insulate adults from the coronavirus, let alone infants, says Galit Alter, an immunologist at the Ragon Institute in Boston and a co-author on Gray’s recent study. For this reason, Gaw, of UCSF, prefers to compare the COVID-19 vaccines to flu vaccines, which are recommended primarily for the protection of pregnant people themselves. Any benefits passed on to the fetus are “kind of a bonus,” she told me. Some of the same fogginess shrouds breast milk. Human milk has long been known to teem with immunity-promoting ingredients that can shore up a baby’s defenses against many pathogens, but whether the new coronavirus is definitely among them remains to be seen. Also unclear is how long antibodies capable of thwarting the coronavirus persist even in the adult body, or whether they reliably travel to fetuses or infants after the pathogen vacates the premises. [Read: Immunology is where intuition goes to die] On top of that, vaccines might not induce the same types of antibodies that a natural infection would, or push the same subsets of them into breast milk. The biggest player in milk is typically an antibody class called Immunoglobulin A, or IgA, which is tailor-made to guard mucus-lined parts of the body, including the airway, where the coronavirus likes to set up shop. At least some COVID-19 shots seem to prompt the production of breast milk that’s richer in another antibody called IgG, the same type that’s shuttled across the placenta and into fetal blood, but is typically somewhat scarcer in milk, says Rebecca Powell, a human-milk immunologist at Mount Sinai in New York. That’s not necessarily a bad thing, Powell told me. But this skew could indicate that vaccines delivered directly to the airway, such as nasal sprays, might eventually be a better option for sharing immunity through breast milk. Still, talk of any protection for babies is a dramatic shift from the early days of the vaccine rollout, when official recommendations seemed to signal “that I had to make a choice between getting vaccinated or nursing,” says Liz Johnson, a 34-year-old microbiologist and infant-nutrition researcher at Cornell University, who is breastfeeding her son, Lucas. Knowing that those two goals aren’t at odds “definitely helps get over that hesitation,” she told me. Some parents are now even considering delaying weaning in their infants to prolong the potential protection. (Unlike placentally transferred antibodies, which persist for months in a baby’s body, most milk antibodies last just hours or days after they move from parent to child.) Kelsey Linn, a 33-year-old pharmacist in Pittsburgh, decided to keep breastfeeding her 13-month-old, Michael, past her planned weaning date after she received her second dose of Moderna’s vaccine on February 14—her son’s birthday. Michael is attending daycare three days a week, and since August, his classroom has been shut down twice due to suspected coronavirus exposures. Ajayi, the pediatrician in San Diego, plans to breastfeed newborn Ayokárí for about a year, and is stirring some of her milk into oatmeal and cereal for her older daughter, Tiwalọlà, who is three and a half, just in case it gives her body a boost. [Read: A bold and controversial idea for making breast milk] In Virginia, Jeanel Little, a vaccinated nurse practitioner at UVA Health, sought out donor milk for her now-ten-month-old daughter, Ruby, after discovering that she had low supply last summer. Little and her husband figured that, odds are, some of their donors have been vaccinated or were infected, and might be providing some coronavirus-fighting antibodies in their milk. As the pandemic wears on, and Ruby remains unvaccinated, “the breast milk has helped to subside some of [our] fears,” Little told me. It’s hard to quantify the increasing optimism about vaccinating pregnant and lactating people, or how influential such changes in perspective might be. More of these individuals are certainly signing up for shots—but shots are also more available now. Still, “I definitely think shifting attitudes could be a factor,” Kristen Nordlund, a CDC spokesperson, told me. Recent data hints that this encouraging trend will continue. Asiodu, at UCSF, began surveying lactating and breastfeeding people about the new vaccines in February. Of the 110 or so people now enrolled in her study, she told me, most haven’t yet had the chance to get a shot. But a majority of them want to. Edlow, who works with patients in Massachusetts, echoes the sentiment: “To me, it seems people are feeling only more positive.” The intense polarization regarding vaccines, and the public scrutiny over eligibility, has also intensified certain debates over pre- and postpartum health, fetal health, and breastfeeding—topics that were charged long before the pandemic began. Early on, “there was real shaming of pregnant and breastfeeding women on social media” who signed up for their shots, Swamy, of Duke University, told me. [Read: Becoming a parent during the pandemic was the hardest thing I’ve ever done] Now there’s danger of stigmatizing vaccinated parents who are unable to, or choose not to, nurse their infants. “These parents aren’t ‘failing’ their children,” Stephanie Langel, an immunologist at Duke, told me. Distancing, hygiene, masking, and vaccinating the adults who interact with the baby will still confer indirect protection, like a cocoon, Edlow, of Massachusetts General Hospital, said. And soon enough, vaccines for infants as young as six months of age will likely be available as well, after going through their own clinical trials. Taylor, the former daycare worker in Alabama, spent a good part of her first trimester battling COVID-19 symptoms that sapped strength from her lungs, brain, and heart. A year later, she’s close to full vaccination, and eager to spare both herself and her daughter from a similar rash of sickness. In addition to breastfeeding, Taylor plans to seek out a pediatric vaccine once the option is available. She hopes the immunity she shares with Ophelia now will tide the baby over, she told me, until she gets a shot—one that’s been vetted for kids her age, and gives her protection that’s long-lasting and entirely her own. The Atlantic’s COVID-19 coverage is supported by a grant from the Chan Zuckerberg Initiative. from https://ift.tt/3wfUf5G Check out http://natthash.tumblr.com
0 Comments
Across the United States, cases have started rising again. In a few cities, even hospitalizations are ticking up. The twists and turns of a pandemic can be hard to predict, but this most recent increase was almost inevitable: A more transmissible and more deadly variant called B.1.1.7 has established itself at the precise moment when many regions are opening up rapidly by lifting mask mandates, indoor-gathering restrictions, and occupancy limits on gyms and restaurants. We appear to be entering our fourth surge. The good news is that this one is different. We now have an unparalleled supply of astonishingly efficacious vaccines being administered at an incredible clip. If we act quickly, this surge could be merely a blip for the United States. But if we move too slowly, more people will become infected by this terrible new variant, which is acutely dangerous to those who are not yet vaccinated. The United States has an advantage that countries such as Canada, France, Germany, and Italy, who are also experiencing surges from this variant, don’t. The Moderna, Pfizer, and Johnson & Johnson vaccines work very well against this variant, and the U.S. has been using them to vaccinate more than 3 million people a day. That’s more than 4 percent of our vaccine-eligible population every three days. An astonishing 73 percent of people over 65, and 36 percent of all eligible adults in the country, have already received at least one dose. More than 50 million people are now considered fully vaccinated, having received either their booster dose or the “one and done” Johnson & Johnson shot. Many states have already opened up vaccination to anyone over 16, and everyone eligible is expected to have a chance to get at least a first dose no later than May. In addition, the United States has had one of the largest outbreaks in the world. This has caused us immense suffering and loss, but it also means that we are now less vulnerable to future waves. So far, 30 million people in the United States have had a confirmed SARS-CoV-2 infection, although the real (unmeasured) number is perhaps as high as 100 million. As expected, those people retain some level of immunity for a substantial amount of time. It’s hard to know exactly how long, because the virus is so new, but for SARS (the related coronavirus that almost sparked a pandemic in 2003), people who were infected retained an antibody response, and thus protection, for an average of two years. Though amazingly, the vaccines appear to provide better immunity than natural infection, those previously infected also gain defenses. Carefully done studies on large populations show a very low rate of reinfection for this coronavirus: less than 1 percent. Plus, many documented reinfections tend to be mild or asymptomatic, an unsurprising outcome given that in these cases the virus is no longer totally novel for the immune system, and thus not as catastrophic in its consequences. [Read: We can now see a virus mutate like never before] It’s pretty clear that large numbers of people in the U.S. already are, or will soon be, protected from COVID-19’s more severe outcomes, such as death and hospitalization, which the vaccines reduce so close to zero that clinical trials have reported hardly any such cases. And it gets better: Yesterday, the CDC released real-life data showing that, just two weeks after even a single dose, the two mRNA vaccines were 80 percent effective in preventing infection. The effectiveness rose to 90 percent after the second, booster dose. People in the study were routinely tested regardless of whether they had symptoms, so we know that vaccines prevented not just symptomatic illness—the vaccine-efficacy rate reported in the trials—but any infection. People who are not infected by a virus cannot transmit it at all, and even people who have a breakthrough case despite vaccination have been shown to have lower viral loads compared with unvaccinated people, and so are likely much less contagious. All of this doesn’t mean that there will be zero deaths or illnesses among the vaccinated. The elderly, who tend to have weaker immune systems, are especially prone to having vaccines fail. In nursing homes, even the common cold can cause deadly outbreaks. But for the vaccinated, the risk from COVID-19 clearly has become comparable to “baseline risk”—it’s not zero, but just like the risks presented by the flu and other viruses, it’s not something for which most of us would put our lives on hold. How do we square all this good news with what happened during a White House briefing yesterday, when CDC Director Rochelle Walensky interrupted the flow, saying, “I’m going to lose the script,” and talked of “the recurring feeling I have of impending doom.” She was visibly emotional and her voice cracked as she said was “scared,” and pleaded with Americans to “hold on a little longer.” I can’t read her mind, but if I were Walensky, I’d be scared because those who are not protected through vaccination or past infection are still at grave risk, a fact that may be overshadowed by all the good news. Even as our vaccines continue to work very well against it, the particular variant we’re facing in this surge is both more transmissible and more deadly for the unvaccinated. Throughout this pandemic, Americans have become used to asking one another to pull together and enact mitigations for everyone’s benefit. One of the slogans for mask wearing was “My mask protects you, and your mask protects me.” Although we were always polarized, and the effects were always unequal—our mitigations helped those who could work from home more than the essential workers who made that possible—at least theoretically, we were all in it together, even if some of us did not act like it. [Read: America is now in the hands of the vaccine-hesitant] You see this appeal to the collective good in the many discussions around achieving herd immunity, too: a goal that will protect us all. That’s still true to some degree, for the future, but it was always an oversimplification. Now, with uneven but increasing rates of vaccination, understanding how those divisions work is even more important, starting with herd immunity. Herd immunity is sometimes treated as a binary threshold: We’re all safe once we cross it, and all unsafe before that. In reality, herd immunity isn’t a switch that provides individual protection, just a dynamic that makes it hard for epidemics to sustain themselves in a population over the long term. Even if 75 percent of the country has some level of immunity because of vaccination or past infection, the remaining 25 percent remains just as susceptible, individually, to getting infected. And while herd levels of immunity will eventually significantly drive down the number of infections, this may not happen without the epidemic greatly “overshooting”—infecting people beyond the levels required for achieving herd immunity, somewhat like a fire burning at full force even though it is just about to run out of fuel. Worse, people’s infection risks are not distributed evenly: Some people have lots of contacts, while others have a few. People are also embedded in different social networks: Some may have a lot of friends and family members who are immune, others not so much. Some work in jobs that increase their risk, others not so much. So it’s perfectly possible for a country as a whole to have herd immunity against a pathogen, but for outbreaks to happen among communities that have a lot of unvaccinated people among them. That’s happened in California, Michigan, and New York for measles among vaccine-resistant communities. In addition, this coronavirus is highly overdispersed. Infections occur in clumps. A single event can result in dozens or even hundreds of people being infected all at once in a super-spreader event. [Read: What if we never reach herd immunity?] Compared with previous surges, case-for-unvaccinated-case, this surge has the potential to cause more illness and more deaths, infecting fewer but doing more damage among them. We can also expect to see more younger, unvaccinated people falling sick and dying. We’ve observed this in other places, including the U.K. and Israel, which started vaccinating the elderly after B.1.1.7 had already taken hold and then had many younger victims. This variant is also very hard to dislodge; the U.K., for example, was able avoid more catastrophic outcomes by delaying booster doses to cover more people initially, but still battled lengthy surges, as did Israel. Even with the U.K.’s ongoing vaccination campaign, which started in early December, almost 50,000 people in the country died from COVID-19 in just January and February this year, equal to nearly two-thirds of the total for all of 2020. Other complications have arisen, too. In some places, we could be seeing what pandemic denialists have been calling “casedemics”—a term that (falsely) implies that the large number of cases amounted to no big deal. In the past, those deniers were wrong because case numbers and infection rates were leading indicators of later hospitalization and death rates. This time, in many places, case upticks may not result in measurable hospital outcomes, because so many elderly people are vaccinated. However, this surge can’t be dismissed as a “casedemic” either, because this virus causes lingering long-term effects—known as “long COVID”—for some portion of the younger population, too. This effect has been observed for other viral diseases, such as influenza and nonbacterial pneumonia, and is clearly an important consideration, especially when so many people are encountering a novel virus for the first time as adults. While we don’t have extensive genomic surveillance, we do have some, and every indication is that the upticks in cases are happening in places with a high percentage of B.1.1.7 variant among reported coronavirus infections: Michigan, New Jersey, Philadelphia, Florida, Southern California, and few others. Tragically, some of those places also have great vaccine inequities. In Michigan, for example, as of mid-March, a mere 28 percent of Black people over 65 had received one dose of vaccine—a number as low as 15 percent in Detroit—even though more than 60 percent of all senior citizens in the state have been at least partially vaccinated. Similar inequities have been reported all over the country, with great disparities in vaccination rates especially among the elderly, who are more vulnerable to severe disease. Frontline and essential workers, who tend to be poorer and are more likely to be Hispanic or Black than the average American worker, also have varying levels of vaccine coverage from state to state. The solution is obvious and doable: We should immediately match variant surges with vaccination surges that target the most vulnerable by going where they are, in the cities and states experiencing active outbreaks—an effort modeled on a public-health tool called “ring vaccination.” Ring vaccination involves vaccinating contacts and potential contacts of cases, essentially smothering the outbreak by surrounding it with immunity. We should do this, but on a surge scale, essentially ring-vaccinating whole cities and even states. A vaccination surge means setting up vaccination tents in vulnerable, undervaccinated neighborhoods—street by street if necessary—and having mobile vaccination crews knock on doors wherever possible. It means directing supply to places where variants are surging, even if that means fewer vaccine doses for now in places with outbreaks under control. It doesn’t make sense to vaccinate 25-year-olds in places with very low levels of circulation before seniors and frontline workers in places where there is an outbreak. Another sensible step would be to delay opening up—especially places with surges and especially for high-risk activities that take place indoors—until the next 100 million Americans are vaccinated, which could be done as quickly as in a single month. It makes no sense to rush to open everything now, when waiting a few weeks could protect so many. In the meantime, we need to protect frontline and essential workers by providing high-filtration masks and paid sick leave while targeting their workplaces with vaccination campaigns. We have already asked so much of them, and they have already suffered so much. I understand the impatience with restrictions—I’m fed up and tired, too—but our restlessness risks creating one last set of victims who could easily be spared. We should not condemn anyone to be the last person to die unnecessarily in a war that we will win, and shortly. The vaccinated can clearly do more, and safely, especially two weeks after their final dose. But it’s a particularly perilous time for the unvaccinated, who deserve our attention, resources, and continued mitigation measures as appropriate. [Read: The coronavirus is evolving before our eyes] More dangerous variants are going to be a huge problem around the world, too. Brazil is facing its own variant and surge, and is registering a record number of deaths day after day, as its hospital system faces a collapse from overload. Multiple countries in Europe are going into another round of shutdowns as they face B.1.1.7-driven surges without sufficient vaccine coverage or supply. Places like India that were relatively spared before are seeing a significant rise in cases and deaths, and once again, B.1.1.7 and other local variants appear to play a role. Many countries have yet to vaccinate a single person, and will now face potential surges driven by more difficult variants. In the HIV pandemic, we went through the same tragic moral failure: Poor countries didn’t get substantive supplies of effective—but expensive—antiviral therapies until almost 10 years after they became available in rich countries. Meanwhile, millions died. Exponential growth—the hallmark of epidemics, but which the B.1.1.7 variant accelerates—is dangerous but also sensitive to small initial changes, giving an advantage to those who act quickly. A slight increase in transmissibility can make the difference between an epidemic petering out or being easy to control with a reasonable amount of mitigation measures, and that same epidemic ravaging a whole country. Starting vaccinations a few weeks earlier can make the difference between being able to largely outrun the virus and being swamped by its exponential growth instead We know what we should do—match variant surges with vaccines and keep up our mitigations for just a little longer. We have the vaccine supply and the infrastructure to do it. We just need to act—now. The Atlantic's COVID-19 coverage is supported by a grant from the Chan Zuckerberg Initiative. from https://ift.tt/3wfUayG Check out http://natthash.tumblr.com The AstraZeneca COVID-19 vaccine is indispensable right now. As one of the first vaccines out of the gate, it’s been at the center of the World Health Organization’s plan to roll out some 2 billion doses to 92 nations by the end of the year. It’s also one of just a handful of vaccines that are already being produced and distributed on such a massive scale that they might change the near-term course of the pandemic. That’s why the past few weeks have felt so catastrophic. The run of bad news might have seemed, at first, to be short-lived. Earlier this month, regulators in more than 20 European countries suspended distribution of the AstraZeneca vaccine. The English-language media cited scattered reports of “blood clots” in recipients as the reason. A few days later, though, the European Medicines Agency’s expert committee weighed in to recommend the vaccine’s continued use. With COVID-19 case rates surging across Europe and more than 3,000 deaths a day, the group concluded that its benefits far outweighed any known or potential risks. Just that short pause sparked despair and condemnation. Commentators and public-health experts called it “stupid, harmful, “quite dangerous,” and a “magnificent example of European failure.” The problem, they said, was that the actual evidence of harm had been very weak—and maybe even nonexistent. Writing in The New York Times on March 22, Heidi Larson, the director of the Vaccine Confidence Project at the London School of Hygiene & Tropical Medicine, noted that just 25 Europeans had developed blood clots, out of 20 million who received the AstraZeneca vaccine. That rate, she said, was lower than what you’d normally see among unvaccinated people. According to the statistician David Spiegelhalter, the furor over blood clots showed our “basic and often creative urge to find patterns even where none exist.” None of these critics said that potential risks should be ignored. They argued instead that, given the available data, the known harms from COVID-19 were clearly many orders of magnitude more significant. The cost of losing time from a temporary pause in vaccination was therefore disproportionate and unbearable; worse, it was likely to exacerbate concerns among vaccine-wary Europeans. Indeed, close to 60 percent of French adults now say they have little or no confidence in the AstraZeneca vaccine; similar poll numbers are turning up in Germany, Italy, and Spain. As Larson suggested in her op-ed last week, the AstraZeneca vaccine may now be back in distribution in many places, but the drama has “heightened anxieties and increased hesitancy.” That effect could spread well beyond Europe, and beyond this particular vaccine. But the challenges here are far deeper than this blizzard of commentary allows. The risk of a dangerous vaccine reaction could be very real, if also very rare—and major European vaccine authorities have not, in fact, been overcautious, political, or innumerate in responding to this possibility. Rather, they’ve been faced with something of a nightmare scenario for vaccine communication. We’re in the midst of a global public-health crisis, and regulators must address the possibility (still unproved) that perhaps one in every 1 million vaccinated people could have a potentially fatal drug reaction—as more than 1 million vaccine doses are being injected each day in Europe alone. It seems as though anything the regulators say about this problem could serve to reduce trust in vaccination, and thus increase the toll of the pandemic. And yet if there does turn out to be a vaccine reaction, even a vanishingly infrequent one, keeping mum won’t make the problem go away. Indeed, it could serve to worsen the effects of the fearmongering about vaccines that will surely grow from here. The reason for the pause was never quite as simple as the critics made it sound. The AstraZeneca vaccine was first authorized for use in Europe at the end of January, then rolled out slowly in February. On March 7, Austrian authorities announced an investigation of a death that was potentially vaccine-related. A few days later, the Danish Health Authority announced that it was investigating a death as well, and then the same thing happened in Norway. On March 15, Germany suspended use of the AstraZeneca vaccine pending the investigation of three deaths and four other incidents. According to the German vaccine authority, the sixth and seventh reports there “put the number of observed cases well above the expected number.” All seven cases involved previously healthy people between ages 20 and 50. At that point, the German regulators advised the government that merely looking into this was not enough. If this weren’t a coincidence—and again, that remains an “if”—then in the course of an investigation, more young people who are not generally at risk of dying from COVID-19 could end up being put at risk by the vaccine. If the regulators were able to identify any clear risk factors for this outcome, the medical community and the general public would need to know as soon as possible. Two days later, on March 17, Gretchen Vogel and Kai Kupferschmidt of Science magazine reported that, across Europe, there had been to that point at least seven deaths from a similar condition, and six other people treated, among the 17 million people who had received the AstraZeneca vaccine. All were healthy before they developed a highly unusual, seemingly contradictory mix of blood disorders: clots throughout the body along with low numbers of platelets, the blood cells that help clots form. In a follow-up article published on Saturday, Vogel and Kupferschmidt cited a German researcher who has named the syndrome “vaccine-induced prothrombotic immune thrombocytopenia,” or VIPIT. A hematologist from Johns Hopkins University told them he wasn’t yet convinced by the “vaccine-induced” part, but he acknowledged that “these cases raise concern that this vaccine is potentially life-threatening in a small subset of patients.” By the time of Vogel and Kupferschmidt’s first article, though, the prothrombotic immune thrombocytopenia problem had already been recast in the English-language media as simply one of “blood clots.” Seen in that context, the decisions to suspend the AstraZeneca rollout were puzzling—and perhaps, as some maintained, driven more by emotions than by data. The European Medicines Agency had helped create this impression, starting with a press release on March 10. In its statement, the agency compared the number of vaccinated people who had blood clots with the baseline rate across the population. Commentators quickly zeroed in on that comparison, or a similar one from an AstraZeneca press release, which stated that the number of events “is much lower than would be expected to occur naturally in a general population of this size.” These generic blood-clot data turned out to have little to do with the very specific, potential risks that several countries were confronting. The EMA said on March 18 that it had found, by then, a possible link to the AstraZeneca vaccine among 25 people who had developed the disturbing blood disorder, including nine who had died from it. All 25 had low platelet counts. Seven also had blood clots throughout their blood vessels—a condition known as disseminated intravascular coagulation, which showed up here at about five times the generally expected rate. The rest had blood clots that prevented blood from draining from their brain—a condition known as cerebral venous sinus thrombosis, which occurred at about nine times the expected rate. Also on March 18, the vaccine authority in the U.K. reported that it was investigating five cases of those cerebral clots in people with low platelets. The original vaccination pause may be over in many countries, but investigations are continuing, and regulators around the world are taking further action. In France, for example, the National Agency for the Safety of Medicines and Health Products has identified nine cases of these blood disorders (including two deaths) out of 1.4 million injections, and described it as a vaccine reaction. In Australia, where there is, at the moment, essentially zero risk of COVID-19 infection, people who have had two very specific, rare blood disorders are now advised to defer any COVID-19 vaccination. Denmark’s health authority just extended its blanket hold on the AstraZeneca vaccine for three more weeks, and so did Norway’s. Since most cases have involved those under 50, several countries are limiting the vaccine’s use to older people as a way to mitigate the risk. We still can’t be sure whether this blood disorder is triggered by vaccination, and we don’t know yet whether the risk—if it’s real—applies equally to all recipients, or only to a subset that might be predisposed. In light of these uncertainties, the balance here between vaccination’s costs and benefits is obvious. Given the present context of COVID-19 transmission throughout Europe, and even assuming the very worst about the risk that the AstraZeneca vaccine might pose, the shot will save many more lives per million doses than it could ever possibly end. It should be just as obvious that health authorities cannot simply look the other way. For these sorts of blood disorders, early diagnosis and appropriate action might be crucial for saving lives. Rajiv Pruthi, a hematologist at the Mayo Clinic, points out that the standard treatment for a cerebral clot—a blood thinner called heparin—could make things worse for patients with this syndrome. At the very least, doctors must be kept informed about potential risks. It’s certainly reassuring that so few safety issues have emerged from COVID-19 vaccination on a global scale. The AstraZeneca vaccine has not yet been approved for use in the U.S., but 145 million doses of other vaccines have been administered since December, and while lots of people have experienced headaches, fever, tiredness, and so on, according to the latest data from the CDC, reactions have almost always ended there. As is the case for vaccines in general, a small number of recipients—just a handful out of every million—have developed severe allergic reactions, which are easily treated. There’s zero indication, at this point, that the Moderna, Pfizer-BioNTech, or Johnson & Johnson vaccines have caused any deaths at all. In other words, the fact that a potential safety issue has emerged for the AstraZeneca vaccine is itself a rare exception. As of now, the EMA is continuing to investigate the blood-related syndrome, and another expert-committee meeting on the subject was scheduled for yesterday. In the meantime, the agency has added a warning to the vaccine’s drug leaflet for the European Union. “Seek immediate medical attention if you develop shortness of breath, chest pain, leg swelling, or persistent abdominal pain following vaccination,” it says. “Also, seek immediate medical attention if you experience after a few days severe or persistent headaches or blurred vision after vaccination, or experience skin bruising or pinpoint round spots beyond the site of vaccination.” Similar warnings have been issued in Canada and Australia. Alerting people to that list of symptoms could save lives. But it might deter some people from vaccination. That’s why even cautious actions like the one taken by the EMA might be seen as dangerously misguided. Any move that shakes confidence in the AstraZeneca vaccine could lead to broader, global harms, warns Paul Offit, the director of the Vaccine Education Center at Children’s Hospital of Philadelphia. “While it’s easy to scare people, it’s very hard to unscare them," he told USA Today. “It creates the perception that these vaccines are dangerous.” But how far should this logic go? Does it matter that other COVID-19 vaccines are on the market—even if they’re more expensive or in short supply? Should vaccine authorities adjust their approach to risk, with the goal of propping up the public’s trust? These questions have no simple answers, and we shouldn’t be surprised that highly qualified experts have come to different conclusions. In fact, we saw something like the same debate unfold late last year, when AstraZeneca and Oxford University first announced their vaccine’s success in clinical trials. The data contained numerous, serious shortfalls: Instead of judging efficacy from a single, large, placebo-controlled trial, the Oxford team merged results from different studies carried out in different ways. The research was so problematic, in fact, that regulators could not agree on whether the vaccine’s demonstrated efficacy against symptomatic COVID-19 was closer to 70 percent, as England’s drug regulator decided, or in the low 60s, per the EMA. The lack of better data was a deal breaker for some health authorities. The U.S. Food and Drug Administration, for example, decided to await results from a large, rigorous trial; Switzerland’s agency, Swissmedic, did the same. But regulators in Europe, along with those in many countries beyond the Continent, went the other way. The EMA recommended authorization of the AstraZeneca vaccine, announcing that “the conduct of studies was sub-optimal” but also that, “given the emergency situation,” the benefits of using it outweighed any risks. In this case, the choice to loosen up paid off: The vaccine has reduced disease and death in recent months, and the more rigorous clinical-trial results—which have only just come in—showed an efficacy of 76 percent. But that doesn’t tell us how regulators should handle the possibility of dangerous reactions to the same vaccine that are too rare to show up in a clinical trial, even one with 32,000 participants. And to some extent, the narrative about those reactions is no longer in their hands. Stories linking people’s deaths to vaccinations have been among the most popular vaccine-related stories on social media in recent months—and that was true long before there were any hints of a real association. Now that health authorities really are investigating a possible, fatal vaccine reaction, these narratives will increase their reach. The first face to be linked prominently to the blood disorders appeared on Facebook on March 22. More seem sure to follow. It may be that at some point soon a non-vaccine cause will be established, or treatments will render the condition manageable. Until that happens, though, regulators must do their best to maintain calm, perspective, and transparency. Imagine if they’d reacted more conservatively from the start, and waited to say or do anything until the number of people who turned up with this condition had reached into the hundreds. More people would have been vaccinated along the way, but the eventual loss of trust in the monitoring system for vaccines could have been far more severe. Addressing concerns about vaccines is a long game, and the biggest challenges will come much later on, when all the eager people have been immunized and it’s time to persuade the holdouts. There are clear precedents for communicating effectively about very rare vaccine reactions. An ordinary flu shot, for example, may cause a tiny number of recipients—just one or two per million—to develop an autoimmune disorder called Guillain-Barré syndrome. The CDC describes this link as being “variable and inconsistent,” but the slightly squishy facts are not concealed from the public.
The Atlantic’s COVID-19 coverage is supported by a grant from the Chan Zuckerberg Initiative. from https://ift.tt/39qeTGz Check out http://natthash.tumblr.com I’ve always been a rule follower. So when I learned that my state, Virginia, was currently vaccinating only people older than 65, people with health conditions, and essential workers, I decided to patiently wait my turn. I didn’t prowl around pharmacies and hospitals at closing time, hoping for an extra dose. A few weeks ago, I signed up for Virginia’s COVID-vaccine waitlist, closed my laptop, and turned on Netflix. I was thrilled when I saw pictures of elderly people getting vaccinated. Finally, the most vulnerable are protected! Then friends with preexisting conditions started posting vaccine selfies, and I was excited for them too. But after that, more and more people my age—in their 20s and 30s—got the vaccine, and I began to question whether so many of my acquaintances were actually secret asthmatics. By now, it feels as if half the people I know have managed to get the vaccine, and I send each of them a “happy for u” text and also a silent ray of resentment. Like Carrie Bradshaw, I’ve been typing away forlornly on my MacBook for the past year, and much like her, I couldn’t help but wonder: Am I a chump for just waiting my turn? Should I take that bad case of bronchitis that my doctor thought might have been asthma and spin it into a bona fide health risk? Should I fudge the fact that I vape e-cigarettes and call myself a smoker? After all, don’t we need to get to herd immunity as quickly as possible? I could be part of making that possible, and get back to yoga to boot. People are definitely fibbing to get the vaccine early, experts say, though no one quite knows the extent of the problem. “I’m hearing a lot of entitled, empowered people, who are used to getting what they want, having conniptions about vaccination,” Arthur Caplan, the chief medical ethicist at NYU, told me. Few people, it seems, consider themselves nonessential. “I’ve asked about 30 people now, ‘Are you important in terms of your job?’” Caplan said. “And guess what? Twenty-nine of them said yes.” (The lone person who deemed themselves nonessential was a bank teller, he said.) States, counties, hospitals, and other vaccine distributors are mostly running on the honor system, says Marcus Plescia, the chief medical officer at the Association of State and Territorial Health Officials. If you say you’re asthmatic or a UPS driver, you’ll probably slide right through. And there’s a good reason for that: People who have documentation of their medical problems are also more likely to have regular doctors and good record-keeping systems—things low-income, disconnected people might not have. I live near Washington, D.C., which is full of people who never met a system they couldn’t game, so I am guessing the cheating is more common here than in areas where many people lack access to transportation or computers. In the southeastern U.S., for example, clinics have had a hard time filling slots, so some states have already opened up vaccination to additional age categories, Plescia told me. Some line-jumpers are simply confused about the categories. Does the cloves phase you went through in college make you a “smoker”? Does working for a school, but not in a public-facing role, qualify you as an “essential worker”? Others are so determined to get a shot that they have signed up for practically every waiting list within a 100-mile radius. [Read: The differences between the vaccines matter] “People who get on multiple sites do tend to be successful,” Plescia said. But the problem is, once these folks get a shot, they forget to cancel their appointment at other sites. “And one of the reasons we think that some of the vaccine clinics are running a little slow is that a lot of people aren’t showing up, because they already got it somewhere else.” I interviewed a few people who had stretched the truth to get a vaccine, and it sounded really tempting, even when the hoops they jumped through were extreme. (I agreed to use only their first names so they wouldn’t get dragged for their, uh, ingenuity.) One man, Alex, drove five hours round-trip to a small town in Wyoming, which he’d heard had extra doses. He truthfully answered all the screening questions except one: He doesn’t actually interact in-person with the general public. Another man, Bob, drove to a Walgreens about an hour away from his county in Virginia. When he got there, he filled out a form saying he’s an essential worker. His claim was technically true, because he works for the government. But he can work from home. I asked him whether he thought I should do the same thing. “I would, I mean, because I did,” he said. “I would encourage others to do the same, because there’s nothing special about me.” [Read: The second COVID-19 shot is a rude reawakening for immune cells] But experts told me that, basically, it’s bad to lie about yourself in order to get something that is still in short supply. “My own husband has not gotten vaccinated, and I’ve not pulled any special strings for him,” Megan Ranney, an emergency physician who teaches at Brown University, told me. “He’s able to, for the most part, stay home. There’s a reason that we have the eligibility requirements that we do, which is to make sure that the people who are at highest risk of getting sick and dying are the first ones to get access.” She said that she thinks I should take the vaccine if it’s offered to me, but not try to sneak around the rules. Plus, if everyone starts jumping the queue, they might create a mad rush for vaccines by motivated young people. “The moment people start feeling like other people aren’t playing by the rules, it changes everyone’s incentives,” says Ashish Jha, the dean of Brown University’s School of Public Health. “They don’t want to be the chump who waited in line.” “I feel like a chump for waiting in line,” I told him. “Thank you,” he responded. Waiting is apparently exactly what I should do. Everyone I interviewed pointed out one important thing: People like me won’t have to wait much longer. At least 31 states have said they will make vaccines available to all adults by mid-April, and some states and jurisdictions have already opened up vaccination to all adults. Virginia will supposedly allow all adults to get vaccinated starting on May 1. Then my vaccine FOMO will be over, and so will my life as a recluse. from https://ift.tt/3waPF8O Check out http://natthash.tumblr.com The vaccines are here, and with them, the promise of getting back to some sort of normal. Over the coming months, many Americans will be returning to offices or schools, traveling to see family and friends, eating cheeseburgers inside sports bars. But the vaccines’ arrival has also provided a more immediate relief: giving people something to talk about. After a year of awkward conversation, the United States has entered vaccine exuberance. People are sharing vaccine selfies, posting photos of their vaccine cards to Instagram, and even just broadcasting tips on where they got appointments or found short lines. “I got my first shot” is news worth hearing. Finally, you have an answer to the dreaded “How’s it going?”: perhaps, “My parents are fully vaccinated as of today. What a relief.” Some people are even comparing the vaccines as if they are catalytic converters or dog shampoos. It’s almost reflexive to bring up which of the Moderna, Pfizer-BioNTech, or Johnson & Johnson vaccines went into the arm. “Which one did you get?” you might ask a friend. (All three are very good.) Of course people are talking about inoculation: It’s the most recent news to process. But the liveliness of vaccine talk makes clear how fitful all previous pandemic conversation has been. Looking back, that void issued a constant, if unseen, stressor on daily life. Now vaccine discourse shows how badly people—Americans especially—want and need small talk. Despite its name, small talk plays an outsize role in socialization. Social scientists refer to this type of speech as phatic communication, which they usually divide into two related but different theories for understanding its function. One theory, devised by the early-20th-century anthropologist Bronisław Malinowski, used phatic speech to account for small talk as an essential part of social bonding. You answer the phone, saunter into a shop, or pass a neighbor on the street. “How are you?” you might ask each other. When this happens, nobody really cares to hear how you are doing. The question is posed for social communion; it’s a way of saying hello, of acknowledging someone’s presence, of beginning a more meaningful interaction. The other theory, put forward by the linguist Roman Jakobson, sees phatic speech as the chatter used to manage the channel of communication. It’s language that cues people in to where, how, and when they should speak. These days, you might pass fewer neighbors and see fewer co-workers, at least in person. Instead, those interactions are largely mediated by technology. And with that comes the need to talk about how to operate those apparatuses and how to behave when using them. “Oh, you’re breaking up,” or, “Your video froze,” or, “Bob, you’re still muted,” or even, “Wait, were we meeting on Zoom or on Teams (or on Slack, or by phone)?” Altogether, phatic speech is the linguistic glue that holds our interactions together. And the pandemic has utterly broken it, making social interactions even more exhausting. First, the Malinowskian, social-bonding flavor of phatic speech has stopped working. Normally, people hear past the meaning of “How are you?” and recognize its social purpose. But as early-pandemic dreams of flattening the curve and getting back to normal devolved into a whole year of online meetings, schooling, piano lessons, and happy hours, each invocation of a phatic greeting became more noticeable—and newly burdensome. Suddenly, asking “How are you?” involved really and truly asking the question, whether you meant to or not. Who knows, after all, if the other party (or someone in their family) might be sick, or has lost their job, or has even just reached a new low of sorrow and terror. While Malinowskian phatic social bonding collapsed, Jakobsonian phatic channel-fluffing ballooned in the worst and most awkward ways. In part, that’s because everyone started using communication technologies unfamiliar to everyday life. Zoom’s 2020 profits swelled fortyfold over the prior year as workplaces and schools shifted to video meetings. Other, similar services, such as BlueJeans, Slack, Skype, and Microsoft Teams, also witnessed huge growth. Figuring out how to get a co-worker into a meeting, a child into a virtual classroom, or a parent into a family videochat required a great deal of irritating meta-discourse. “Is it a phone call, or is it on Zoom?” “Meet in mine, or are you sending an invite?” “Oh, we don’t have a subscription, so you’ll have to host if it’s more than two of us.” When it works best, phatic speech disappears into the background. A hello begets a conversation. But when coordinating speech loses its phatic function, it has to be dealt with as actual speech—and today, as speech fraught with emotion: “I guess I’m okay, under the circumstances.” Then the rest of the interchange floods with phatic channel-management. Bob’s still on mute, your camera won’t work, or the connection is bad. Even after the introductory awkwardness ceases, it gets replaced with piles of apparatus-wrangling. Together, the combined failures of the two kinds of phatic speech are a lot worse than either one breaking down on its own. That’s made pandemic small talk less effective and more onerous. It joins a host of other behaviors and habits the pandemic has altered, some perhaps for good. Last spring, my colleague Megan Garber nailed the coffin shut on handshakes. Hugs and cheek kisses also fell out of favor as greetings, perhaps for good. As the pandemic spread through North America and Europe, my colleague Uri Friedman hypothesized that those continents’ residents might begin wearing masks regularly, as many East Asian nations do, long after the world has tamed COVID-19. Likewise, it’s possible that the pandemic has changed phatic speech for good. Perhaps the utility of a salutatory “How are you?” is forever poisoned. But I don’t think so. The long winter of lockdown is breaking, and vaccines promise hope of a return to a new, if different, normal. The sense of dread and despair that made casual greetings feel notable and oppressive for so many people has begun to lift. Small talk’s function remains a little marred—I find myself still answering the literal meaning of phatic utterances, only now with statements of measured optimism: “I’m good, starting to see some light at the end of the tunnel.” But small talk’s use in social bonding is returning. “Which vaccine did you get?” has become a low-stakes way to move from phatic communion to small talk to business. As the pressure eases off the pregnant How are you?, the unfair demands placed on that phrase will ease. Language and culture also just don’t change so quickly. Even at the nadir of pandemic small talk, people still made it work. “Oh, you know,” you might have found yourself telling someone asking how you are. And that person probably just responded, “Yeah.” Social communion succeeds, if with a stutter. A friend of mine even invented a new stock response to the ubiquitous how-are-you greeting: “I’m Covid-OK,” she says, chasing the rogue exchange back into its phatic cage. Human speech is resilient and adaptable. It is baked into our embodied experience of the world. As more of that world returns, so will the old patterns of speech we left behind in the shops and parks and offices we abandoned. Americans in particular are obsessed with social pleasantries, and it will be difficult for us to resist the urge to send off a casual “How’s it going?” at the earliest opportunity. Recovering the normalcy of small talk might alleviate more pandemic fatigue than you’d think. Maybe phatic communion will even feel newly invigorating, after a year of unexpected decline. Think how delightful it will feel to say “I’m fine” and not notice, because you mean it. The Atlantic's COVID-19 coverage is supported by a grant from the Chan Zuckerberg Initiative. from https://ift.tt/3w2DFWK Check out http://natthash.tumblr.com Trying to remember March 2020 feels like sticking your head into a parallel universe. This time last year, Americans were just going into lockdown—presumably for two weeks—to protect themselves from a mysterious but deadly virus. We disinfected mail but didn’t wear masks. Few of us knew that COVID-19 symptoms could last for months, that you might lose your sense of smell, or that your toes might break out in purple lesions. The possibility that millions would die was real but incomprehensible. The pandemic today is almost unrecognizably different. In the United States, an acute, terrifying catastrophe has given way to the monotony of lowered expectations. There are no makeshift morgues in the streets. Businesses are opening despite a thousand American deaths a day. This week, Mayor Bill de Blasio ordered New York City employees back to work, regardless of their vaccination status, while case counts in the city are on a high plateau. The pervasive sense is that we can’t wait forever for the pandemic to end. When, exactly, will we reach a point that could be considered a finish line? It’s the natural question, but I think it’s a counterproductive one. Not only because, as Anthony Fauci told me recently, the most honest answer is “We just don’t know.” The inability to give a definitive answer is contributing to misperception of risk, conflating better with good enough. It’s also true that much of what defined the COVID-19 crisis at its worst is no longer an issue. Many health-care workers are vaccinated, and the need to “flatten the curve” is in the past. Tests are widely available, and there are better treatments for the disease. Death rates are falling quickly. The SARS-CoV-2 pandemic may drag on for years, but the nightmare of last year—of an entirely new viral illness, emerging in a specific sociopolitical context—is behind us. Instead we’re facing a new set of challenges, and they are not easily comparable to what has come before. It’s worth considering a new way of thinking about the period of the pandemic now ahead of us—one that leads us neither to complacency nor to paralyzing despair. In many ways COVID-19 is already over. What lies ahead is COVID-21. Diseases are not static things. Pathogens change, hosts change, and environments change. In the case of COVID, all three are now different than they were in 2020. What began as one coronavirus has infected well over 100 million people and evolved into new forms that appear to transmit more readily and infect us in subtly different ways. Our immune systems have changed as well, as a result of fending off infections. And, of course, our lifestyles have changed, as have social standards, medical systems, and public-health programs. COVID-21 is the product of all these changes in aggregate. It’s the disease as it will be experienced in the months and years to come: with new variants of the virus, new public policies and health behaviors, various degrees of immune memory, and—most important—a cavalcade of new vaccines. One-quarter of all Americans have now received at least one shot, and that number is racing up. This month, New Yorkers lined up outside Yankee Stadium throughout the night at a makeshift 24/7 vaccination site, until the supply ran out. “If we open 3,000 appointments, they will immediately fill,” says Ramon Tallaj, a physician who oversees clinical care in underserved communities across New York City. Demand seems to be growing. If there were sufficient supply, Tallaj told me, his team could be giving out 40,000 doses every day. And this should happen soon; the White House says that shortages will end in the coming weeks. The vaccination effort is sure to change the nature of COVID in unexpected ways. The habitat for the virus is changing: It may still stick in the nasal passages of an immunized person, but it shouldn’t continue on its way into the lungs, much less the toes. The key question is just how long this protection will last, especially against a rapidly mutating virus. Clinical trials have shown the vaccines to be fantastic at preventing serious illness so far, but haven’t yet been able to observe how protection might dissipate over long periods. Because SARS-CoV-2 hasn’t been infecting humans for much longer than a year, it’s impossible to say exactly how immune responses will play out. The common-cold coronaviruses can reinfect the same person after a year or two. Early research on COVID vaccination shows that people develop high levels of antibodies, but that these begin to decline about a month after the first dose. The CDC’s official position on how long immunity lasts after vaccination is “We don’t know.” Antibodies are not the whole story, though. Monica Gandhi, an infectious-disease specialist at UC San Francisco, believes that we’ll be well protected by other immune mechanisms, even after antibody levels drop. Her research focuses on how HIV evades and weakens the body’s immune system, particularly the T cells. She reminded me that T cells, and also B cells, store a memory of prior infections, and are generally more important than antibodies for maintaining long-term protection against viruses. Reassuring evidence has already emerged indicating that these cells can form durable memories of SARS-CoV-2. Recently, a group of researchers biopsied the lymph nodes of vaccinated individuals and found “remarkably” strong B-cell development. In a February Science paper, another team found that the T cells generated in people who have had COVID-19 seem to have similar half-lives to the T cells you get from being vaccinated against yellow fever—and yellow-fever protection usually lasts a lifetime. Another promising sign comes from those who contracted the original SARS coronavirus in 2003. The T cells of people who were infected at the time reliably recognized the spike protein from the virus in lab experiments 17 years later. Gandhi believes that this memory, while not always as protective as having high levels of neutralizing antibodies in your blood, will likely be sufficient to prevent severe disease. “Do I think that we’ll have lifelong immunity from severe infection?” she said. “I am very heartened that we will.” If that’s the case, then COVID-21 will eventually be a milder, less deadly version of the illness that we started with last year. “The worst-case scenario is we render it a cold,” Gandhi said. “The best-case is we reach herd immunity and the virus goes almost entirely away.” But others expect a much worse worst-case scenario, in which immunity to severe disease is only temporary. The biologist and former Harvard professor William Haseltine warns against the rosy view: “It seems to me clear that the T-cell theory isn’t going to hold up,” he told me. Although our memory cells could continue to recognize the virus, that won’t necessarily be enough to give us meaningful protection. The disease might end up being milder the second time around, or after vaccination, but he worries that, as the virus mutates, it also could get worse. As for herd immunity, Haseltine called that a “fantasy.” “The best we’ll get is seasonal herd immunity. We have 60 years of experience with coronaviruses, and they come back every year.” Even the bad version of COVID-21 would be far different from the depths of COVID-19, though. Millions of cases of severe disease would be prevented with vaccines, but boosters would have to be given out at regular intervals. “The Moderna and Pfizer vaccines are shockingly good mimics of natural infection,” Haseltine told me. “But it’s really important to stress the fact that these vaccines are likely to be temporary protection. A year or maybe two.” That means we’d need a more enduring system of vaccine production and distribution. It will be an enormous challenge to keep the public up-to-date with annual or semiannual injections—and if uptake flags and the virus remains pervasive, even immunized people won’t be 100 percent free from risk. In the end, Haseltine said, we might hope for a universal vaccine that protects against all strains of SARS-CoV-2, as well as future coronaviruses that might emerge. Early research has shown some promise using nanoparticle immunization technology, which combines fragments of different viruses. Fauci and others have been pursuing a universal influenza vaccine for years, and they are now, at last, seeing some indications of success. A universal coronavirus vaccine should theoretically present fewer obstacles, because the viral structure is more straightforward, and it changes less readily. As the race to develop the current generation of COVID-19 vaccines finishes, the race for a universal vaccine begins. Between Gandhi’s vision and Haseltine’s is another, quite disturbing, one. Imagine that the vaccines work well, but not indefinitely. The virus continues to spread and mutate. COVID can still have severe, even life-threatening, effects. Vaccination brings rates of serious disease and death down substantially, but not close to zero. And we come to think of this as pretty much okay. In other words, imagine a world in which the disease persists, and is accepted, as something that is far less deadly than it was last year—more like a bad flu than a common cold. As with influenza, the world might lose hundreds of thousands of people to this illness each year. And yet we would come to see its toll as being within the bounds of acceptable loss. As with diseases like malaria, HIV, influenza, and so many others, enormous effort and resources would go into preventing infections and treating sick people. But the singular global war against the SARS-CoV-2 virus that began in 2020 would fade in intensity. Instead of working toward a post-COVID future, we’d come to see the disease as yet another unfortunate but inevitable feature of the modern world. This version of COVID-21 would be most dangerous, not because the virus has developed some new, sinister mutation, and not because our vaccines turn out to be inadequate. The risk instead would come from the way that it’s normalized. As the bioethicist Jackie Scully wrote in 2004, diseases morph “partly as a result of increasing expectations of health [and] partly due to changes in diagnostic ability, but mostly for a mixture of social and economic reasons.” They change with how we perceive them, and react to them. We are at an inflection point that will change the reality of this disease. The most insidious future is one in which we fail to change our moral benchmarks, and end up measuring the danger of COVID-21 by the standards of 2020. If wealthy countries with early access to vaccines abandon continued, global coronavirus-vaccination efforts as their cases fall or when the disease becomes milder for them, a still-severe disease could haunt the world indefinitely—and lead to rebounds everywhere. Avoiding this myopia is the central challenge of COVID-21. It extends to the systemic problems highlighted by this pandemic. Much of the damage the virus has wrought has come indirectly, by exacerbating food and housing insecurity, for example, or restricting access to medical care. The Biden administration has elevated science and begun to focus on comprehensive approaches to prevention. No longer is federal leadership hawking hydroxychloroquine, suggesting injections with “disinfectant,” or stoking xenophobic sentiment. But this sudden sense of order is a beginning, not an end. Last year’s sense of terror and panic belongs behind us. This is the phase of the pandemic when we can move from haphazard emergency plans to concerted measures to eradicate a life-threatening illness. Despite lingering unknowns about exactly how long immunity will last and how many cases we’ll continue to see, we now have the knowledge and resources to become much more certain very quickly. If we beat COVID-21, the numbering could end there. The Atlantic's COVID-19 coverage is supported by a grant from the Chan Zuckerberg Initiative. from https://ift.tt/3w1LP1I Check out http://natthash.tumblr.com Brushing my teeth is a struggle. I brush so hard, and for so long, that sometimes my gums bleed. I can’t spit until I’ve touched each tooth carefully with the tip of my tongue. I open and close the medicine cabinet repeatedly, pressing my palm into the pointy corner of the mirror, until it feels like enough. I can’t leave the bathroom until I’ve flipped the light switch on and off a dozen times. Some nights, the routine takes 30 minutes. Some nights, I lean over the sink and cry. My obsessive-compulsive disorder manifests in rituals: small, repeated behaviors that my anxious little brain demands. If you do not do this thing, my brain explains, something terrible will happen to someone you love. Fear of contracting a deadly virus, combined with the total disruption of my work and social life, has multiplied my compulsions, which now require much more of my time. The same is true for others living with OCD, many of whom are preoccupied by germs or illness. Society may be eagerly preparing for the summer to end all summers, but people with anxiety and an intolerance for uncertainty are not entirely optimistic. “The majority of people who don’t have OCD—their life will go back to normal,” Elizabeth McIngvale, the director of the McLean OCD Institute in Houston, told me. For many people with OCD, returning to “normalcy” isn’t as simple as eating indoors at restaurants again. It means recalibrating their brain. One of my earliest memories of my OCD is from July 2007, when the last Harry Potter book came out. I was about to start high school, my family was moving to a new house, and I was a sweaty bundle of nerves. To cope, I immersed myself in the world of house elves and horcruxes, and made a compromise with my brain: Everything will be okay if I read every sentence three times. I finished the 784-page book long after my friends had spoiled the ending. I wasn’t officially diagnosed with OCD until 10 years later; for most of that decade, I just thought I was weird. But the disorder is fairly common. Roughly 1.3 percent of Americans have symptoms that would warrant an OCD diagnosis—one in every 80 people—according to Chris Pittenger, a psychiatry professor and the director of the Yale OCD Research Clinic. The disorder can be broken into a few broad categories, but they tend to bleed into one another. Some people with OCD have obsessions and compulsions, such as hand-washing, related to cleaning and contamination. Others have a desire for symmetry or an urge to organize or do things according to a specific number. And some have uncomfortable thoughts they can’t escape, such as visualizations of death or illness or injury. I’ve always thought of OCD as the state of being biologically superstitious. The children’s sidewalk rhyme goes, “Step on a crack or you’ll break your mother’s back.” But a person with OCD may have to step on seven consecutive sidewalk cracks, three times in a row, and if she doesn’t, her mother will develop terminal cancer. Stress, illness, and major life transitions can make OCD worse, which is why the pandemic exacerbated many people’s symptoms. “Every therapist has a waitlist; everyone is looking for more help,” Jeff Szymanski, the executive director of the International OCD Foundation, told me. “People can’t find enough OCD specialists to hire.” For some people with OCD, the pandemic has affected their symptoms in a more general way, Pittenger said: More stress means more obsessive thoughts and compulsions, but not necessarily thoughts and compulsions related to the virus. That’s certainly been the case for me. Over the past 12 months, I’ve developed intricate new rituals for closing Ziploc bags and washing dishes. I have to read the entire label on the waist of my sweatpants before I can put them on. I even have a strange new tic: vigorous nodding. At certain points throughout the day, I feel the urge to bob my head back and forth until it hurts. I have to do it, or something bad will happen: Maybe I’ll contract COVID-19, or maybe my parents will get into a car accident. Sometimes I nod while I walk through the park next to my house, and people give me funny looks. At home when I nod, my boyfriend politely ignores me. [Read: The coronavirus is a special mental-health disaster] OCD can feel utterly enormous, so I found it comforting to talk with others who have it for this story. Jeff Whitmire, who is 44 years old and lives in Lititz, Pennsylvania, has had OCD since he was a child. For him, it often manifests as overanalysis of events and interactions. Years ago, when Whitmire hit a stick on the road while driving his car, he couldn’t stop thinking about the fact that he hadn’t actually seen the stick. Which meant, he thought, that there was a chance that stick could have been a person. Whitmire drove 30 miles in distress before deciding to turn the car back around to check. Whitmire’s compulsions calmed significantly when he entered his 40s: He was able to go off his medication and stop attending therapy. But when the pandemic hit, his anxiety shot up, and the compulsions came flooding back. “It was like going back to square one,” he told me. For a while, he was too anxious to call his best friend on the phone, because he didn’t want to spend the rest of the day overthinking their conversation. For some people with contamination OCD, the pandemic has complicated their fears about germs and viruses—and many of them have become overwhelmed, Pittenger said. Chelsea Ridener, a 24-year-old pediatric nurse in Tulsa, Oklahoma, had mild contamination OCD before the pandemic. When the world grew fixated on a highly contagious virus, her compulsions became almost debilitating. Ridener now wipes down her grocery cart for 10 or 15 minutes before shopping and scrubs her hands with sanitizer after touching anything in a public space. (Scientists have concluded that the coronavirus is much more likely to be transmitted through the air than on surfaces.) At Walmart recently, Ridener’s 2-year-old son touched something in the bathroom and then immediately grabbed her hand. Picturing the germs spreading from his body to hers sent Ridener into a panic attack. She sat in a back hallway of the store, shaking and crying for nearly an hour. Surprisingly, although the past year has been terrible for some people with contamination OCD, others have not experienced an increase in contamination-related thoughts and behaviors, Pittenger and Szymanski told me. People like me, who don’t have compulsions related to health, have been more likely to report exacerbated OCD symptoms, at least according to preliminary research, they said. This could be because people with contamination OCD actually found a strange relief in the pandemic: They were exceptionally well prepared to live through a global health crisis. “My therapist said, ‘You’ve been prepping for this your whole life,’” says Dotty Dart, a 30-year-old who lives in Detroit and who has rituals associated with germs and a fear of vomiting. “It was weirdly comforting,” she told me, to know that other people finally understood the daily panic she’d always felt. Seeing people take public health seriously, wear masks, and wash their hands more often made her feel less anxious. But when Dart thinks about the world opening up again—people crowding restaurants and bars and stores, coughing and sneezing and touching things—that relief disappears. “It makes me a little nervous, thinking about people just going back to being gross adults.” The pandemic will eventually retreat, but anxiety is a much stickier thing. Like some people with OCD across the country, I’m worried that I’m stuck with these new compulsions for the foreseeable future—that this time next year, I’ll still be struggling to put on sweatpants and walking around the park nodding at no one in particular. My OCD is still manageable. It does not tend to seriously disrupt my life. But sometimes I ask myself: What if my symptoms only get worse from here on out? What if 2020 was the year my brain broke? I explained those fears to Pittenger, and he offered an alternative future: “As the world gets less stressful, the symptoms should calm down” at least a little, he told me. I’ll have to work on it, though, and employ common treatments for stress: good sleep, exercise, meditation, and mindfulness. But he and other experts are still concerned that some people with contamination OCD “will continue to struggle with these triggers” long after the pandemic ends. Ridener told me she already knows she’ll never be able to ditch her face mask: “I’ll be the person that is always wearing one, for the rest of my life,” she said. The Atlantic’s COVID-19 coverage is supported by a grant from the Chan Zuckerberg Initiative. from https://ift.tt/3cqk8aQ Check out http://natthash.tumblr.com The recent shootings in Atlanta highlighted a surge of anti-Asian violence in the United States throughout the pandemic. Disease stigma and racism have together shaped pandemic response and policy for centuries. And so to better understand this history, on the podcast Social Distance, co-hosts James Hamblin and Maeve Higgins speak with Alexandre White, a sociologist and medical historian at Johns Hopkins University. He shares his views on how a legacy of prejudice tied to disease should lead us to reexamine how we respond when outbreaks occur. Listen to their conversation here: Subscribe to Social Distance to receive new episodes as soon as they’re published. What follows is a transcript of the episode, edited and condensed for clarity: James Hamblin: How did you get into this line of research? Alexandre White: I became very interested in the ways in which epidemic moments seem to key off of, or become more severe as a result of, existing social, economic, and political inequalities. I found this most clearly when I was conducting research on HIV/AIDS and tuberculosis infections in South Africa. And I was really struck by the ways in which histories of apartheid and ongoing racial inequities would shape who got sick, who got better, and—ultimately—why. And I became very interested in looking at international epidemic responses and the ways in which economic ideologies, political ideologies, histories, and legacies of colonialism and racism shape international epidemic response. In the early days of my research, I was exploring an earlier case of racially segregated responses to an epidemic of bubonic plague in Cape Town in 1901. And I was doing this research at the same time we were living through the West African Ebola epidemic. We were seeing highly policed, militarized quarantining of poorer neighborhoods in Monrovia, with violence ensuing. And I was like: There must be something connecting these two phenomena in some way. And as I continued my research, I started to see [that] the way in which we as a globe have responded to the threat of infectious disease spread—the threat of epidemics and pandemics—is to, in so many ways, double down on the rooted and continuing social imbalances as a way of not only ascribing difference to populations but also as a way of providing differential care. And we see the ways in which this has very disparate outcomes in who lives and who dies from epidemic disease. There’s a wonderful quote by Roderick McGrew from his study on cholera that says: “Epidemics do not create abnormal situations, but rather sharpen existing behavior which ‘betray deeply rooted and continuing social imbalances.’” What I was seeing was an example of what sociologists would call the “social determinants of health.” We could see, especially in the legacies of apartheid, the ways in which racial segregation, unequal access to housing resources, [and] political violence really shape how people live and, unfortunately, also the diseases they get and ultimately how they die. And as we’ve seen in the United States, especially over the last year, racism in a variety of different ways, whether it’s political violence or whether it’s the effects of structural racism leaving you vulnerable to contagion and infectious disease, it quite literally kills. Hamblin: You mention the social determinants of health. If you’re in a place that’s high-stress, you can’t sleep, can’t eat well, don’t have space, you’re probably going to be in a worse place in this pandemic than otherwise. So there’s been an important need to say that this pandemic is not affecting people equally. How do you highlight that disparity without contributing to notions that this is a disease that is associated with certain populations? White: That’s a wonderful question. Since the 14th century and perhaps even earlier, the arrival of an epidemic has been grounds for ascribing difference and assigning blame to certain populations—generally marginalized populations—for causing the spread of the disease. And we can look to, for instance, massacres of Jews in Europe and especially the Strasbourg massacre of 1349. The Jewish population of the city was blamed for the spread of plague and ultimately massacred. Maeve Higgins: And that was because there was already deeply rooted hatred of Jewish people and the plague was used as an excuse. White: That’s exactly right. And you have to remember that the understanding of disease in the 14th century was very different from what we have now. There wasn’t an understanding of contagion or germ theory. Rather, there was an understanding that this pestilence had arrived and we’re going to blame these particular populations for that spread. But in the late 19th century, you see similar actions at work, just under new and different understandings of disease. With the acceptance of germ theory and an understanding of the ways in which diseases are capable of traveling, disease becomes really a basis for justifying already latent exclusions—whether they’re internal to a nation or a city or in terms of immigration and global travel. So disease becomes a way of further ascribing difference and otherness in a way that is both biological, cultural, and enduring. Higgins: You’ve mentioned examples of disease bias from that time period in Africa. What are some cases we saw in the U.S.? White: I think there are several very disturbing historical cases that resonate today as we see so much anti-Asian discrimination and violence and racism. There were two notable events of bubonic plague occurring on U.S. soil. One was in Honolulu, which was at the time part of the American colony of Hawaii. There was great concern, in that case, of Hawaii being seen fundamentally as an Asiatic colony because of this stigma around the spread of infectious disease coming from the Asian continent. And what resulted was an incredibly violent, racist, and xenophobic quarantine of the city’s Chinatown, whereby Chinese homes and businesses were segregated away from the rest of the city. People were unable to travel in and out. But at the same time, the region around this Chinatown, and even within, was gerrymandered such that [for] American and white-owned businesses and homes, you could travel without encumbrance. The public-health authority of the city attempted to burn down and sanitize plague-infected homes, and ultimately these fires got out of control and engulfed much of the Chinatown in flames, obviously leaving many homeless, without employment, without a job, without a place of work. Higgins: On top of a plague. White: Indeed. And we saw similar racially segregated quarantines occur in San Francisco’s Chinatown from 1900 to 1904 as they were battling the plague. And those quarantines also played out in rather similar and oppressive ways. Higgins: Back in April of last year, you wrote: “As we witness spates of xenophobic violence, Sinophobia and other anti-Asian sentiment, it is important for us to notice whose perspective dominates responses to epidemics.” What have you been thinking about as we’ve seen this anti-Asian harassment and violence escalating? White: I’ve been both incredibly saddened by this and also frustrated. This history of anti-Asian racism runs very much through histories of epidemics, of immigration, of colonialism that the United States often doesn’t discuss. What this ignores is the long history of structurally racist action against Asian populations broadly. And this goes back to the latter half of the 19th century, reaching a sort of apex with two major federal acts that would control immigration from Asia to the United States. The first was the Page Act of 1875, which banned the immigration of Chinese women, and which was justified on the basis that Chinese women were perceived to be immoral or guilty of sexual misdeeds. And this conflation of sexual and moral perversity was linked fundamentally with a medical justification that somehow the venereal diseases that Chinese women might bring and spread as sex workers were somehow more virulent than those brought by either other European migrants or that existed in the United States. So there was this grim and horrific conflation of gender, sexuality, race, and the foreignness and concern for the diseases that were more threatening because they were fundamentally arriving from Asia. Higgins: And we saw an apparent attack specifically on Asian women working in massage parlors over 100 years later. White: The other major coercive, racist, and anti-Chinese act that emerged in the late 19th century is the Chinese Exclusion Act, which banned the immigration of Chinese men as well, doubling down on the Page Act. This was once again justified by beliefs of the threat of contagion arising from Asia and somehow poisoning the moral and epidemiological space of the United States. And it’s really important to note that these acts were not solely effective against Chinese or broadly Asian populations, but the sheer fact that these acts were passed really allowed for the slews of racist and xenophobic immigration acts that we saw in the 20th century and 21st century against South American and Central American populations. Even former President [Donald] Trump’s Muslim ban is rooted in this legacy that really emerges out of a very specific, racially targeted form of exclusion in the Chinese Exclusion Act. And this is something that Erika Lee and many others have written about in great detail, and I think is really important to keep in mind, especially when we attempt to understand the complexities of the violence that we’ve seen in recent weeks and the violence we’ve seen broadly across 2020. A troubling aspect in [how] the United States responded to COVID-19—and I would include the United Kingdom in this response as well—is that for the 19th century and 20th century, so much of Western beliefs of fundamental superiority of civilization and justifications for colonialism emerged out of this mythology of the West being the most sanitary, the most hygienic space, and being the most hygienic civilization on the planet. Rudyard Kipling’s infamous poem The White Man’s Burden, for instance, was written about American colonial actions in the Philippines, where he writes: “Take up the White Man’s burden— / The savage wars of peace— / Fill full the mouth of Famine, / And bid the sickness cease.” It was very much his belief that Western civilization, and explicitly American civilization, was the most hygienic, the most sanitary, and that the rest of the world was responsible for the diseases that could pollute that civilization. And we see that same rhetoric coming up today. But we also see that myth falling apart as we recognize that the U.S. COVID-19 response up to vaccination delivery has been one of the worst—one of the most unequal and most deadly in the world. Hamblin: I have a particular interest in the history of hygiene. That myth that you talk about of the Western world being uniquely hygienic—it’s actually the inverse of that. Christian countries were late to and sometimes actively discouraged things like baths because they were lewd and you had to be naked. When Marco Polo traveled, he was taken by hygiene standards elsewhere that were much higher than in Europe. And Europe certainly had its share of plagues and infectious disease. So that was always a baseless idea, right? White: Absolutely. And it’s [an] idea that really emerges in the aftermath of 19th-century European colonization of the rest of the world. When we look at the history of international infectious-disease control, that emerges really in the 19th century out of what were called the International Sanitary Conferences, which was a set of conferences that began in [1851] and continued into the 20th century, that focused on creating the first international infectious-disease controls for regulating the spread of infectious disease among people. But the focus of these controls were not health for all or some sort of humanitarian principle. Rather, it was: How do we allow for the maximum speed and pace of trade and traffic with also the maximum control of infectious disease? It was really about minimizing the effect on trade and traffic while also controlling infectious disease. And unsurprisingly, especially as these conferences were driven by European imperial powers—the particular concern over disease traveling from colonial sites, especially in Africa, the Indian Ocean, and then ultimately also in South and Southeast Asia—the focus became on how to maintain lucrative sea lanes and shipping without spreading diseases that were becoming very dangerous in the eyes of Europe, like cholera, plague, and yellow fever. So this myth emerges. And it’s a mythmaking process that I think is actually central to Europe and the West coming to envision itself as an entity apart from the rest of the world. And in my work, I call this “epidemic Orientalism.” We see the ways in which the need to maintain trade, colonial, and resource exploitation becomes bound up with controlling particular bodies and people who were seen to be in opposition to a sanitary global trade regime. And this is where you get a lot of the racist and xenophobic ideologies we’ve talked about already, and ideas that we see still in the present when we associate diseases with certain parts of the world, essentially slurring the names for an epidemic like COVID-19 in a variety of ways that ascribe blame to certain countries or certain areas. Hamblin: Right. That draws out this interesting distinction: There’s a lot of scapegoating and blaming of immigrants during these heightened times of infectious-disease spread. But the actual issue is just travel. If there is an outbreak in a particular place that you need to contain, you can ban travel to and from that area. Sometimes that’s a legitimate and necessary public-health measure. But why would you ever specifically say that it has something to do with immigration and yet people can travel to these places? White: Framing of threat through disease allows for the pathologization of peoples and cultural practices as somehow distinct and different from one’s own. So it’s a way of creating difference. If an epidemic is occurring in a certain region, there are certainly justifications for containing that epidemic, controlling it, and mitigating its spread. I think it’s when you start applying differential systems of control. For instance, in the 19th century, the diseases spreading from Europe were not regulated or controlled in these International Sanitary Conventions, [which] essentially allowed disease to spread from Europe to the rest of the world, but policed diseases traveling from elsewhere, namely colonial sites to European metropoles, which created a fundamentally differential system of travel regulations rooted in disparities and in systems of oppression. Hamblin: Connecting the idea of a place or group of people to a pathogen has occurred throughout history. In 1919, people referred to the Spanish flu despite it seeming to have originated in the U.S. Donald Trump used the phrase “China virus” a long time into the pandemic when that was not at all an appropriate term. Now we are seeing things like “U.K. variant” or “variant that originated in the U.K.,” or South Africa or Brazil. Is there a more sophisticated nomenclature that would avoid inappropriate conflation of a certain group of people or a place with a pathogen? White: We could go with the scientific variant names. The U.K. variant is known as B.1.1.7. Hamblin: Though that is hard to do in popular media, especially now that there’s [at least] five variants of concern here in the U.S. and they all jumble up and sound the same. White: I think there’s a slightly more philosophical question related to this, which is: Obviously, epidemics may begin in a certain place, but to what extent do origins actually matter? Especially when we’ve seen the epicenter of this pandemic move from China to Italy to take up home for a very long time in the United States. How do we equate geography and threat when epidemic epicenters do tend to move and shift? And this is something that the WHO has challenged—the naming of diseases for their point of origin. Several diseases have been renamed to reduce that stigma. One of the reasons COVID-19 is COVID-19 and SARS-CoV-2 is [because those names are] completely devoid of any geographic signifiers. The one disease that I think really sticks in the minds of people today is still Ebola virus disease, which is named after the Ebola River. So what we’re seeing—and I think the variants are bringing up this conversation again—is while it’s important to understand and control the disease within a specific geography, the conflation of a place as somehow the cause of the emergence or spread of the disease is where we run into very real challenges, where culturally specific, racially specific, nationally specific stereotypes and anxieties start to emerge. And that’s really what we fundamentally need to combat against because it leads to very, very bad public-health policy. And it also leads obviously to very significant resentments, which simmer over and lead to oppression in so many different ways. from https://ift.tt/3fdQFTB Check out http://natthash.tumblr.com When the group of teenagers surrounded my father, he might have been standing by a crate of watermelons, one hand palming a fruit, the other knocking at it for hollowness. Or maybe he was looking at the fish nestled in ice, assessing whether the cod or the halibut appeared fresher. I don’t know; I wasn’t there. What I do know is that the teenagers, white and maskless, coughed all over him. “You’re a piece of shit,” one of them said, sneering. It was right at the start of the pandemic, last February or March. I don’t know all of the details, because my father never told me anything about the encounter. I heard about what happened only months later, in June, when my mom mentioned it over the phone in a quick aside, before moving on as if she had never said it. “But don’t worry about us. Just focus on staying healthy,” she said. At that point, my parents lived in a different state, and I hadn’t seen them all year. “Do you want us to mail you more masks?” I still haven’t really discussed the incident in depth with my dad. After so long, the silence has hardened, even as anti-Asian violence has surged in the United States, including last week, when a gunman in Atlanta killed six women of Asian descent. The first time I asked my dad about his experience was when I told him I was writing this story. Many immigrants such as my dad (and my mom, who has faced her fair share of racism) have built up a code of silence with their children to not discuss the daily indignities of being Asian American. Even a moment as painful as this one is merely starting to chip away at it. [Read: Why this wave of anti-Asian racism feels different] During my childhood, my parents almost never talked about race. When they did, they fed me the immigrant clichés: We left China in the ’80s with only a few dollars and determination; we worked long, difficult hours for the careers and lives we dreamed of. See how we’ve succeeded; see how you can succeed too. Racism was something that happened to other people but never my parents. When they saw news of police brutality, they condemned it as if it were a spectacle from a distant land playing out on the screen. The few times they would break their silence have stuck with me. In the car ride home after seeing a movie as a child, I once declared that I’d be an actor when I grew up. “It’s going to be really hard,” my mother said, staring straight ahead at the road. I countered that she and Dad had said I could do anything as long as I put in the work. “But be prepared for no one to hire you. You’re Asian,” she said. I don’t remember the movie we saw that day, or what my mom said after that. I do remember my own silence for the rest of the drive. Late last year, I moved in with my parents in suburban New Jersey, hoping to spend more time with them (and save on rent) during the pandemic. I thought living with them would allow for us to have more conversations about race. But the news reports that kept appearing about racism toward Asians seemed to describe a different world from the one our household pretended to exist in. My parents have discussed recipes, my dad’s painting hobby, and my teenage brother’s college applications with me. I know they know about the stories of anti-Asian racism that are swirling around us, and they know I know, but they haven’t acknowledged them. Unsettled but unsure about disturbing the illusion, I’ve followed their lead, a thousand unsaid things on my tongue. Only when I pressed my mom for details did I learn that after the incident at the grocery store, when my dad would go back, he would drive into a parking spot, turn off the engine, and just sit there, in the quiet of his car, mustering up the nerve to go inside. When I asked my dad why he hadn’t told me about the incident, he said he must have forgotten about it. “It wasn’t a big enough deal,” he said. He didn’t say more about it after that. I told Jennifer Louise Young, a postdoctoral scholar at Stanford University who has studied Asian American families, about my dad’s silence. She wasn’t surprised. Young has found that Asian parents don’t really talk with their children about racism, whether toward Asians or other communities. She suggested that when racism targets them, parents may especially struggle to talk about their experiences because of denial or shame. Jennifer Lee, a sociologist at Columbia University who studies Asian Americans, pointed out that Asian parents might not tell their children about racism because of the vulnerability it requires. “Your father [wished] to protect you from racism and xenophobia because you’re his daughter, and obligations to protect typically run vertically from parents to children,” Lee told me. “For immigrant parents to admit that they are now the ones who need protection is a blow to their sense of well-being.” Silence is also insulation. Immigrants like my parents might stay quiet about experiences of alienation in hopes that it will help with assimilation, for themselves but especially their children. But this moment, in which we’ve seen Asians harassed, threatened, punched, stabbed, and killed, has exposed the fallacy of that bargain. Immigrants from my parents’ generation may dream of a post-racial America, but it’s a tenuous dream, one with cracks that are papered over. This dream, lovely and false, can’t possibly hold for much longer. [Read: What it’s like when the racism comes for you] Writing this story forced me to finally ask my parents why they never talk about anti-Asian racism with me or my brother. When I brought it up over dinner one night, they seemed surprised. They were quiet for a bit. “We didn’t want you two to grow up with this shadow over you,” my mom finally said. We didn’t want you to feel bad about being different.” I was surprised by her candor. “We didn’t want to place that psychological burden on you,” my dad added. They didn’t speak of denial or shame. They didn’t speak of their own injuries at all. They centered everything around my brother and me, still insulating us as they opened up about their silence. The tragedy of anti-Asian racism is that we partly can’t see it. If stories of racism aren’t shared within families, they’re likely even scarcer in official tallies of anti-Asian violence. The true scale and horror of violence against Asians in America may never be known. Although reported hate crimes against Asian Americans have risen over the past year, “I think that’s just the tip of the iceberg,” says Connie Chung Joe, the CEO of the Los Angeles chapter of Advancing Asian American Justice, an advocacy group. “We’ve seen a lot of people just not knowing, when this happens, where to go for help or to get support. And so they go nowhere at all.” At first, after the Atlanta shootings, my parents and I chatted about everything except what had happened. We talked about the best ways to stir-fry salmon (dice it into cubes) and my dad’s progress on a watercolor landscape (he had the clouds down, but the trees were rough). The weight of the news slowly descended upon us. Finally, a few days later, unable to endure the silence anymore, I brought up the shootings as we idled in the kitchen one afternoon. Yes, they’d heard the news. Such terrible news. “When you move back to the city, don’t go out after dark,” my mom said. “Don’t go out alone.” When I pointed out that most of the Atlanta victims were her age, and that she should take care as well, she shrugged. Then she finished washing the bowl of strawberries my dad had bought at the grocery store and placed it before me. from https://ift.tt/3vY924F Check out http://natthash.tumblr.com When I spoke with Letícia Soares on March 12, day 335 of her battle with COVID-19, she was celebrating an anniversary of sorts. It had been 11 months to the day since the start of her illness—an unrelenting sickness that has pinwheeled her through more than 65 symptoms, including fatigue, nausea, migraines, diarrhea, chest pain, hair loss, asthma, abdominal pain, brain fog, heart problems, and painful inflammation in both eyes. When the vaccine rollout began, she and her partner, who also has long COVID, couldn’t help but worry. “Is it safe?” she recalled thinking at the time. “Could it exacerbate our symptoms?” The clinical trials, for any of the vaccines, had no answers: None set out to study the safety and efficacy of the shots in this population. And although long COVID is a chronic and debilitating condition, it is not among the chronic and debilitating conditions that currently qualify someone for a vaccine. Soares and her partner intend to get their shots when they become eligible. Still, when news of the vaccines’ success broke, “we didn’t know what it meant for us,” Soares, a 36-year-old biologist at Western University in Ontario, Canada, told me. “There was no empirical evidence to reduce our anxiety.” Many long-haulers are still lining up for vaccination, in hope of guarding against a future tussle with the coronavirus and a more severe bout of disease. (Early evidence hints that COVID-19 survivors do produce a strong immune response to the virus, but might need the extra jolt offered by vaccines to keep their defenses high.) Now, as more shots roll out, a second potential perk has emerged: A scattering of long-haulers report that their COVID-19 symptoms have mysteriously faded after their shots—an astounding and unexpected pattern that’s captured the attention of experts worldwide. Stories of symptoms that subside after the shots are intriguing, experts told me. But no clinical trials have tested whether the vaccines can act as makeshift therapeutics for long COVID, either. It’s still unclear how common these ebbs in illness are, or how fleeting they might be. In patient-led surveys, at least as many long-haulers are reporting no postvaccination change in symptoms; a small percentage said that the shots have so far made their illness worse. Long COVID, with its constellation of debilitating, life-altering symptoms, is one of the most serious outcomes of a coronavirus infection. But it remains one of the least understood parts of the pandemic. A year into the greatest global health crisis in a century, scientists still have not settled on a consensus definition for long COVID, let alone a standard set of tests or treatments. Now long-haulers are tackling one of the biggest data vacuums yet: the collision of their condition with vaccines. If all goes well, vaccines could chip away at the long-hauler population on two fronts: preventing long COVID, and perhaps bringing some cases to an end. But as the world rushes toward the promise of a finish line, the science of long COVID once again lags behind. Until that gap is closed, our race against the virus cannot be won. My colleague Ed Yong was one of the first to report on long COVID, in June. In the nine months since, the condition has gained international recognition and sparked a small but growing number of efforts to scientifically suss out its causes, including several that will be funded by the National Institutes of Health. Without firm answers, progress on palliatives and preventives for the disease will be halting and patchwork; in many trials studying treatments for coronavirus infections, long-COVID patients have simply been left out. That’s also been the case for immunizations. When many vaccine developers’ clinical trials began last spring, long COVID wasn’t yet widely known, making it difficult to enroll people who had begun to suffer its symptoms or to check whether the shots affected the risk of contracting the condition. The result was erasure: Not asking was easier. While billions of people around the globe have seen themselves reflected in vaccine trials and their dazzling success, long-haulers have so far been offered only a distant window into someone else’s reality. That oversight may have opened up a big gap in the armor that vaccines are meant to offer. Recent studies suggest that 10 to 30 percent of people with documented coronavirus cases have experienced long-term consequences. Some lingering impacts are the products of severe coronavirus infections, which can leave organs riddled with damage that lasts months. In this population, “I’m optimistic that the vaccines will make a big dent,” Lekshmi Santhosh, a pulmonologist and long-COVID researcher at UCSF, told me. But vaccines are less likely to block the mildest forms of disease, muddying the forecast for long-COVID cases that sprout from more silent infection. Many long-haulers never became sick enough to be hospitalized; some even started out with mild or symptomless infections that only later blossomed bafflingly into debilitating disease. [Read: Don’t be surprised when vaccinated people get infected.] Akiko Iwasaki, an immunologist at Yale, has proposed three explanations for long COVID. In one, the coronavirus might linger in the nooks and crannies of some long-haulers’ bodies, evading ready detection, but still replicating enough to raise the ire of the immune system. In another, fragments of viral genes or proteins—though not infectious themselves—might remain adrift in the system, duping immune cells into launching a prolonged and unnecessarily vigorous attack. Or, perhaps, no trace of the pathogen is left; rather, its transient presence sets the immune system askew, leaving disoriented cells squabbling among themselves. Researchers haven’t yet teased these very plausible ideas apart; these hypotheses also aren’t mutually exclusive. A vaccine could, in theory, combat all of Iwasaki’s proposed scenarios by simply thwarting the virus. “If you’re not even getting infected,” she told me, the chances of long COVID disappear. Even people who aren’t rendered impervious to the virus might still have enough immunological juice to pen the pathogen in place. Researchers think some cases of long COVID could involve the virus spreading unchecked throughout the body, infiltrating tissues where it might not belong. Sequestering it early could head off its more insidious effects, says Rachel Rutishauser, an immunologist at UCSF. But none of that has yet been confirmed. Foggier still is the potential impact of vaccines on existing long-haulers. Many long-COVID survivors are understandably nervous about introducing into their body something reminiscent of the pathogen that catalyzed their illness—something that could, in theory, rouse immune cells into doubling down on their overzealous attacks. “There’s a lot of anxiety,” Denyse Lutchmansingh, a critical-care physician and long-COVID researcher at Yale, told me. “Some of these patients feel so awful that you really do not want to do something that might trigger them.” The vaccines have also been linked with a bevy of side effects that, while not inherently unsafe, echo the fevers, aches, and fatigue that long-haulers often experience. People who have already encountered the virus also seem more likely to have an initially rough go with their shots. Una Osato, a 38-year-old New York performer, writer, and educator who has had COVID-19 for more than a year, spent several days in the vise grip of flu-like symptoms after she received Pfizer’s vaccine. “It was almost a reprise of my [initial] COVID experience,” Osato told me. But she has no regrets about getting her vaccine. “I would have done it again,” she said. A small number of long-haulers might experience a longer dip in well-being after their shots, or mixed outcomes in improvement. Andrew Gold, a 64-year-old chef and cookbook editor in New York, felt some symptoms worsen after he received the Pfizer vaccine. His fatigue, shortness of breath, and aches became more severe; his blood-oxygen levels dropped. His sense of taste and smell, which had recently started to creep back, retreated once again. But he’s focusing on the positives: His erratic heartbeat has quieted slightly, and his fevers have lessened a notch. The day he got his second dose, he walked home with a bag of groceries, without stopping, for the first time in eight months. John Wherry, an immunologist at the University of Pennsylvania, told me he thinks unilateral deteriorations will be the minority. Although viruses and vaccines share features in common, the crucial differences that make the shots safe will also reduce the chances that they’ll stoke the symptomatic flames of long COVID. Many pathogens, including the new coronavirus, have evolved to purposefully discombobulate the immune system in various ways, allowing them to batter the body with ease. Vaccines, which contain no active viruses, don’t run this risk. One small study, not yet peer-reviewed, seems to bolster this idea. Researchers tracked the symptoms of 66 previously hospitalized long-COVID patients for more than eight months, 44 of whom received a vaccine earlier this year. Most of the shot recipients battled a brief bout of flu-like symptoms after their vaccination. But the side effects melted away after a couple of days. A month after the inoculations, the researchers found no evidence that the shots had consistently worsened people’s long-term symptoms. “I think there’s increasing evidence that these vaccines are not causing dramatic harm” to long-haulers, Fergus Hamilton, an infectious-disease specialist at the University of Bristol, in England, and the study’s lead author, told me. For many long-haulers, the hope that vaccines won’t exacerbate their illness might have been enough to sway them into getting their shots. But in recent weeks, hundreds of recently vaccinated long-COVID patients around the world have reported feeling not just a lack of bad side effects from their shots, but immense relief from their symptoms. For some, the improvements have already endured for weeks or months—the most extended calm some of them have had since their sickness began. When Kim Wills-Rinaldi, a 58-year-old geriatric-and-palliative-care social worker in Connecticut, first received a chance at vaccination in January, “I completely panicked,” she told me. She had spent the past 10 months dueling COVID-19 symptoms, developing shingles, arthritis, and rashes; her hair had fallen out in clumps. “I kept thinking, I’ve been so sick for a year. What if this makes me really bad again?” But two days after receiving her first dose of the Pfizer vaccine on March 12, Wills-Rinaldi awoke and found that almost all of her symptoms had vanished. “For me, this is like a miracle,” she said. Wills-Rinaldi hasn’t yet gotten her second shot, and there’s no telling whether the respite will stick. Most immunologists are still hesitant to draw firm conclusions about how common these remissions might be, but the idea of using vaccines as therapeutics “isn’t new,” Sulggi Lee, an infectious-disease physician and immunologist at UCSF, told me. A number of therapeutic vaccines are being developed against HIV and certain cancers, in the hope that they will rev up immune cells to purge roaming pathogens, or destroy aberrant or infected cells. If typical vaccines are study guides given to students before big exams, therapeutic vaccines are a next-best resource—open-book tests. Still, speculating on what soothes long COVID layers the theoretical on top of the theoretical. In a recent blog post on Medium, Iwasaki, the Yale immunologist, expanded on her three original hypotheses, appending explanations of how the vaccine might tackle each of them. In long-COVID survivors whose immune systems have struggled to evict bits of the virus, Iwasaki told me, the vaccines might marshal a wave of antibodies and T cells—some of the body’s most essential fighters—that boots out these unwanted tenants and their scrappy remains. Alternatively, the vaccines could restore balance to an unhinged immune system, refocusing its resources on guarding against pathogens instead of attacking healthy tissues. There’s precedent for this, Iwasaki said: Some treatments for autoimmune conditions, such as multiple sclerosis, counterintuitively involve riling up other branches of the immune system. This last possibility is perhaps the most precarious, as it could be “a temporary suppression” of the long-haul condition, she told me. Lutchmansingh, at Yale, likened the idea to “a kick in the pants for the immune system.” The emotional relief that many people feel after receiving their shots, and their confidence in the protection of vaccination, could also be helping long-haulers, Rutishauser, of UCSF, told me. The vaccine is “associated with a return to normalcy,” she said. The improvements documented so far shouldn’t be dismissed as a meaningless placebo effect, she added: Physical and psychological well-being can spur each other forward as some people’s sickness abates. Long COVID has been “such a lonely place,” Kelly House, a 52-year-old long-hauler in North Carolina, told me. “You almost feel like, what’s wrong with you that you can’t get past this?” House’s fatigue and headaches, which have plagued her since July, retreated the morning after she received her first dose of the Pfizer vaccine on March 10, taking a hefty slice of self-doubt and confusion with them. “I finally have good news now,” she said. Since the start of the pandemic, long-haulers have been navigating their own illness, paving paths for researchers to follow. Online support groups have swollen to many thousands of members, who have spearheaded efforts to bring recognition to their sickness. When some long-haulers first started to report that the vaccines had seemingly driven their symptoms into hiding, others rushed to immortalize those stories in data. One patient-led survey, run by the filmmaker Gez Medinger, found that among 345 long-haulers—most of them in the United Kingdom—who said they had received their first dose of a COVID-19 vaccine at least two weeks earlier, roughly a third of respondents felt that their symptoms had improved. About a fifth of the participants felt worse, and half experienced no change. Diana Berrent, the founder of Survivor Corps, a long-COVID support group, told me that similar results emerged from her group’s survey, which is tracking the symptoms of about 850 vaccinated long-haulers and counting, some 40 percent of whom say their symptoms have waned post-vaccination. (Another 45 percent said their symptoms were unchanged, while 15 percent said they had worsened.) Hannah Davis, of Body Politic, another support group, is amassing similar accounts. The mood in the past few weeks, several long-haulers told me, has started to tip toward cautious buoyancy as stories trickle in, no two quite alike. After spending 10 months with a steady drumbeat of fatigue, chest pain, congestion, shortness of breath, and burning body pain, Jean Bratman, 62, of Maryland, received her first dose of the Pfizer vaccine in January. The week after the shot, she took her first walk in three months. Now seven weeks out from her second dose, she is fully vaccinated—and for the first time in a year, “I feel nearly normal, almost symptom-free,” she said. “It’s wonderful.” In Seattle, Anne McCloskey, 54, rediscovered the taste of oranges and sushi—food that had, for the better part of a year, been colorful textures, devoid of flavor—after finishing her full course of Moderna’s vaccine in February. The shots stripped away her insomnia, heart problems, and cognitive issues that had caused her to forget her son’s birthday. Long COVID “felt like someone threw a weight on me and sunk me, like an anchor,” McCloskey told me. She is finally unmoored. [Read: Unlocking the mysteries of long COVID] Still, the numbers collected in early surveys won’t necessarily be representative. Some of the experts I talked with said they weren’t seeing rates of improvement quite so high among their own patients. Most of the patients in the University of Bristol study, for instance, “did not experience a dramatic change” in their symptoms, Hamilton told me. People’s postvaccination outcomes are “all over; it’s anecdotal,” Melissa Pinto, a nurse and long-COVID researcher at UC Irvine, told me. “We don’t even know what makes a person at risk for long COVID or how long COVID happens without a vaccine.” The shots, Pinto said, just add another perplexing variable to the jumble. “It’s a fool’s errand to try and quantify some of this yet,” Berrent, of Survivor Corps, told me. “We’re still qualifying it.” Even the best vaccines aren’t perfect preventives; they won’t be panaceas for ongoing disease, either. Nevertheless, “there’s something kind of consistent in these reports,” Iwasaki told me. “I’m hopeful that there is something real underneath.” In the coming weeks, months, and years, researchers will try to home in on what that something is. Certainly not all long-COVID survivors will experience vaccination in the same way. And the shots alone won’t magic away the scars of damaged tissue or the numbing heft of depression brought on by months of sickness. Many of the long-haulers I spoke with whose health had been ostensibly boosted by their shots said their thoughts had been consumed with the prospect of those benefits slipping away. Others who hadn’t experienced relief from their shots felt guilty that they hadn’t lived up to expectations. In New York, Osato has been flooded with messages from friends and family eager to spread the news of post-vaccine recoveries; she’s worked to gently tune it out. “I’ve needed to not focus on the possibility of my symptoms disappearing, because it sets me up to feel disappointed, sad, and hoping on what seems like a lottery,” she told me. Long COVID is not a monolith. Its origins and end points won’t be either. For every long-hauler who has gotten a vaccine, there are still dozens more who haven’t. Soares, in Toronto, is one of them. As the vaccine rollout in her region continues, she is watching with a mix of optimism and trepidation. She and her partner spend their days in a delicate dance, searching for the rare moments in which they both feel well. Perhaps, Soares told me, a vaccine will put their life back on track. But Soares isn’t betting on that possibility. What counts most, she told me, is getting the vaccine for what it was intended to do: protect against the virus itself, should she meet it again. Although what sits at the intersection of long COVID and vaccines is murky, Soares said, “my fear of reinfection is worse.” The Atlantic's COVID-19 coverage is supported by a grant from the Chan Zuckerberg Initiative. from https://ift.tt/2P8xW15 Check out http://natthash.tumblr.com |
Authorhttp://natthash.tumblr.com Archives
April 2023
Categories |