There’s something strange about this coronavirus pandemic. Even after months of extensive research by the global scientific community, many questions remain open. Why, for instance, was there such an enormous death toll in northern Italy, but not the rest of the country? Just three contiguous regions in northern Italy have 25,000 of the country’s nearly 36,000 total deaths; just one region, Lombardy, has about 17,000 deaths. Almost all of these were concentrated in the first few months of the outbreak. What happened in Quito, Ecuador, in April, when so many thousands died so quickly that bodies were abandoned in the sidewalks and streets? Why, in the spring of 2020, did so few cities account for a substantial portion of global deaths, while many others with similar density, weather, age distribution, and travel patterns were spared? What can we really learn from Sweden, hailed as a great success by some because of its low case counts and deaths as the rest of Europe experiences a second wave, and as a big failure by others because it did not lock down and suffered excessive death rates earlier in the pandemic? Why did widespread predictions of catastrophe in Japan not bear out? The baffling examples go on. I’ve heard many explanations for these widely differing trajectories over the past nine months—weather, elderly populations, vitamin D, prior immunity, herd immunity—but none of them explains the timing or the scale of these drastic variations. But there is a potential, overlooked way of understanding this pandemic that would help answer these questions, reshuffle many of the current heated arguments and, crucially, help us get the spread of COVID-19 under control. By now many people have heard about R0—the basic reproductive number of a pathogen, a measure of its contagiousness on average. But unless you’ve been reading scientific journals, you’re less likely to have encountered k, the measure of its dispersion. The definition of k is a mouthful, but it’s simply a way of asking whether a virus spreads in a steady manner or in big bursts, whereby one person infects many, all at once. After nine months of collecting epidemiological data, we know this is an overdispersed pathogen, meaning that it tends to spread in clusters, but this knowledge has not yet fully entered our way of thinking about the pandemic—or, our preventive practices. [Read: Herd immunity is not a strategy] The now-famed R0 (pronounced as “r-naught”) is an average measure of a pathogen’s contagiousness, or the mean number of susceptible people expected to become infected after being exposed to a person with the disease. If one ill person infects three others on average, the R0 is three. This parameter has been widely touted as a key factor in understanding how the pandemic operates. News media have produced multiple explainers and visualizations for it. Movies praised for their scientific accuracy on pandemics are lauded for having characters explain the “all-important” R0. Dashboards track its real-time evolution, often referred to as R or Rt, in response to our interventions. (If people are masking and isolating or immunity is rising, a disease can’t spread the same way anymore, hence the difference between R0 and R.) Unfortunately, averages aren’t always useful to understand the distribution of a phenomenon, especially if it has widely varying behavior. If Amazon’s CEO Jeff Bezos walks into a bar with 100 regular people in it, the average wealth in that bar suddenly exceeds $1 billion dollars. If I also walk into that bar, not much will change. Clearly, the average is not that useful a number to understand the distribution of wealth in that bar, or how to change it. Sometimes, the mean is not the message. Meanwhile, if the bar has a person infected with COVID-19, and if it is also poorly ventilated and loud, causing people to speak loudly at close range, almost everyone in the room could potentially be infected—a pattern that’s been observed many times since the pandemic begin, and that is similarly not captured by R. That’s where the dispersion comes in. There are COVID-19 incidents in which a single person likely infected 80 percent or more of the people in the room in just a few hours. But, at other times, COVID-19 can be surprisingly much less contagious. Overdispersion and super-spreading of this virus is found in research across the globe. A growing number of studies estimate that a majority of infected people may not infect a single other person. A recent paper found that in Hong Kong, which had extensive testing and contact tracing, about 19 percent of cases were responsible for 80 percent of transmission, while 69 percent of cases did not infect another person. This finding is not rare: Multiple studies from the beginning have suggested that as few as 10 to 20 percent of infected people may be responsible for as much as 80 to 90 percent of transmission, and that many people barely transmit it. This highly-skewed, imbalanced distribution means that having an early run of bad luck with a few super-spreading events, or clusters, can produce dramatically different outcomes even for otherwise similar countries. Scientists looked globally at known early-introduction events, in which an infected person comes into a country and found that in some places, such imported cases led to no deaths or known infections, while in others, they sparked sizable outbreaks. Using genomic analysis, researchers in New Zealand looked at more than half the confirmed cases in the country and found a staggering 277 separate introductions in the early months, but also that only 19 percent of introductions led to more than one additional case. A recent review shows that this may even be true in congregate living spaces, such as nursing homes, and that multiple introductions may be necessary before an outbreak takes off. Meanwhile, in striking contrast, in Daegu, South Korea, just one woman, dubbed Patient 31, generated more than 5,000 known cases in a megachurch cluster. [Read: The pastors already planning to rebel against future shutdowns] Unsurprisingly, SARS-CoV, an earlier novel coronavirus and the previous incarnation of SARS-CoV-2 that caused the 2003 SARS outbreak, was also overdispersed in this way: The majority of infected people did not transmit it, but a few super-spreading events caused most of the outbreaks. MERS, another coronavirus cousin of SARS, also appears overdispersed, but luckily, it does not—yet—transmit well among humans. This kind of behavior, alternating between being super infectious and fairly noninfectious, is exactly what k captures, and what focusing solely on R hides. Samuel Scarpino, an assistant professor of epidemiology and complex systems at Northeastern, told me that this has been a huge challenge, especially for health authorities in Western societies, where the pandemic playbook was geared toward the flu—and not without reason, because pandemic flu is a genuine threat. However, influenza does not have the same level of clustering behavior. We can think of disease patterns as leaning deterministic or stochastic: In the former, an outbreak’s distribution is more linear and predictable; in the latter, randomness plays a much larger role and predictions are hard, if not impossible, to make. In deterministic trajectories, we expect what happened yesterday to give us a good sense of what to expect tomorrow. Stochastic phenomena, however, don’t operate like that—the same inputs don’t always produce the same outputs, and things can tip over quickly from one state to the other. As Scarpino told me, “Diseases like the flu are pretty nearly deterministic and R0 (while flawed) paints about the right picture (nearly impossible to stop until there’s a vaccine).” That’s not necessarily the case with super-spreading diseases. Nature and society are replete with such imbalanced phenomena, some of which are said to work according to the Pareto principle, named after the sociologist Vilfredo Pareto. Pareto’s insight is sometimes called the 80/20 principle—80 percent of outcomes of interest being caused by 20 percent of inputs—though the numbers don’t have to be that strict. Rather, the Pareto principle means that a small number of events or people are responsible for the majority of consequences. This will come as no surprise to anyone who has worked in the service sector, for example, where a small group of problem customers can create almost all the extra work. In cases like those, booting just those customers from the business or giving them a hefty discount may solve the problem, but if the complaints are evenly distributed, different strategies will be necessary. Similarly, focusing on the R alone, or using a flu-pandemic playbook, won’t necessarily work well for an overdispersed pandemic. Hitoshi Oshitani, a member the National COVID-19 Cluster Taskforce at Japan’s Ministry of Health, Labour and Welfare and a professor at Tohoku University who told me that Japan focused on the overdispersion impact from early on likens his country’s approach to looking at a forest and trying to find the clusters, not the trees. Meanwhile, he believes, the Western world was getting distracted by the trees, and got lost among them. To fight a super-spreading disease effectively, policy makers need to figure out why super-spreading happens, and they need to understand how it impacts everything, including our contact-tracing methods and our testing regimes. There may be many different reasons a pathogen super-spreads. Yellow fever spreads mainly via the mosquito Aedes aegypti, but until the insect’s role was discovered, its transmission pattern bedeviled many scientists. Tuberculosis was thought to be spread by close-range droplets until an ingenious set of experiments proved that it was airborne. Much is still unknown about the super-spreading of SARS-CoV-2. It might be that some people are super-emitters of the virus, in that they spread it a lot more than other people. Like other diseases, contact patterns surely play a part: A politician on the campaign trail or a student in a college dorm is very different in how many people they could potentially expose compared with, say, an elderly person living in a small household. However, looking at nine months of epidemiological data, we have important clues to some of the factors. In study after study, we see that super-spreading clusters of COVID-19 almost overwhelmingly occur in poorly ventilated indoor environments where many people congregate over time— weddings, churches, choirs, gyms, funerals, restaurants, and such—especially when there is loud talking or singing without masks. For super-spreading events to occur, multiple things have to be happening at the same time, and the risk is not equal in every setting and activity, Muge Cevik, a clinical lecturer in infectious diseases and medical virology at the University of St. Andrews and a co-author of a recent extensive review of transmission conditions for COVID-19, told me. [Read: I have seen the future—and it’s not the life we knew] Cevik identifies “prolonged contact, poor ventilation, [a] highly infectious person, [and] crowding” as the key elements for a super-spreader event. Super-spreading can also occur indoors beyond the six-feet guideline, because SARS-CoV-2, the pathogen causing COVID-19, can travel through the air and accumulate, especially if ventilation is poor. Given that some people infect others before they show symptoms, or when they have very mild or even no symptoms, it’s not always possible to know if we are highly infectious ourselves. We don’t even know if there are more factors yet to be discovered that influence super-spreading. But we don’t need to know all the sufficient factors that go into a super-spreading event to avoid what seems to be a necessary condition most of the time: many people, especially in a poorly ventilated indoor setting, and especially not wearing masks. As Natalie Dean, a biostatistician at the University of Florida, told me, given the huge numbers associated with these clusters, targeting them would be very effective in getting our transmission numbers down. Overdispersion should also inform our contact-tracing efforts. In fact, we may need to turn them upside down. Right now, many states and nations engage in what is called forward or prospective contact tracing. Once an infected person is identified, we try to find out with whom they interacted afterward so that we can warn, test, isolate, and quarantine these potential exposures. But that’s not the only way to trace contacts. And, because of overdispersion, it’s not necessarily where the most bang for the buck lies. Instead, in many cases, we should try to work backwards to see who first infected the subject. Because of overdispersion, most people will have been infected by someone who also infected other people, because only a small percentage of people infect many at a time, whereas most infect zero or maybe one person. As Adam Kucharski, an epidemiologist and the author of the book The Rules of Contagion, explained to me, If we can use retrospective contact tracing to find the person who infected our patient, and then trace the forward contacts of the infecting person, we are generally going to find a lot more cases compared with forward-tracing contacts of the infected patient, which will merely identify potential exposures, many of which will not happen anyway, because most transmission chains die out on their own. The reason for backward tracing’s importance is similar to what the sociologist Scott L. Feld called the friendship paradox: Your friends are, on average, going to have more friends than you. (Sorry!) It’s straightforward once you take the network-level view. Friendships are not distributed equally; some people have a lot of friends, and your friend circle is more likely to include those social butterflies, because how could it not? They friended you and others. And those social butterflies will drive up the average number of friends that your friends have compared with you, a regular person. (Of course, this will not hold for the social butterflies themselves, but overdispersion means that there are much fewer of them.) Similarly, the infectious person who is transmitting the disease is like the pandemic social butterfly: The average number of people they infect will be much higher than most of the population, who will transmit the disease much less frequently. Indeed, as Kucharski and his co-authors show mathematically, overdispersion means that “forward tracing alone can, on average, identify at most the mean number of secondary infections (i.e. R)”; in contrast, “backward tracing increases this maximum number of traceable individuals by a factor of 2-3, as index cases are more likely to come from clusters than a case is to generate a cluster.” Even in an overdispersed pandemic, it’s not pointless to do forward tracing to be able to warn and test people, if there are extra resources and testing capacity. But it doesn’t make sense to do forward tracing while not devoting enough resources to backward tracing and finding clusters, which cause so much damage. Another significant consequence of overdispersion is that it highlights the importance of certain kinds of rapid, cheap tests. Consider the current dominant model of test and trace. In many places, health authorities try to trace and find forward contacts of an infected person: Everyone they were in touch with since getting infected. They then try to test all of them with expensive, slow, but highly accurate PCR (polymerase chain reaction) tests. But that’s not necessarily the best way when clusters are so important in spreading the disease. PCR tests identify RNA segments of the coronavirus in samples from nasal swabs—like looking for its signature. Such diagnostic tests are measured on two different dimensions: Is it good at identifying people who are not infected (specificity), and is it good at identifying people who are infected (sensitivity)? PCR tests are highly accurate in both dimensions. However, PCR tests are also slow and expensive, and they require a long, uncomfortable swab up the nose at a medical facility. The slow processing times means that people don’t get timely information when they need it. Worse, PCR tests are so responsive that they can find tiny tiny remnants of coronavirus signatures long after someone has stopped being contagious, which can cause unnecessary quarantines. Meanwhile, researchers have shown that rapid tests that are very accurate for identifying people who do not have the disease, but not as good at identifying infected individuals, can help us contain this pandemic. As Dylan Morris, a doctoral candidate in ecology and evolutionary biology at Princeton, told me, cheap, low-sensitivity tests can help mitigate a pandemic even if it is not overdispersed, but they are particularly valuable for cluster identification during an overdispersed one. This is especially helpful because some of these tests can be administered via saliva and other less-invasive methods, and be distributed outside medical facilities. In an overdispersed regime, identifying transmission events (someone infected someone else) is more important than identifying infected individuals. Consider an infected person and their 20 forward contacts—people they met since they got infected. Let’s say we test 10 of them with a cheap, rapid test and get our results back in an hour or two. This isn’t a great way to determine exactly who is sick out of that 10, because our test will miss some positives, but that’s fine for our purposes. If everyone is negative, we can act as if nobody is infected, because the test is pretty good at finding negatives. However, the moment we find a few transmissions, we know we may have a super-spreader event, and we can tell all 20 people to assume they are positive and to self-isolate—if there is one or two transmissions, it’s likely there’s more exactly because of the clustering behavior. Depending on age and other factors, we can test those people individually using PCR tests, which can pinpoint who is infected, or ask them all to wait it out. [Read: The plan that could give us our lives back] Scarpino told me that overdispersion also enhances the utility of other aggregate methods, such as wastewater testing, especially in congregate settings like dorms or nursing homes, allowing us to detect clusters without testing everyone. Wastewater testing also has low sensitivity; it may miss positives if too few people are infected, but that’s fine for population-screening purposes. If the wastewater testing is signaling that there are likely no infections, we do not need to test everyone to find every last potential case. However, the moment we see signs of a cluster, we can rapidly isolate everyone, again while awaiting further individualized testing via PCR tests, depending on the situation. Unfortunately, until recently, many such cheap tests had been held up by regulatory agencies in the United States, partly because they were concerned with their relative lack of accuracy in identifying positive cases compared with PCR tests—a worry that missed their population-level usefulness for this particular overdispersed pathogen. To return to the mysteries of this pandemic, what did happen early on to cause such drastically different trajectories in otherwise similar places? Why haven’t our usual analytic tools—case studies, multi-country comparisons—given us better answers? It’s not intellectually satisfying, but because of the overdispersion and its stochasticity, there may not be an explanation beyond that the worst-hit regions, at least initially, simply had a few unlucky early super-spreading events. The cities that were vulnerable are not pure luck: Dense populations, older citizens, and congregate living, for example, made cities around the world more susceptible to outbreaks compared with rural, less dense places and those with younger populations, less mass transit, or healthier citizenry. But why Daegu in February and not Seoul, despite the two cities being in the same country, under the same government, people, weather, and more? As frustrating at it may be, sometimes, the answer is merely where Patient 31 and the megachurch she attended happened to be. Overdispersion makes it harder for us to absorb lessons from the world because it interferes with how we ordinarily think about cause and effect. For example, it means that events that result in spreading and non-spreading of the virus are asymmetric in their ability to inform us. Take the highly publicized case in Springfield, Missouri, in which two infected hairstylists, both of whom wore masks, continued to work with clients while symptomatic. It turns out that no apparent infections were found among the 139 exposed clients (67 were directly tested; the rest did not report getting sick). While there is a lot of evidence that masks are crucial in dampening transmission, that event alone wouldn’t tell us if masks work. In contrast, studying transmission, the rarer event, can be quite informative. Had those two hairstylists transmitted the virus to large numbers of people despite everyone wearing masks, it would be important evidence that, perhaps, masks aren’t useful in preventing super-spreading. Comparisons, too, give us less information compared with phenomena for which input and output are more tightly coupled. When that’s the case, we can check for the presence of a factor (say, sunshine or Vitamin D) and see if it correlates with a consequence (infection rate). But that’s much harder when the consequence can vary widely depending on a few strokes of luck, the way that the wrong person was in the wrong place sometime in mid-February in South Korea. That’s one reason multi-country comparisons have struggled to identify dynamics that sufficiently explain the trajectories of different places. Once we recognize super-spreading as a key lever, countries that look as if they were too relaxed in some aspects appear very different, and our usual polarized debates about the pandemic are scrambled, too. Take Sweden, an alleged example of the great success or the terrible failure of herd immunity without lockdowns, depending on whom you ask. In reality, although Sweden joins many other countries in failing to protect elderly populations in congregate-living facilities, its measures that target super-spreading have been stricter than many other European countries. Although it did not have a complete lockdown, as Kucharski pointed out to me, Sweden imposed a 50-person limit on indoor gatherings in March, and did not remove the cap even as many other European countries eased such restrictions after beating back the first wave. (Many are once again restricting gathering sizes after seeing a resurgence.) Plus, the country has a small household size and fewer multigenerational households compared to most of Europe, which further limits transmission and cluster possibilities. It kept schools fully open without distancing or masks, but only for children under 16, who are unlikely to be super-spreaders of this disease. Both transmission and illness risks go up with age, and Sweden went all online for higher-risk high-school and university students—the opposite of what we did in the United States. It also encouraged social-distancing, and closed down indoor places that failed to observe the rules. From an overdispersion and super-spreading point of view, Sweden would not necessarily be classified as among the most lax countries, but nor is it the most strict. It simply doesn’t deserve this oversize place in our debates assessing different strategies. Although overdispersion makes some usual methods of studying causal connections harder, we can study failures to understand which conditions turn bad luck into catastrophes, and we can also study sustained success because bad luck will eventually hit everyone, and the response matters. The most informative case studies may well be those that got hit by terrible luck early on, like South Korea, and yet managed to bring about significant suppression. In contrast, Europe was widely praised for its opening early on, but that was premature; many countries there are now experiencing widespread rises in cases and look similar to the United States in some measures. In fact, Europe’s achieving a measure of success this summer and relaxing, including opening up indoor events with larger numbers, is instructive in another important aspect of managing an overdispersed pathogen: Compared with a steadier regime, success in a stochastic scenario can be more fragile than it looks. Once a country has too many outbreaks, it’s almost as if the pandemic switches into “flu mode,” as Scarpino put it, meaning high, sustained levels of community spread even though a majority of infected people may not be transmitting onward. Scarpino explained that barring truly drastic measures, once in that widespread and elevated mode, COVID-19 can keep spreading because of the sheer number of chains already out there. Plus, the overwhelming numbers may eventually spark more clusters, further worsening the situation. As Kucharski put it, a relatively quiet period can hide how quickly things can tip over into large outbreaks and how a few chained amplification events can rapidly turn a seemingly under-control situation into a disaster. We’re often told that if Rt, the real-time measure of the average spread, is above one, the pandemic is growing, and that below one, it’s dying out. That may be true for an epidemic that is not overdispersed, and while an Rt below one is certainly good, but it’s misleading to take too much comfort from a low Rt when just a few events can reignite massive numbers. No country should forget South Korea’s Patient 31. That said, overdispersion is also a cause for hope, as South Korea’s aggressive and successful response to that outbreak—with a massive testing, tracing, and isolating regime—shows. Since then, South Korea has also been practicing sustained vigilance, and has demonstrated the importance of backward tracing. When a series of clusters linked to nightclubs broke out in Seoul recently, health authorities aggressively traced and tested tens of thousands of people linked to the venues, regardless of their interactions with the index case, six feet apart or not—a sensible response, given that we know the pathogen is airborne. Perhaps one of the most interesting cases has been Japan, a country with middling luck that got hit early on and followed what appeared to be an unconventional model, not deploying mass testing and never fully shutting down. By the end of March, influential economists were publishing reports with dire warnings, predicting overloads in the hospital system and huge spikes in deaths. The predicted catastrophe never came to be, however, and although the country faced some future waves, there was never a large spike in deaths despite its aging population, uninterrupted use of mass transportation, dense cities, and no formal lockdown. It’s not that Japan was better situated than the United States in the beginning. Similar to the U.S. and Europe, Oshitani told me, Japan did not initially have the PCR capacity to do widespread testing. Nor could it impose a full lockdown or strict stay-at-home orders; even if that had been desirable, it would not have been legally possible in Japan. Oshitani told me that in Japan, they had noticed the overdispersion characteristics of COVID-19 as early as February, and thus created a strategy focusing mostly on cluster-busting, which tries to prevent one cluster from igniting another. Oshitani said to me that he believes that “the chain of transmission cannot be sustained without a chain of clusters or a megacluster.” Japan thus carried out a cluster-busting approach, including undertaking aggressive backward tracing to uncover clusters. Japan also focused on ventilation, counseling its population to avoid places where the three C’s come together: crowds in closed spaces in close contact, especially if there’s talking or singing—bringing together the science of overdispersion with the recognition of airborne aerosol transmission as well as presymptomatic and asymptomatic transmission. Oshitani contrasts the Japanese trifecta, nailing almost every important feature of the pandemic early on, with the Western response, trying to eliminate the disease “one by one” when that's not necessarily the main way it spreads. Indeed, Japan got its cases down, but kept up its vigilance: When the government started noticing an uptick in community cases, it initiated a state of emergency in April and tried hard to incentivize the kinds of businesses that could lead to super-spreading events, such as theaters, music venues, and sports stadiums, to close down temporarily. Now schools are back in session in person, and even stadiums are open—but without chanting. It’s not always the restrictiveness of the rules, but whether they target the right dangers. As Morris put it, “Japan’s commitment to ‘cluster-busting’ allowed it to achieve impressive mitigation with judiciously chosen restrictions. Countries that have ignored super-spreading have risked getting the worst of both worlds: burdensome restrictions that fail to achieve substantial mitigation. The U.K.’s recent decision to limit outdoor gatherings to six people while allowing pubs and bars to remain open is just one of many such examples.” Could we get back to a much more normal life by focusing on limiting the conditions for super-spreading events, aggressively engaging in cluster-busting, and deploying cheap, rapid mass tests—that is, once we get our case numbers down to low enough numbers to carry out such a strategy? (Many places with low community transmission could start immediately.) Once we look for and see the forest, it becomes easier to find our way out. from https://ift.tt/3cO7ukD Check out http://natthash.tumblr.com
0 Comments
Dear Dr. Hamblin, My partner and I are both blind. Since March, our primary means for getting anywhere has been walking. We haven’t ridden public transit and very rarely ride as a passenger in a car. However, we do have two tandem bikes. In normal times, our sighted friends would captain them (which is to say, be the front riders). Because this is an outdoor activity, and not face-to-face, we are wondering what the level of risk would be if both riders were masked. Is it safe to go tandem biking? Lisa Larges For all the volumes of research that have been published on COVID-19 so far, none has specifically focused on tandem bicycles. The Centers for Disease Control and Prevention has issued no guidelines. But we’re all making decisions based on imperfect information these days, and I think we know enough to confidently apply some other studies to your scenario. Generally speaking, biking is an ideal pandemic activity. It’s a great transportation alternative to riding in a car, and the presence of the bike itself mostly enforces physical distancing. Cycling has proved so opportune for the moment that in many places, the demand for bikes and the subsequent strain on the supply chain has made a decent bike almost as hard to come by as hand sanitizer that doesn’t smell like urinal cakes and vodka. I’m far from the only person endorsing pandemic cycling; in July, New Yorkers recorded 80 percent more bike rides in the exercise app Strava than they did at the same time last year. Riding a bike feels manifestly good in a world where almost nothing else does. [Tom Vanderbilt: The pandemic shows what cars have done to cities] The issue of tandem biking—or riding in close proximity to other people, as other cyclists have asked me about—is more interesting. It would, hypothetically, create some potential for transmission. You’re closer than six feet, unless you have the world’s longest tandem bicycle. Your friend in the front would be generating little aerosolized particles while they breathe—as we all do—and the airflow would direct those particles back toward you. The number of particles would increase if the other person is breathing hard (as people on bikes tend to) or talking loudly over the din of a busy street. This could all theoretically raise the chances of you inhaling some virus if your friend is contagious. That sounds bad. But we also know that several factors would be working in your favor. First, you have safety in the fact that you’re not facing each other. Because the front rider is projecting their breath forward, and you’re sitting directly behind, their head serves as a physical barrier that parts the current of air. You’d get more of their breath in your face if you were at a 45-degree angle behind them (in their “slipstream”). Second, because you’re moving, the air around you is constantly turning over. Your breaths are being washed away into the sea of air around you. The situation is entirely different than if you were on a stationary tandem Peloton in a basement. (I don’t think those exist, and I’m not sure they ever should, but the pandemic would be an especially inopportune moment to launch them.) Though no one has studied your specific scenario, some Dutch engineers published a controversial model earlier this year that suggested safe distances for outdoor exercise. Based on experiments on airflow patterns in wind tunnels, they concluded that to be entirely safe from ever inhaling anything that came out of another person’s mouth, you would need to be 16 feet behind someone who’s walking, 33 feet behind a runner, and even farther behind someone moving faster, including most bikers. These numbers made news and terrified more than a few people. [Read: Why Americans really go to the gym] The big problem with the model is that it didn’t measure whether anyone actually got infected or sick. It’s interesting to know that you could theoretically be inhaling a microscopic speck of some stranger’s sputum at such a distance, but it doesn’t mean that anything contagious is traveling that far. Nor does it mean that you could be exposed to enough of the virus to be at risk of getting infected. Researchers have yet to document cases of outdoor transmission at anywhere near 16 feet. So forget those specific figures above. Just remember that no number of feet is magic, not even six, and that any distance guideline depends on the context and length of time you’re exposed. Personally, I don’t worry about passing an oncoming runner or biker at a close distance; but I do try not to trail people closely for long. (It’s generally a weird thing to do anyway.) Technically this is sort of what you’d be doing, so I can’t tell you that tandem biking is zero risk. I can’t recommend that you go tandem cycling with a new captain every day. But if it’s one friend whom you’d trust to let into your bubble as a monogamous cycling partner, I’m going to suggest that you go ahead and saddle up the tandem bike—if you can enjoy it without worrying too much. With masks on, and assuming your friend isn’t sick or having lots of high-risk contacts, you can worry less about the virus than you would about potholes or oblivious people opening car doors into the bike lane. Whatever risk you might incur would have to be balanced against the risk of not biking. The exercise has value, socializing has value, sunlight has value, and just getting out of your same surroundings as we drag into the ninth month of the pandemic absolutely has value. from https://ift.tt/30jKncN Check out http://natthash.tumblr.com I have recently been reminded, asked, or commanded to vote approximately 6 million times. These nudges have come from the people and places I’d expect—candidates, local officials, civic and political organizations—but also, more so than in any other election year I remember, from the places I wouldn’t. Uber, Nike, Postmates, the ticket service AXS, the New York Mets, and the fast-casual restaurant chain Dig have all reminded me to check my voter registration, at least once in the past two weeks. Others, including Amazon and the home-decor retailer Lulu and Georgia, have nestled links to voting information in their usual marketing emails. Seemingly every time I open Facebook or Instagram, I am greeted by a notification about the importance of voting. Voting advocacy from people outside of traditional politics isn’t particularly new in the United States—the nonprofit Rock the Vote first partnered with MTV in 1990, producing videos with celebrities such as Madonna and Janet Jackson that implored the network’s young audience to go to the polls. But efforts from brands to get out the vote among their own customers are a recent-enough phenomenon that none of the experts I spoke with knew of any data on how common they are. The trend seems to be a logical outgrowth of the widespread activist marketing that reached a fever pitch this year. All summer, after the killing of George Floyd, brands that sell everything from lipstick to digital surveillance technology weighed in on racism and police violence—even those that profit from the abuse of Black Americans. Brands’ pivot to registering voters has made similarly strange bedfellows of some companies and their new messages. Facebook, a company whose platform is a limitless abyss of antidemocratic disinformation, is asking its users to do their duty to democracy before fully addressing the ways in which the company’s products have eroded it, both in America and abroad. (Facebook did not respond to a request for comment.) [Read: Brands have nothing real to say about racism] Now, in the face of a contentious election that’s just five weeks away, new companies join the chorus seemingly every day. No matter what they sell or how they sell it, they all seem to be comfortable marketing themselves as advocates of democracy and civic engagement, so long as their customers are willing to do the heavy lifting. Having the right to vote become fodder for corporate marketing is bleak enough. What’s worse is the reminder that even at a time when millions of people are fearful for their future and unsure of their safety, companies will nonetheless find a way to profit. Getting out the vote in America is really, really hard, and no matter who sends the emails, they can do only so much to move the dial. Relatively few people vote in America, because exercising the right can be onerous and confusing. In the 2016 presidential election, a little less than 56 percent of voting-age Americans cast a vote, a rate that lags behind that of recent national elections in Germany, Mexico, South Korea, and most developed countries. The proportion of nonvoters is even higher among young people, poor people, the working class, and immigrants. Tactics to encourage voting take many different forms, with varying levels of efficacy. Christopher Mann, a political scientist at Skidmore College who studies voting and elections, says that there is a reliable hierarchy of maneuvers to mobilize voters: The most effective is face-to-face canvassing, followed by personal phone calls. These are things that, by their very nature, brands are unlikely to engage in, because of the resources and manpower necessary to pull them off. Getting out the vote via email, as most of these brands have elected to do, isn’t totally ineffective, but its impact is far smaller. Mann says he’s not aware of any research on how effective it might be for consumer brands to send out voting information in emails or pop-up notifications. But based on how things go when political organizations use the same tactics, he’d expect it to have a marginally positive effect if done consistently and with links to resources—maybe a 1 to 2 percent bump in registrations among people who receive the information, and a quarter of a percent increase in actual votes. But in order to achieve even this level of effectiveness, companies would ideally be targeting people who are poorly served by more traditional voter outreach—poor and working-class people who don’t feel included and generally don’t participate in American politics. For many of the brands most vocal about voting, those people simply aren’t their customers. “There’s some perverse incentives here,” Mann told me. “The brands for whom there’s the most payoff for being a good citizen in this regard may have the least impact” on actually registering or motivating voters. That’s because brands that think that these kinds of messages will be beneficial to their image are likely targeting a pool of people who are already well acquainted with the electoral process—people wealthier, whiter, and more formally educated than the population at large. Facebook, a free service with more than 200 million American users, is better positioned to do real good than Sweetgreen, which sells $13 salads. [Read: Fashion’s racism and classism are finally out of style] Emails and pop-up notifications may have a negligible impact on voting when used by most companies, but they have some significant upsides for brands: They’re fast, cheap, and well liked. “Encouraging registration is a way for a corporation to project a civic-minded, nonpartisan image at little cost,” Donald Green, a political scientist at Columbia University who studies voting, told me in an email. Although messages around how to vote have become more explicitly political during the 2020 presidential campaign, Green told me, the encouragement of voting as a concept is generally unlikely to incite real rage among a company’s customer base, as long as it doesn’t endorse a candidate. So far, none of the major companies has, even though many of them lace their statements with references to the vaguely progressive values likely held by their clientele. Nike, for example, has spent years aligning itself with left-leaning causes in advertising, and its voter-outreach email simply said, “No more sitting on the sidelines. You can’t stop our voice.” The messages end up mealymouthed—these companies are willing to gesture at the maintenance of a minimally functional democracy, but are not willing to say it with their chests. Republicans buy sneakers too. All of these feel-good public efforts elide what many American corporations are: an impediment to voting, not a facilitator of it. More than 2 million people told the Census Bureau that they didn’t vote in the 2016 election because they didn’t have the time, and state laws vary widely on what kinds of accommodations employers are required to make in order to allow their employees to vote. In some states, in-person voting is restricted to a single date, lines can take hours, polls close as early as 6 p.m., and people who leave work to vote are generally not paid for that time. For those who work low-wage service jobs—people who are more likely to be younger, poorer, and from minority racial groups than the average enthusiastic voter in America—those circumstances are enough to make exercising their right to vote very difficult. Many companies that blast out emails telling customers to vote are less forthcoming with details of what, if anything, they’re doing to help their own workers get to the polls, even though that can have much more than a marginal impact. A year-long 2018 campaign by Blue Cross Blue Shield of Minnesota, for example, ended with 88 percent of its employees voting, more than 30 percentage points higher than the nationwide voting rate. But these types of voluntary efforts depend on the benevolence of the company in question. Uber recently announced that it is giving all its employees Election Day off to make sure they can vote, but that accommodation isn’t being extended to drivers, whom the company has fought vehemently to prevent from being categorized as employees. An Uber spokesperson confirmed to me that although the company has made efforts to encourage voter registration among drivers, they will not receive any reimbursement for time they spend voting. [Read: How capitalism drives cancel culture] This is all a choice, of course. If they wanted to, American politicians could do the things many other rich nations do: make voter registration automatic for all citizens, allow lengthy early-voting periods, end restrictions on voting by mail, and make Election Day a federal holiday. They could restore the Voting Rights Act to continue the fight against the country’s long history of voter suppression against Black Americans. They could open more polling places and return voting rights to people who have completed prison sentences for felonies. They could do any number of things to meaningfully address the actual reasons so few people in the United States vote, and none of them would require an email from a store that once sold me throw pillows. As long as America’s leaders decline to make the system-wide changes that would help more people vote, corporations with something to sell will seep into the void. And they’ll act out of self-interest. After all, it’s hard to continue businesses as usual in a country where the economy and social order are breaking down, as American companies that have also begun voting advocacy in Western Europe have admitted. Even when the people leading some of these companies feel a real moral obligation to encourage participatory democracy, simple corporate outreach efforts won’t fix the structural problems that mar American voting—but they can form the inexpensive basis of a nice little marketing campaign. from https://ift.tt/346N6HK Check out http://natthash.tumblr.com Editor’s Note: The Atlantic is making vital coverage of the coronavirus available to all readers. Find the collection here. On the day that a COVID-19 vaccine is approved, a vast logistics operation will need to awaken. Millions of doses must travel hundreds of miles from manufacturers to hospitals, doctor’s offices, and pharmacies, which in turn must store, track, and eventually get the vaccines to people all across the country. The Centers for Disease Control and Prevention, along with state and local health departments, coordinates this process. These agencies distributed flu vaccines during the 2009 H1N1 pandemic this way, and they manage childhood vaccines every day. But the COVID-19 vaccine will be a whole new challenge. “The COVID situation is significantly different and more complex than anything that we have had to deal with in the past,” says Kris Ehresmann, an infectious-disease director at the Minnesota Department of Health. [Read: A vaccine reality check] The two leading vaccine candidates in the U.S.—one developed by Moderna, the other by a collaboration between Pfizer and the German company BioNTech—have progressed so quickly to clinical trials precisely because they are the fastest to make and manufacture. They rely on a novel vaccine technology whose advantage is speed, but whose downside is extreme physical fragility. These vaccines have to be frozen—in Pfizer/BioNTech’s case, at an ultracold –94 degrees Fahrenheit, colder than most freezers—which will limit how and where they can be shipped. The ways these vaccines are formulated (without added preservatives) and packaged (in vials that hold doses for multiple people) also make them easier to develop and manufacture quickly but harder to administer on the ground. In other words, speed is coming at the expense of convenience. “For this first generation of vaccines, we won’t trade off safety. We don’t want to trade off effectiveness,” says Kelly Moore, the associate director of immunization education at the Immunization Action Coalition. So instead, the U.S. is planning for a vaccine that requires brutally complicated logistics. Public-health departments in states, territories, and major cities are currently drawing up vaccine plans for the end of October. It’s still unclear whether these vaccines are safe and effective—and it’s extremely unlikely that data will be available by the end of October. But the departments are getting ready. Many are already stretched thin by the ongoing pandemic, and they are now helping plan, as Moore puts it, “the largest, most complex vaccination program ever attempted in history.” The leading vaccine candidates both deploy a new, long-promised technology. Their core is a piece of mRNA, genetic material that in this case encodes for the spike protein—the bit of the coronavirus that helps it enter human cells. The vaccine induces cells to take up the mRNA and make the spike protein and, hopefully, stimulates an immune response. By using mRNA, vaccine makers do not need to produce viral proteins or grow viruses, methods that are used in more traditional vaccines and that add time to the manufacturing process. This is why Moderna and Pfizer/BioNTech have been able to get their vaccines into clinical trials so quickly. Moderna went from a genetic sequence of the coronavirus to the first shot in an arm in a record 63 days. To get a naked strand of mRNA inside a cell, scientists have learned to encase it in a package called a lipid nanoparticle. mRNA itself is an inherently unstable molecule, but it’s the lipid nanoparticles that are most sensitive to heat. If you get the vaccine cold enough, “there’s a temperature at which lipids and the lipid structure stop moving, essentially. And you have to be below that for it to be stable,” says Drew Weissman, who studies mRNA vaccines at the University of Pennsylvania and whose lab works with BioNTech. Keep the vaccine at too high a temperature for too long, and these lipid nanoparticles simply degrade. Moderna’s and Pfizer/BioNTech’s vaccines have to be shipped frozen at –4 degrees and –94 degrees Fahrenheit, respectively. Once thawed, Moderna’s vaccine can then last for 14 days at normal fridge temperatures; Pfizer’s, for five days. [Read: America is running low on a crucial resource for COVID-19 vaccines] The freezer temperature required by Moderna’s vaccine makes it difficult to ship; the ultracold temperature required by Pfizer and BioNTech’s vaccine is nearly impossible to maintain outside of a large hospital or academic center with specialized freezers. For this reason, Pfizer has devised “thermal shippers” that, unopened, can keep the vaccines frozen for up to 10 days;once opened for the first time, they have to be replenished with dry ice within 24 hours then every five days. These shippers are supposed to be opened no more than twice a day to take out vials, and must be closed within one minute. The real catch, though, is that these shippers hold, at a minimum, 975 doses of the COVID-19 vaccine. A large hospital in a city could deal with that volume, but in rural areas, a 975-dose shipment will need to be broken up into smaller ones—all while making sure the vials stay ultracold. “The other potential would be only shipping that vaccine to our more urban areas,” says Molly Howell, North Dakota’s immunization program manager, “but then we’re leaving out a lot of people who are health-care workers in rural areas or at high risk in rural areas.” To get the vaccine out to those places, her department is looking into buying frozen-transport coolers and potentially a dry-ice machine. If North Dakota is allocated, for example, 2,000 doses, the state will have to open the thermal shipper, repackage smaller allotments in dry ice, and physically drive them to rural clinics across the state. The vaccines are too precious to risk shipping conventionally. [Read: What if the vaccine works only half the time? ] The storage and handling requirements for these vaccines are especially stringent, but they’re also especially uncertain. In time, it may turn out that these mRNA vaccines can be stored at higher temperatures or can be reformulated to be stored at higher temperatures, as other vaccines have been. Scientists are actively trying to create more stable lipid nanoparticles, and Pfizer says it is working on a freeze-dried version of its vaccine that can be kept in normal freezers. These incremental improvements in storage are a normal part of the vaccine-development process, but they take time. For example, Kathleen Neuzil, a vaccine researcher at the University of Maryland, points out that the flu vaccine FluMist initially needed to be frozen but can now be stored at normal fridge temperatures. (Neuzil is also an investigator on the Pfizer/BioNTech-vaccine trial.) In the August CDC meeting where Pfizer unveiled the thermal shipper, a CDC official interjected to tell stakeholders not to go out and buy freezers in anticipation of a vaccine. The agency was exploring other storage solutions, and the requirements could change. And in fact, between that August meeting and the publication of the CDC’s vaccine-distribution playbook in September, the number of days Pfizer and BioNTech’s vaccine could be stored at fridge temperature increased from one to five. The vaccine is so new that even its manufacturer is still figuring out its minimum storage requirements. It sounds absurdly simple, but how the mRNA vaccines are packaged also imposes logistical challenges. Currently, they’re in multidose vials that have to be used or discarded within six hours of opening. Moderna’s vaccine comes in 10-dose vials; Pfizer and BioNTech’s, in five-dose vials. Unused doses can degrade over time at high temperatures and, more dangerous, can become contaminated with bacteria, because the vaccines lack preservatives. Both the multidose vials and the lack of preservatives help get a vaccine out faster, says Moore: Experts have been worrying about a shortage of glass for vaccine vials, and preservatives add complexity that can slow down vaccine development. Vaccine providers in the U.S. are unaccustomed to giving multidose, unpreserved vaccines, though. Administering them will require scheduling appointments with extra care in order to minimize waste, but also discarding unused doses if needed for safety. When multidose vaccines are used outside the U.S., according to Moore, who chairs a World Health Organization immunization committee, some waste is built into the vaccination program. “It’s okay to open a vial for one baby,” she says, because a program that doesn’t waste any doses is probably erring on the side of turning people away. But this mindset might seem counterintuitive, especially while COVID-19 vaccines remain scarce. Lastly, both Moderna’s and Pfizer/BioNTech’s vaccines require two doses per person over time, and the second dose has to come from the same manufacturer as the first dose. It also has to be administered exactly 28 days, for Moderna’s, or 21 days, for Pfizer and BioNTech’s, after the first dose—in both cases longer than the vaccines can be stored in the fridge. All of this means that having the right number of vaccines for the right people will require extensive and careful record keeping. [Read: How we survive the winter] Individual states maintain electronic immunization registries that track which residents have gotten which vaccines. What needs to be reported to the registries varies state by state; many vaccine providers, such as pharmacies and pediatrician’s offices, directly connect their records to the registry. But doctors who don’t routinely give vaccinations, such as those who see adults, might not be connected, which could mean manually inputting the data for every patient into the immunization registry. New connections to the system can also take weeks or months to establish, because of the complexity of electronic health records, Moore says. The CDC is rolling out a new Vaccine Administration Management System (VAMS) to supplement existing state registries, and it is expected to offer features such as scheduling and supply management. But VAMS has also added confusion, says Rebecca Coyle, the executive director of the American Immunization Registry Association. One issue is that VAMS requires collecting identifiable information that some states are not allowed to share from their existing immunization registries. If that’s not reconciled, vaccine providers might have to spend hours manually inputting patient data into the new system. “There’s a lot of clarification that still needs to happen,” Coyle says. “The clock has started with states to finalize their response plans, and yet there are giant chunks of information that are missing.” The two-dose requirement for these vaccines also runs up against the problem of human nature: People forget. They can’t get off work. They can’t find child care. They might even move. “That’s just normal human behavior outside of COVID,” says Azra Behlim, a senior director at the health-care-services firm Vizient. The CDC is planning to send physical vaccination-record cards for each patient along with vaccine supplies when states order their doses. It is also encouraging public-health departments and hospitals to send reminders about a second dose. This is important because even a full course of a vaccine may offer only partial protection against COVID-19, and one dose is likely to offer even less. If a vaccine is fast-tracked through an emergency use authorization rather than formally licensed by the Food and Drug Administration, that too could create bureaucratic hurdles. For example, Medicare doesn’t cover the costs of emergency-use drugs. So while the government intends to pay the cost of the vaccine and of supplies like syringes, hospitals would be on the hook for storage, scheduling, record keeping, and paying staff to actually give the injections. “Hospitals are not happy about that—at all,” Behlim says. A fix will likely have to come from Congress. Another worry for hospitals: having to juggle multiple vaccines that are not interchangeable, especially after more become available in the future. “What they’re concerned about is: I get a vaccine now in November, and then another manufacturer launches in January, and then another manufacturer in March, and three more launch in May,” Behlim says. Immunization registries can record who got which vaccine, but hospitals and clinics will still have to decide which ones to stock and how much of each. One vaccine might be more effective, but another one easier to store. A third might be most effective in older people, while a fourth could have the advantage of requiring only a single dose. The more vaccines there are on the market, the harder vaccine management becomes. In fact, with dozens of vaccines currently in clinical trials, the U.S. will very likely have multiple COVID-19 vaccines from multiple manufacturers next year. Two other vaccines are just behind Moderna’s and Pfizer/BioNTech’s mRNA vaccines, in Phase III clinical trials in the U.S. One of those is made by AstraZeneca and the other by Johnson & Johnson; both insert the genetic code for the coronavirus spike protein into a harmless virus. These vaccines take slightly longer to manufacture, because they require growing viruses, and they are also a relatively new technology. But they do not have to be frozen, and Johnson & Johnson’s can be given in just a single dose. Close behind these two are more traditional vaccines that use proteins purified from the virus, which will likely have traditional storage requirements. Of course, clinical trials still need to be completed before scientists will know whether any of these vaccines are safe and effective. “Which vaccine or vaccines will prove the safest and the most effective and the most deployable? I think we don’t know yet. And that’s why having redundancy is good,” says Dan Barouch, a vaccine researcher at Harvard. (His lab is a collaborator on Johnson & Johnson’s vaccine.) In the short run, speed is of the essence. But in the long run, these other characteristics—safety, effectiveness, and ease of use—will determine which vaccines get widely distributed. Julie Swann, who studies supply chains at North Carolina State University and who worked with the CDC during the 2009 flu pandemic, says she’s disappointed that the U.S. has put its weight behind these mRNA vaccines, which rely on new technology and whose handling imposes extra requirements on states and vaccine providers. It will be even harder to use them in developing countries. “There’s no way we can use this in some countries around the world,” she says. The good news is that more deployable vaccines are moving fast through the pipeline too. The race to a vaccine has dominated hopes for an end to the pandemic. But the first COVID-19 vaccine may not ultimately be the most important COVID-19 vaccine. from https://ift.tt/3cE6WxB Check out http://natthash.tumblr.com Experts have long feared the virus will peak again in winter. The days are now getting shorter, life is moving indoors, and the pandemic isn’t contained. How bad could the next few months get? Katherine Wells wants to know what to expect and how to prepare. She was joined at a live Atlantic Festival taping of Social Distance by her co-host, staff writer James Hamblin, and Alexis Madrigal, staff writer and co-founder of the COVID Tracking Project at The Atlantic. Listen to the episode here: Subscribe to Social Distance on Apple Podcasts, Spotify, or another podcast platform to receive new episodes as soon as they’re published. What follows is a portion of their conversation, edited for length and clarity: Katherine Wells: We’ve reached a pretty grim milestone. Two hundred thousand deaths and we’re heading into winter. I’ve been worried about winter since the beginning. We’re so dependent on being outside right now. A couple of months ago, CDC Director Robert Redfield said the winter is “going to be probably one of the most difficult times that we’ve experienced in American public health.” That’s terrifying. James Hamblin: Yeah, it seems like the writing is on the walls. As you go through New York, the solution to so much life has been: just do it outside. Open windows. Push people into empty parking spaces that are makeshift restaurants. And now, fall is starting to be in the air. Restaurants are starting to allow for 25 percent [indoor] capacity. Schools are reopening. Kids—not all kids but some kids —are meeting in class. It’s this sort of perfect storm that makes a lot of people worry about resurgence. Wells: There’s so much regional variation and there’s so much uncertainty. Alexis, you’ve been following the numbers the whole time. What do you think the winter is going to look like? Alexis Madrigal: I think the base case here, the default scenario, is that things get a lot worse. There is an alternative scenario, though. If we really look at what happened during the Sunbelt surge, we were actually better able to contain it than I thought as we were going through it at the time. A lot of overlapping half steps and a lot of imperfect but smart things came together to bring transmission rates down and eventually contain those outbreaks in Arizona and Texas and Florida without very extreme measures. We didn’t actually get rid of the virus. But we stopped runaway growth. I think the big question for me this winter is whether that same thing will happen. We know cases are going to grow. If we’re sitting on this plateau of 40,000 cases a day, the virus is pretty much everywhere. So if you’ve got community transmission everywhere, and you then increase the mobility and interaction that people have, you’re going to see more cases. It’s just happened time and time again. There is a scenario in this pandemic, though, where masking helps not only with COVID-19, but also with the flu, where testing begins to catch more contagious people, where a vaccine rolls out among crucial populations. And maybe you don’t see the darkest winter in public health. When I really look at the scenarios, you see this tremendous divergence. Maybe it’s only 500 people dying a day at the end of December. Or maybe it’s 1,500. That’s a huge difference. You’re talking 80,000 people in the hospital at any given time versus 20,000 people in the hospital. These are hugely different on-the-ground realities and it’s very hard to know precisely how to weight them. Though, like I said, I think the base case here is that things don’t go well. Wells: There’s no scenario where we get this under control soon. This is definitely with us through the winter in a devastating way. Is that your sense? Madrigal: That would be my sense, yeah. Hamblin: If Alexis said anything other than that, I would jump in and correct him. The talk of a vaccine existing has been conflated with the idea of a vaccine being widely distributed. We need to plan for a winter where a vaccine is not part of our lives. [Anthony] Fauci said that he would be happy if the vaccine were 50 percent effective. Ideally, it would be closer to 75 percent. Right now, you have polls saying about 50 percent of Americans would try a vaccine if it were available now. So, a vaccine is not going to get rid of this. Alexis is following cool testing developments, which can help and we’re hoping in November, there are rollouts of rapid tests, but those are not going to be perfect. They’re not going to be instantly everywhere. And the confluence of weather and a lack of economic stimulus ... I think people are reaching a breaking point. There are going to be a lot of things coming together right at the same time. Wells: On the vaccine, Jim, you mentioned that it may only be 50 percent or 70 percent effective. Can you explain what that means? Hamblin: No vaccine is perfect, just like no medicine is perfect. No test is perfect. At best, a vaccine offers you a really good shot that if someone coughs in your face while they’re infectious, that you’re going to be protected. But our best vaccines are not 100 percent. There will always be some people who don’t mount an effective immune response or whose immune response fades. There’s been discussion about what the effectiveness of these vaccines against this coronavirus will end up being, and how effective they would need to be to even be worthwhile. We don’t know yet. We’re waiting on these clinical trials. It’s very possible, even likely, that that effectiveness will end up being between 50 and 75 percent, meaning that you’re very likely to be protected if you have it, but you would probably still want to avoid really high risk scenarios. Once you get a whole population that’s vaccinated at that level, it’s effectively gone. But when you’re just rolling it out to start with, it doesn’t mean that you go back to doing things exactly like you used to. It would be miraculous in terms of the number of cases dropping, number of fatalities dropping, but as long as there’s still that possibility, it means life does not go back totally to normal. Wells: Right. Okay, let’s talk about testing. What are the realistic prospects of mass availability of cheap rapid at home antigen testing? Is this the kind of thing where, in December, I’ll be able to go into a drugstore, buy a box of paper-strip antigen tests and test myself every day? Is that going to happen or are we really far away from that? Madrigal: I think there will be something available, maybe not in December. But later in the winter and into the spring, I think there’ll be such tests available. One hope might be that the antigen test can soak up some of the less vital demand for tests so that PCR tests can be targeted at people who did have a high-risk exposure or who have presented with symptoms. And other technologies are coming along. For schools in particular, pooled testing, where you take a bunch of different samples and run them through the same machine in one test. This technology is kind of like coming along and has some features that are quite nice for workplaces and schools—places where you know the group, you can assign risk factors to them and you know you’re going to have continued interaction. This goes back to my main theme which is: you have all of these things coming online that could help in some way, and when you layer them all on top of each other, does that get you somewhere? That really is the question for me. I don’t think there’s any way that all those things are going to knock the virus out. But does it get you to what we’ve been doing so far: bumping along with a rate of transmission about one, which means, each person that gets infected basically infects one other person. You don’t get runaway growth of transmission, but you also don’t really suppress the thing and you continue to have community transmission out there. We’ve just been balanced on this knife edge of Rt=1. And over the winter, are we going to see that go way up or are we going to see it go way down? Or are we going to be able to stay balanced on this knife edge even as winter comes because we have this set of tools that help us stay close to that number? from https://ift.tt/363qOsZ Check out http://natthash.tumblr.com Editor’s Note: This article is part of our coverage of the The Atlantic Festival. Learn more and watch festival sessions here. In April 2018, I spoke with Bill Gates about two near certainties—that the world would eventually face a serious pandemic and that it was not prepared for one. Even then, Gates acknowledged that this was the rare scenario that punctured his trademark optimism about global progress. “My general narrative is: Hey, we’re making great progress and we just need to accelerate it,” he told me. “Here, I’m bringing more of: Hey, you thought this was bad? [You should] really feel bad.” Two years on, COVID-19 has infected at least 31 million people around the world. The confirmed death toll is nearing 1 million. Both numbers are likely underestimates. The annual “Goalkeepers Report” from the Bill & Melinda Gates Foundation, which is usually a hopeful account of an improving world, is instead a litany of loss. The global economy will decline by at least $12 trillion by the end of 2021. About 37 million people have already been pushed into extreme poverty. Twenty-five years of progress in vaccine coverage have disappeared in 25 weeks. [Read: America is trapped in a pandemic spiral] Today at The Atlantic Festival, I talked (virtually) with Gates again about the lessons that the world—the United States in particular—must learn from the coronavirus pandemic. This interview has been edited for length and clarity. Ed Yong: Bill, we last spoke about this topic in 2018, a very different time. How do you feel about the way the pandemic has played out this year? Bill Gates: Well, sadly, I think the most pessimistic view of how unprepared we were has actually played out, particularly in the United States. With something that can grow exponentially, like infectious disease, a little bit of preparedness makes such a difference. A few countries have distinguished themselves, but most countries have not. Yong: And looking at how the U.S. has fared, what has surprised you, and where do you see we’ve gone wrong? Gates: The U.S. had a lot of assets going into this. We weren’t ground zero, so the U.S. had more time to get ready. The U.S. has more PCR [polymerase chain reaction] machines than all other countries per capita. We are very blessed with an expensive medical infrastructure. And we have groups like the CDC [Centers for Disease Control and Prevention] and BARDA [the Biomedical Advanced Research and Development Authority]. So the U.S. had done more to get ready than other countries had in advance. I would have expected us to get the commercial [testing] providers up and going like South Korea or Germany or Australia did. There were so many phone calls about, We have to get diagnostic capacity up and we have to get quick results. I participated in a lot of those calls. And yet, to this day, that’s just a complete mess. Yong: I think you are one of the few people who has had direct contact with the president and the administration about the matter of pandemic preparedness. What is your assessment of America’s leaders and their response to this pandemic? Gates: Even though the U.S. didn’t do a very good job, most other countries didn’t. There were a few that had been hit by SARS or MERS that had practice understanding, Oh, wow, diagnosis, contact tracing is super important, so they are among the countries that did the best. So I’d give the U.S., like, a C–. Once it hit, the first community spread of coronavirus in the United States should have set off such alarms. This notion that the travel ban was some beneficial thing, that’s just not true. And then after the pandemic starts, there hasn’t been any coherence. [Read: How the pandemic defeated America] Now the R&D funding, I will say that’s where the U.S. actually does get the highest grade in the world. We need to complement that with funding the factories and the procurement for the global response, in which the U.S. has been absent so far. But I’m still hopeful that if there’s another supplemental bill, we’ll get about $8 billion for international COVID activities into that. Yong: Do you think that the pandemic should change the way we think about global health? In this crisis, many of the richest countries have fared appallingly, whereas many poorer ones, Senegal to Vietnam, have actually done really well. Do you think that this should be cause for humility and change in our approach? Gates: Certainly humility is called for because the damage—whether it’s economic, educational, mental health—is so large. Other than a world war, this is the worst thing that’s happened in over a century. And so we should all say, “Wow, we didn’t understand about masks; we didn’t understand about asymptomatics.” Even the medical profession. We haven’t taken understanding these different respiratory diseases quite as seriously as we should. So everyone has lessons here. Yong: I think that one of the things the pandemic has highlighted is the relevance of social interventions. The pandemic has so much widened inequities, both around the world and domestically, between rich and poor. It has disproportionately hit Black and Latinx and Indigenous communities. How are you thinking about those disparities and what needs to be done to address them? Gates: Yeah, it’s kind of unbelievable that every dimension of inequity has been exacerbated here. Every other year, [our “Goalkeeper’s Report”] has been this positive story of gradual progress—less children dying, less malnutrition, longer life spans. We get to say to the world, “Hey, pay attention to that steady progress.” This report had to deliver the news that if you only look at COVID deaths, you’re actually missing the scale of the setback. Because it’s also routine immunization, malaria, getting HIV medicines. Things are so disrupted, even gathering the numbers for that was very, very difficult. But we dropped our routine-immunization levels by over 14 percent. There’s going to have to be a stronger equity agenda, hopefully on a global basis, once we get out of this. Thirty-seven million people have been driven into extreme poverty. That’s really just gut-wrenching. [Read: The pandemic experts are not okay] Most of the time when we talk about infectious diseases, our problem is, the world doesn’t pay attention to malaria or TB. Here, because people care so much about getting the [COVID-19] vaccines, they’re actually saying, “Okay, we should maybe be even less generous.” The kind of generosity that historically has helped might even go down. Yong: Do you see those kinds of inequities also play out in the U.S.? One of my concerns is that the groups that have been disproportionately burdened by this pandemic and by this long-standing history of systemic discrimination will be last in line to receive the vaccine. What work should and can be done to reduce that inequity back home? Gates: One way to help with that is to have so much volume that you’re not making superhard trade-offs. With our vaccine expertise in the foundation, we’re trying to help with that. If multiple [vaccines] get approved, actually, the volumes could be quite large. We should look at the risk levels. And based on that, you would say that communities including Blacks and Hispanics would have higher priority. You can come up with what the equitable priority ranking should be, [but] I’m not seeing that sense of gathering the data to come up with those algorithms. It’s kind of bizarre that you have these overoptimistic projections that the vaccine will come soon. When you read the 67-page report about how it’s distributed, it doesn’t actually concretely identify the criteria or how the information is going to be gathered to do the prioritization. It’s just like everything with this—the vacuum of leadership and the unwillingness of people to step forward because it’ll say, “Oh, you know, this thing’s a mess.” Yong: You and your foundation have shaped a lot of the research, the funding space, the thinking around global health. Looking at what is happening with a pandemic this year, with the benefit of hindsight, do you see any mistakes? Would you do anything differently in the future? Gates: I think the prescription is still the same as it was before this pandemic, and the cost of doing it is in the tens of billions, not hundreds of billions. Compared to, say, defense budgets, this is not a gigantic additional burden. And, in fact, if it’s done appropriately, it will drive progress and will help us with diseases that are here today. I think we can be ready for the next time, so that if something that’s not much worse than this hits, the impact would be, you know, 5 percent of what it’s been here. Yong: Do you think that this crisis will actually spur introspection? Gates: Yes. People didn’t think about infectious diseases, mostly because we’ve made so much progress that rich countries kind of ignore them. But this thing has cost trillions of dollars. The [cost of] preparedness, as a percentage of the damage this thing has done, is not even close to 1 percent. There’s basically no country that hasn’t had very big damage. If you care about education, and if you care about race, if you care about mental health, if you care about gender, if you care about government budgets and having money to do things that you want the government to do, this has cost so much. So yes, it takes rich people getting sick. It takes rich economies being affected. But when that happens, the world gets together. If this had hit 20 years ago, with the state of biology, digital infrastructure, you would have had to just pray that it didn’t come back. Now we do have all the things that we need so that a pathogen like this wouldn’t be a big deal in the future. Yong: I hope you are right, Bill. Thank you so much for taking the time to speak to us today. Really appreciate it. Gates: Great to talk to you. from https://ift.tt/3kLqzHc Check out http://natthash.tumblr.com Editor’s Note: This article is part of our coverage of the The Atlantic Festival. Learn more and watch festival sessions here. Yesterday, after weeks of reports about political interference in the efforts of government scientists and public-health experts to inform Americans about the pandemic, Anthony Fauci, the director of the National Institute of Allergy and Infectious Diseases, directly addressed the two Trump-administration officials at the center of the recent controversy: Michael Caputo, a spokesperson for the Department of Health and Human Services, and Caputo’s former science adviser, Paul Alexander, who attempted to censor what scientists, including Fauci, said about the coronavirus. “Caputo enabled Alexander,” Fauci told me over email. “Alexander is the one who directly tried to influence the CDC (he may have succeeded, I cannot really say) and even me (I told him to go take a hike).” Fauci’s comments came after his appearance at The Atlantic Festival yesterday evening. As first reported by Politico, Alexander tried to directly intervene in the publication of the Centers for Disease Control and Prevention’s well-known publication Morbidity and Mortality Weekly Report, and wrote scorching emails about CDC officials. He also tried to prevent Fauci from advocating for children to wear masks. Caputo ranted on Facebook Live about “deep state” operatives in the public-health infrastructure. The interference from Caputo’s team had drawn sharp rebukes from the public-health community, especially as it does indeed appear to have been at least partly successful at influencing the CDC’s messaging. Caputo is now on medical leave, and Alexander was dismissed from HHS last week. (Alexander and HHS did not immediately return requests for comment.) Watch: Atlantic staff writer alexis madrigal in conversation with anthony fauciAt the festival, Fauci urged Americans to maintain faith in the nation’s public-health institutions, despite the battles between political appointees at HHS and CDC researchers. “I think we could put that behind us right now,” he said. “I would trust the CDC, and I would trust the FDA.” The agencies’ troubles haven’t disappeared with Alexander’s departure: This week, the CDC again ran into controversy when it posted, then retracted new guidance on how the coronavirus spreads. But the most serious problems of the American response to the pandemic, Fauci asserted, were much broader and deeper. With at least 200,000 Americans now dead from COVID-19, he said, “obviously the numbers speak for themselves.” After the virus hit the Northeast, exacting a fearsome toll, Fauci said, states across the Sun Belt allowed case numbers to grow over the summer, which meant the U.S. was never able to get the baseline of cases low enough to mitigate the risks of reopening. “We’re looking at 40,000 new cases per day,” he said. “That’s unacceptable, and that’s what we’ve got to get down before we go into the more problematic winter.” [Read: How we survive the winter] Fauci’s message conveyed a new level of urgency about the challenges ahead. Two weeks ago, he told The Atlantic that the country had to get new daily cases down to 10,000 over “the next few weeks” to guard against surges in the winter, when containment will be even harder in many parts of the country as the weather grows colder. Cases, however, have remained near that 40,000-a-day plateau. There are signs that some states, such as Wisconsin, may be on the verge of bigger outbreaks. Time is running out to bring down viral spread. How might the U.S. get those cases down? The path is well known, and Fauci ticked off the public-health mantras: ubiquitous masking, physical distancing, avoiding crowds, doing things outdoors when possible, and washing your hands. What’s less clear is how anything might change in the U.S. over the next few months, because public-health officials have long been saying that these things were necessary to constrain the virus. Fauci pointed out that their advice continues to be met with furious resistance and violent rhetoric from America’s right-wing fringe. “People have been threatening me as a public-health person, literally threatening me and my family,” Fauci said, “because I’m saying we should be doing public-health things like wearing a mask and physical distancing, as if I’m doing something that is harmful to them … not that the virus is hurting us.” [Read: Anthony Fauci, lightning rod] Fauci is much more optimistic about the development of a vaccine, which has progressed at an unprecedented speed. He cited the large-scale, Phase 3 clinical trials currently under way in the U.S. “The results that we have actually do look good,” he said. (One trial, AstraZeneca’s, remains partly on hold after two participants developed serious neurological illnesses.) The federal government’s investments in vaccine development and production are a bright spot in the American response, which otherwise has been uncoordinated, chaotic from the top down, and predicated on pinning blame on individual states. By contrast, Operation Warp Speed, a name Fauci often decries because it sounds reckless, has been well funded, organized, and effective. In normal circumstances, vaccine makers would wait until after clinical trials conclude to begin manufacturing, but government funds have allowed them to begin over the past several months. “If we get an answer, let’s say, November, December—it’s possible it could be earlier, but I think it’s going to be likely November, December,” Fauci said, “we can then start vaccinating people, starting with the health-care workers, … the elderly, and those with underlying conditions.” The Trump administration’s political rhetoric about vaccine development has raised alarm among other public-health experts. In the lead-up to the election, Trump has begun teasing that a vaccine could be available in weeks. Some have wondered whether the design of the current trials, released after substantial public pressure, will actually reveal the information that’s needed about these new vaccines. “The trials need to focus on the right clinical outcome—whether the vaccines protect against moderate and severe forms of COVID-19—and be fully completed,” wrote Eric Topol, a molecular-medicine professor at Scripps Research, and Peter Doshi, a professor at the University of Maryland School of Pharmacy, in a New York Times op-ed yesterday. People across the political spectrum also are expressing uncertainty about taking the vaccine, which could blunt the positive effects of its availability. So, as we approach winter, there are two wildly different stories to tell about what might happen. In the storybook ending, a vaccine becomes available, more testing reduces the number of contagious people, and the country brings the virus under control. In the darker scenario, vaccines are delayed, or even if one arrives, few people accept it as safe. Testing is ineffective, and collapsing social cohesion leads to less adherence to simple, effective public-health measures. [Read: A vaccine reality check] Throw in a presidential election, flu season, climate chaos, rampant misinformation online, and the path the country may end up on is not at all clear. “What the general public needs is a message that’s consistent, and that they can believe,” Fauci said. “And what’s happened, unfortunately—and I think you’d have to be asleep not to realize this—is that we are living in a very divisive society right now; there’s no doubt about that … It’s politically charged, and what’s happened is that public-health issues and public-health recommendations have taken on a we-versus-them approach.” Can America’s science-and-technology infrastructure save us from a crumbling politics of grievance and anger? Not even a public servant with a record like Fauci’s can predict that. from https://ift.tt/2FTlRrY Check out http://natthash.tumblr.com Editor’s Note: Every Wednesday, James Hamblin takes questions from readers about health-related curiosities, concerns, and obsessions. Have one? Email him at [email protected]. Dear Dr. Hamblin, I heard an immunologist on the radio today say that a coronavirus vaccine could be only 50 percent effective, in which case we’d still have to “live” with the virus even after it arrives. With all the talk of the vaccine being the way out, this is terrifying. What if the vaccine isn’t totally effective? Will the virus really be with us forever? Sydney Levitt Toronto, Canada No vaccine is perfectly effective. That isn’t bad news; it’s just a basic fact. No medicine is perfectly effective, no parachute is perfectly effective, and no person is perfectly effective at … whatever it is they do. But though vaccines are only partly effective at protecting a single person, they can still be extremely effective collectively. Vaccine “effectiveness” takes into account lots of different factors: What percentage of vaccinated people develop antibodies? How many antibodies? How long do the antibodies last? How well do they protect the person from disease? Ultimately, you’re left with a rough average: what percentage of people who get vaccinated are protected for a meaningful amount of time. [Read: A vaccine reality check] The most successful vaccines that we have, such as those against measles, are about 97 percent effective—meaning almost everyone develops fully protective, long-lasting immunity. Not every vaccine is so reliable. Technically, all that a vaccine does is stimulate our immune systems. From there, it’s up to our bodies to develop and maintain immunity—without inadvertently attacking our own cells in the process. Vaccines are developed to try and thread the needle of stimulating a robust and lasting antibody immune response while not making anyone too sick. As we’ve seen with the flu vaccine, which fewer than half of Americans choose to get most years, even a slight chance of a sore arm or a mild fever after a shot will deter some people from getting it—let alone a one-in-a-million chance of a more serious reaction. The variability of our immune responses is the quintessential challenge of vaccine making. It is why safe and effective vaccines take so long to develop. Even once you have an effective formula, the process of vaccination has historically happened over decades, not months or years. The first polio inoculation studies were initiated in the 1930s, and a viable vaccine wasn’t discovered until the 1950s. Even though global eradication efforts began in the 1980s, there are still dozens of known cases of the disease every year, mostly in children. Through a century of vaccination efforts, smallpox is the only virus that has ever been totally eliminated through vaccination. Developing a vaccine is never easy, but the coronavirus makes it uniquely challenging. The virus can affect people in many ways and to varying degrees of severity, largely because our immune systems respond very differently from person to person. When the vaccines eventually come, we should expect that some people will respond differently than others. For that reason, especially with a new vaccine that’s being produced at a fraction of previous record speeds, drugmakers and regulatory agencies could have an incentive to err on the side of under-stimulating the immune system, rather than overstimulating it and potentially causing unwanted symptoms. This would mean that fewer people would be fully protected after taking the vaccine, but might mean that more people take the vaccine. (The Food and Drug Administration doesn’t specify an exact minimum level of effectiveness in order to take a product to market.) We don’t know how the numbers will play out yet, but we should have a preliminary sense as clinical trials wrap up near the end of the year. Each vaccine candidate—and there are dozens—could have different numbers. During the Phase 3 trials that are happening right now, people are being monitored to see whether they contract COVID-19 despite having been vaccinated. The process could have been sped up with a controversial approach known as vaccine challenge trials, in which people volunteer to be purposely exposed to the virus. But the scientific community opted not to do that for ethical reasons. Instead, we are waiting to see whether people are infected organically. This takes time. The longer that trials go on, the more valuable the results. But even if a trial lasted five years, the results wouldn’t be able to account for every possible long-term, real-world condition. The process can give only a window into what’s likely to happen when billions of people take the product. But do not expect a vaccine to give you 100 percent certainty of protection. [Read: America is running low on a crucial resource for COVID-19 vaccines] Still, if everyone in a population takes a vaccine that is, say, 70 percent effective, the effects add up quickly. The result is a population that is protected—and that more quickly achieves “herd immunity” than a population with a less effective vaccine. Occasional cases of COVID-19 might arise, but enough people will be protected to prevent widespread outbreaks. When Anthony Fauci, the head of the National Institutes of Allergies and Infectious Diseases, mentioned the possibility of a vaccine being 50 percent effective, he wasn’t saying it as though the vaccine would be a failure. He was saying he would consider it a success—an intervention worth using, and better than nothing. Though, his hope would be to start with a product that’s somewhere closer to 75 percent effective. No matter how effective the coronavirus vaccines prove themselves to be, their overall impact will ultimately depend on how many people take them. That means how many people have access to them globally, as well as how many people consent to taking them. In a Pew Research Center poll out this week, only 21 percent of Americans surveyed said they would “definitely” take a vaccine if it were available now. This rate is half of what it was in May, and has decreased in step with the president’s unsubstantiated and impossible claims about a vaccine being widely available before the election. People will rightly require transparency and rigor from their politicians and public-health officials if a vaccine is to be widely trusted and used. The most valuable thing that any population can have in a pandemic is clear, accurate information. Without this, even a mythical, perfectly effective vaccine could fail to stop the pandemic. “Paging Dr. Hamblin” is for informational purposes only, does not constitute medical advice, and is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. By submitting a letter, you are agreeing to let The Atlantic use it—in part or in full—and we may edit it for length and/or clarity. from https://ift.tt/3kIBHoc Check out http://natthash.tumblr.com Sometime this week, alone on a hospital bed, an American died. The coronavirus had invaded her lungs, soaking them in fluid and blocking the exchange of oxygen and carbon dioxide that makes up our every breath. Her immune system’s struggle to fight back might have sparked an overreaction called a cytokine storm, which shreds even healthy tissue. The doctors tried everything, but they couldn’t save her, and she became the 200,000th American taken by COVID-19—at least according to official counts. In reality, the COVID-19 death toll probably passed 200,000 some time ago. And yet “the photos of body bags have not had the same effect in the pandemic” as after other mass-casualty events such as Hurricane Katrina, says Lori Peek, a sociologist at the University of Colorado Boulder who studies disasters. “Is our national empathy—our care and love and concern for one another—at such a low level that we are not truly feeling, in our bones, in our hearts, and in our souls, the magnitude of the loss?” It’s hard for anyone to comprehend the sheer horror of mass death. As I wrote in April, “compassion fade” sets in when victims are no longer individuals but statistics, and few Americans have witnessed something of this scale before. But there’s an additional explanation for this empathy deficit: Part of the reason this majority-white, majority-non-elderly country has been so blasé about COVID-19 deaths is that mostly Black people and old people are dying. Eight out of 10 American COVID-19 deaths have been among people older than 65; the rest of the dead are disproportionately Black. White people’s brains psychologically sort minorities as “out-groups” that stir less empathy. Segregated neighborhoods have also helped insulate white Americans from the horror Black Americans face, because the ambulance sirens and the packed hospital wards are typically far from their own zip codes. “We literally don’t see those deaths in the same way we might if we didn’t experience segregation,” says Nour Kteily, a management professor at Northwestern University who studies hierarchies. Ageism reduces human beings’ capacity for caring too. Globally, people don’t value elderly lives as much as they do young people’s, research shows. When it comes to deciding who lives or dies, there’s a disregard for the elderly, even among the elderly. Discrimination against the old is perplexing, because age will ultimately catch us all. Though no white person will ever be a Black person, every person, if all goes well, will get old. But several studies that forced people to imagine life-and-death decisions hint at how little society values the elderly. One major insight into this phenomenon comes from a 2018 study called the “Moral Machine experiment,” which invites participants to determine how to program a self-driving car. People who play the Moral Machine game are shown two images, each of which depicts an out-of-control car driving into a different group of people (or, in some of the images, a cat or a dog.) For example, the game might tell the player that if you let the car plow ahead, the car will kill three little girls and two adult men. But if you swerve to the right, the car will instead kill two elderly men, two elderly women, and another, non-elderly woman. Would you swerve, or stay straight? Who would you kill? After it launched in 2016, the Moral Machine experiment went viral a few times, which meant that millions of people in 233 countries and territories ultimately played it. Through the game, its authors were able to glean country-specific preferences for sparing or sacrificing different types of lives. The strongest signals that came out of all those sessions were that people preferred to spare a greater number of lives, to spare human lives, and yes—to spare young lives. The most likely lives to be saved in these simulated car accidents were those of babies, children, pregnant women, and male and female doctors. Male or female homeless people and overweight men, meanwhile, were likely to be sacrificed. Overall, older men and women were some of the least likely to be spared, ranking just above dogs, human criminals, and cats—disturbingly, in that order. (“People like dogs,” says Azim Shariff, a social psychologist at the University of British Columbia and one of the authors of the study. This could explain why the large number of coronavirus cases in prisons has also provoked a collective yawn from policy makers.) Interestingly, people of all ages and backgrounds generally agreed on who to kill. Older players were less likely to sacrifice the older pedestrians than younger players were, but they still did it. As Texas Lieutenant Governor Dan Patrick, himself a septuagenarian, has said, “As a senior citizen, are you willing to take a chance on your survival in exchange for keeping the America that America loves for its children and grandchildren? And if that is the exchange, I’m all in.” “All things being equal, people were willing to place a priority on sparing a younger person to sacrifice an older person,” Shariff says. This preference for sacrificing the old to save the young was found in every country. The only places where people showed a weaker preference for killing the old—though they still preferred it to sacrificing the young—were in East Asian countries, such as Japan and Taiwan, and in majority-Muslim countries, such as Pakistan and Saudi Arabia. The two countries where people most preferred to sacrifice the elderly, meanwhile, were France and Italy. At the peak of the pandemic, this question became real for Italians, and doctors in the most affected regions of Italy used 80, or even 65, as their “cutoff age” for access to scarce ventilators. Shariff and his team didn’t ask people why they preferred to kill the old, but judging by anecdotal reports, such as YouTubers playing the game for their viewers, people seemed to rationalize that the elderly had fewer years left to live. Indeed, doctors follow a similar logic. In a May paper in the New England Journal of Medicine, a group of doctors from different countries suggested that hospitals consider prioritizing younger patients if they are forced to ration ventilators. “Maximizing benefits requires consideration of prognosis—how long the patient is likely to live if treated—which may mean giving priority to younger patients and those with fewer coexisting conditions,” they wrote. Perhaps, on a global scale, we’ve internalized the idea that the young matter more than the old. The Moral Machine is not without its criticisms. Some psychologists say that the trolley problem, a similar and more widely known moral dilemma, is too silly and unrealistic to say anything about our true ethics. In a response to the Moral Machine experiment, another group of researchers conducted a comparable study and found that people actually prefer to treat everyone equally, if given the option to do so. In other words, people didn’t want to kill the elderly; they just opted to do so over killing young people, when pressed. (In that experiment, though, people still would kill the criminals.) Shariff says these findings simply show that people don’t like dilemmas. Given the option, anyone would rather say “treat everybody equally,” just so they don’t have to decide. Bolstering that view, in another recent paper, which has not yet been peer-reviewed, people preferred giving a younger hypothetical COVID-19 patient an in-demand ventilator rather than an older one. They did this even when they were told to imagine themselves as potentially being the older patient who would therefore be sacrificed. The participants were hidden behind a so-called veil of ignorance—told they had a “50 percent chance of being a 65-year-old who gets to live another 15 years, and a 50 percent chance of dying at age 25.” That prompt made the participants favor the young patient even more. When told to look at the situation objectively, saving young lives seemed even better. To Shariff, his study and others support what many already suspect to be true—that certain deaths bother us more than others do. “If it was attractive, 15-year-old, blond, soccer-playing children who are dying, then we would have more of a concern,” he says. At 74 years old, President Donald Trump falls smack in the COVID-19-death demographic. Yet he has also minimized the threat of the virus repeatedly. This makes sense: The elderly themselves don’t care much about protecting the elderly because they typically don’t think of themselves as such, says Susan Fiske, a Princeton psychologist who has studied ageism and other prejudices. The “old” are always just a little bit older than ourselves. For the rest of us, there might be a more sinister impulse behind ageism. Most of us know someone who is elderly, be they an aging parent or grandparent, and those ties make us subconsciously crave control over how the elderly behave, Fiske says. Younger people subconsciously want to be sure that the elderly don’t hog a disproportionate amount of time and resources. “Older people are expected to step aside,” she told me. The only American cultures that have consistently positive views of the elderly are African Americans and Native Americans, Fiske has found in surveys. She’s not sure why, but speculates that the adversity these communities have faced has made them prize older people’s wisdom and experience. Likewise, some experts have pushed back against the assumption that young COVID-19 patients are more worth saving than the old. Fifty-year-olds, for example, might be more useful for the economy because they have skills and experience that 20-year-olds don’t have. Utilitarians would argue that policy makers should simply maximize the total number of years people have left to live; the young certainly have more. But the fact that mostly older people are dying has helped justify something that isn’t justifiable. It’s helped public officials look away when they should be taking action. from https://ift.tt/3iTTIPz Check out http://natthash.tumblr.com Editor’s Note: The Atlantic is making vital coverage of the coronavirus available to all readers. Find the collection here. Last Monday, when I called the cardiologist Amy Kontorovich in the late morning, she apologized for sounding tired. “I’ve been in my lab infecting heart cells with SARS-CoV-2 since 6 a.m. this morning,” she said. That might seem like an odd experiment for a virus that spreads through the air, and primarily infects the lungs and airways. But SARS-CoV-2, the new coronavirus behind the COVID-19 pandemic, can also damage the heart. That much was clear in the early months of the pandemic, when some COVID-19 patients would be hospitalized with respiratory problems and die from heart failure. “Cardiologists have been thinking about this since March,” said Kontorovich, who is based at Mount Sinai. “Data have been trickling in.” Autopsies have found traces of the coronavirus’s genetic material in the heart, and actual viral particles within the heart’s muscle cells. Experiments have found that SARS-CoV-2 can destroy lab-grown versions of those cells. Several studies have now shown that roughly 10 to 30 percent of hospitalized COVID-19 patients had high levels of troponin—a protein released into the blood when the heart’s muscle cells are damaged. Such patients are more likely to die than others with no signs of heart injury. This is worrying for people with severe symptoms, but more recently, a few studies suggested that COVID-19 can cause heart inflammation, or myocarditis, even in people who showed mild symptoms, or had recovered. These results were controversial but concerning. Myocarditis is frequently caused by viruses, and resolves on its own in many cases. But it can progress to more severe heart problems, and is one of the leading causes of sudden death in young adults. These studies contributed to decisions by two college football conferences—the Big Ten and the Pac-12—to cancel their fall season. (The Big Ten has since reversed its call, and the Pac-12 is considering doing the same) These developments have only added to COVID-19’s mystique. News stories and scientific articles have spun a narrative about a bizarre virus that behaves like no other, and a supposedly respiratory illness that should perhaps be reconsidered as a vascular disease. But several cardiologists and virologists I’ve talked with say such claims are overblown. COVID-19 is a severe disease that should be taken seriously, but it’s not all that strange. It seems that way in part because it is new and extremely widespread, and so commands our full attention in the way that most viral illnesses don’t. Hundreds of researchers are studying it. Millions of people have been infected by it. And every study, every news story, and every unusual detail quickens the pulse. From a virus’s point of view, the heart is both an easy target and a terrible one. It is easy to reach and invade because it collects blood from all over the body and, unlike the brain, has no protective barrier. But infecting the heart also risks killing the host without triggering symptoms that would allow a virus to easily spread—coughing, sneezing, diarrhea, or vomiting. For that reason, viruses that affect only the heart “do not exist,” says Efraín Rivera-Serrano, a virologist at the University of North Carolina at Chapel Hill. But viruses can incidentally affect the heart. They do so often enough that in the Western world, they are the most common cause of myocarditis. At least 20 known viruses can trigger this condition, including those that cause influenza, Zika, dengue, and measles. The list also includes the original SARS virus: One Toronto-based study found its genetic material in seven of 20 autopsied hearts. These hearts also had myocarditis. By contrast, autopsied hearts with traces of the new coronavirus typically don’t (with some exceptions). The virus was there, but whether it was actually doing anything is unclear. But a virus doesn’t need to be in the heart to wreak havoc. It can cause indirect damage by attacking the lungs and starving the heart of oxygen, or by triggering an inflammatory immune response that affects the entire body. Even viruses that primarily affect the gut (like enteroviruses) or the respiratory system (like adenoviruses) can cause myocarditis in this way, when molecules produced at the site of infection travel through the bloodstream and inflame the heart. Coxsackie B, for example, is the most widely studied cause of viral myocarditis, but is primarily a gut virus that spreads through fecal contamination; it can infect the heart, but it does much of its damage via the immune system. “To say a virus is cardiac or vascular or respiratory simplifies things too much,” says Paul Checchia, a cardiologist at Texas Children’s Hospital. “Anytime a pathogen invades the body, the whole body reacts.” SARS-CoV-2 is no exception. The immune system’s response to this coronavirus can be slow to kick off, but then prolonged and severe. These immune overreactions are similar in kind to those triggered by other respiratory viruses, like influenza, but greater in degree. The heart could potentially be caught in this stronger crossfire. But how often does that happen? In the early months of the pandemic, it seemed clear that the risk of heart injuries was “directly proportional to the severity of the illness,” says Neel Chokshi, a sports cardiologist at the University of Pennsylvania. But in July, a team led by Valentina Puntmann at University Hospital Frankfurt, in Germany, complicated that picture. The researchers showed that 78 percent of people who had recovered from COVID-19 (including many who had never been hospitalized) still had some kind of heart abnormality that was detectable on MRI scans two months later. About 60 percent still had signs of myocarditis. The study was explosive. It spawned a wave of articles and papers about the possibility that COVID-19 could inflict stealthy and prolonged harm upon the hearts of people who aren’t outwardly sick, and reportedly influenced decisions about whether college athletes should be allowed to play. These intense discussions sparked intense criticism. Other scientists slammed the study for several errors, including data that were missing, reported incorrectly, or analyzed with the wrong statistical tests. The Frankfurt team corrected its paper, and says the main conclusions still stand. “I think the data are good,” says Tiffany Chen of Penn Medicine, who specializes in cardiac imaging and was not involved in the study. “These were relatively healthy, mild cases of COVID-19, and they had a lot of abnormalities. It’s unsettling.” But the clinical implications of these findings—what they mean for COVID-19 patients whose symptoms have abated, but whose MRI scans are abnormal—aren’t yet understood, she says. Viral myocarditis isn’t always a problem. It’s entirely possible that you have had the condition at some point in your life without ever realizing it. Some people recover but have persistent scarring that weakens their heart and increases the risk of problems years down the line. And in a third group, the inflammation rapidly worsens, leading to faulty heartbeats, heart failure, or even death. The latter two outcomes are rare, but “it’s really hard to give accurate percentages,” says Chokshi. Doctors typically see cases of viral myocarditis only when they fall into the third group, and severe symptoms warrant MRIs and other diagnostic tests. “We don’t do MRIs on everyone who has the flu, so we don’t know how many have inflammation or what their long-term outcomes are,” says Martha Gulati, the cardiology chief at the University of Arizona. For example, in two small pilot studies, Checchia found signs of heart damage in 40 and 55 percent of children who were hospitalized with RSV—a common respiratory virus. “On discharge, they seemed perfectly fine,” he says. “But we couldn’t get funding to look at them months or years down the line.” Without that information, it’s hard to know what to make of the Frankfurt COVID-19 study or others like it. Yes, some patients have myocarditis—but what does that mean? How do the numbers compare to other respiratory viruses? Will COVID-19 patients with myocarditis recover fully, or will some have long-term problems? Is this virus doing something strange, or are researchers just studying it more intensely than other viral infections? For now, it’s difficult to say. The worry is that COVID-19 is doing whatever it’s doing at scale. The original SARS epidemic of 2003 infected only 8,000 people, killed slightly fewer than 800, and was over in three months; its impact on the heart was “lost in the historical bin of the scientific literature,” says Checchia. SARS-CoV-2, by contrast, has infected at least 31 million people and killed at least 960,000. Its effects are thousands of times more obvious than its predecessor’s. Even if it’s no worse than any other viral illness, its sheer scope means that a tiny risk of severe long-term problems would still translate to a lot of failing hearts. Reassuringly, “there hasn’t been an obvious influx of patients being admitted to the hospital with unexplained myocarditis, despite the huge numbers who have had COVID-19,” says Venkatesh Murthy, a cardiologist and radiologist at the University of Michigan. “I don’t find it convincing that there is a major amount of serious clinically relevant myocarditis in people who are feeling well.” Still, he and others say that long-term studies are important. “We’re still early,” says Chen. “I don’t think there’s a defined time point when we’d expect to see heart failure, so we have to follow these patients for months or years down the road.” That can be unnerving for people who are currently sick. Long-haulers, who are struggling with months of debilitating COVID-19 symptoms, are “responding to the media’s interpretation of these studies and, to put it bluntly, are rightfully freaking out,” said Kontorovich, who is part of a team that provides care for long-haulers. But for now, she sees the myocarditis issue and the long-hauler phenomenon as separate matters. Some long-haulers have been diagnosed with dysautonomia—a group of disorders that disrupt involuntary bodily functions, including heartbeats (which can become inexplicably fast) and blood pressure (which can suddenly crash). But people who have lingering heart problems after viral myocarditis don’t usually experience the chronic symptoms that long-haulers do, and they typically have measurable changes to their hearts that long-haulers don’t. “There may be a connection, but it hasn’t been proved,” Kontorovich said. College athletes are also facing immediate decisions. In just the past two months, the 27-year-old basketball player Michael Ojo died from a heart attack during a practice, while the 20-year-old football player Jamain Stephens Jr. died from a blood clot in his heart. Both had previously contracted COVID-19. In a recent study, a research team at the Ohio State University scanned the hearts of 26 college athletes who tested positive for COVID-19 and had mild or absent symptoms. Four of them—15 percent—had signs of myocarditis. But the Ohio study didn’t examine a control group of similar athletes who didn’t have COVID-19, and even healthy athletes experience changes in their heart as they train, including features that are “similar to what you might see with infections or scarring,” says Gulati, the cardiologist at the University of Arizona. If athletes come down with clinical myocarditis—that is, with obvious signs of heart problems—they’re taken out of play for at least three months to let the infection run its course and to give the heart a chance to bounce back. The question now is: What to do about the people who have subclinical myocarditis after COVID-19, which presents with no symptoms and can be seen only on a medical scanner? Chokshi, the sports cardiologist, says the risk that these abnormalities will lead to heart failure “is very, very low,” but “the outcome is catastrophic.” The American College of Cardiology published guidance advising that all athletes who test positive for COVID-19 rest for at least two weeks, even if they show no symptoms. Setting myocarditis aside, it still makes sense to stop players from spreading the virus to one another, especially when so many colleges are facing large outbreaks. “There are plenty of reasons to not play football independent of this issue,” Murthy says. “We already have plenty of evidence to take COVID-19 seriously.” As pandemics get wider, they feel weirder. Ebola was identified in 1976, but its ability to affect eyes, linger in semen, and afflict survivors with long-term complications wasn’t fully appreciated until it infected 28,000 people in West Africa, from 2014 to 2016. Zika was identified in 1947, but its ability to cause microcephaly—a condition where babies are born with small heads—wasn’t noted until the explosive epidemic of 2015. When millions of people become infected, rare events become commonplace, and phenomena that might typically have gone unnoticed suddenly become prominent. This creates a deceptive sense that the disease in question is stranger than most, and has uprooted the world because there’s something inherently odd about it. COVID-19 is different only in that everyone is encountering it for the first time during a pandemic. The world has gone from complete ignorance to an onslaught of detail in a matter of months, and those details can seem jarring. The virus affects the heart. Also, the brain. Odd symptoms. A multisystem inflammatory syndrome in children. Cases of reinfection. Some of these phenomena will be particular to SARS-CoV-2. Others would also show up if any new virus infected millions within months. This is not to downplay the severity of the pandemic. Some claims about COVID-19’s effect on the heart may be overwrought, but that doesn’t mean the virus is harmless. Conversely, the claims that COVID-19 is equivalent to the flu are clearly wrong, but that doesn’t mean anything goes. The reality lies between this false dichotomy and is still grim, as evidenced by the sheer number of infections, deaths, and lingering disabilities. “It’s hard to find a balance,” says Rivera-Serrano. “It’s not an apocalyptic zombie virus that’s so different from everything else and can suddenly do all these things to the body. But you also don’t want to trivialize what is happening.” Indeed, by bringing underappreciated aspects of viral infections to light, COVID-19 might help to change our understanding of diseases in general. The long-term consequences of viral myocarditis, for example, are still unclear, because “it can be really hard to identify hundreds of people who have all been exposed to the same virus in a relatively short amount of time,” Murthy says. That’s no longer true. And beyond making studies possible, the pandemic also clarifies that such studies are worthwhile. “We have a mindset that this is a problem we need to work on,” Murthy adds. The heightened focus on COVID-19 allows hype and sensationalism to flourish, but also shines a spotlight on phenomena that have long been consigned to the shadows. For example, many of the lingering symptoms that long-haulers are facing are similar to known chronic conditions such as dysautonomia and myalgic encephalomyelitis, which can be triggered by other viral infections. These illnesses have been dismissed and trivialized for decades. Few doctors know how to deal with them. Few scientists study them. That might change as thousands of people with similar problems are emerging all at once, and are pushing for recognition and research. In a pandemic, experiences that might once have been dismissed grab attention. Perhaps that tells us they should never have been dismissed at all. from https://ift.tt/2Hf9CWR Check out http://natthash.tumblr.com |
Authorhttp://natthash.tumblr.com Archives
April 2023
Categories |