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  1. Aunty Mabel on Facebook thinks he is a Bond baddie (spoiler: he's not) Microsoft founder and philanthropist Bill Gates stuck an oar into tinfoil-hat-infested waters once again today with a pretty reasonable plan to deal with the ongoing global pandemic. In an opinion piece for Tortoise Media, His Billness laid out a three-part plan for eliminating the grim threat of coronavirus and, unsurprisingly, it all hinges on those pesky vaccines. Gates reckoned that likely more than one vaccine will be available by the early part of next year, but dealing with the pandemic would first require the capacity to make enough of the stuff, and then ensure a global reach for dosages. "Right now," he said, "most of the world's supply of COVID-19 vaccines is slated to go to rich countries." Those countries at the other end of the scale are not so lucky: "As things stand now, these countries will be able to cover, at most, 14 per cent of their people." Taking the ethics and morality of the situation aside, the result, according to Gates, is the virus continuing its rampage through large chunks of the world and wealthy nations risking reinfection because, after all, not everybody will leap at the chance of a needle stuffed full of special sauce. "The only way to eliminate the threat of this disease somewhere is to eliminate it everywhere," insisted Gates. "New modeling from Northeastern University helps illustrate what will happen if vaccine distribution is so unequal. The researchers there analyzed two scenarios. In one, vaccines are given to countries based on their population size. Then there’s another scenario that approximates what’s happening now: 50 rich countries get the first 2 billion doses of vaccine. In this scenario, the virus continues to spread unchecked for four months in three quarters of the world. And almost twice as many people die." "This would be a huge moral failing. A vaccine can make Covid-19 a preventable disease, and no one should die from a preventable disease simply because the country they live in can’t afford to secure a manufacturing deal," he added. As well as upping manufacturing capacity (and noting the unusual sight of pharmaceutical companies sharing facilities), Gates also called for more funding to pay for both the vaccines and infrastructure to get doses to patients. "There's a lot to be learned from the ongoing effort to eradicate polio," he said. And the Bill and Melinda Gates Foundation knows a lot about polio. Gates has been forced in recent months to deny that his support for vaccine research is actually a cover for something altogether more nefarious. Lurking within the recent Windows XP source code leak were all manner of conspiracy videos, and social media posts concerning Gates' involvement in the spread of the virus have fanned the flames licking up those 5G (or, indeed, 4G) masts. When asked in a recent interview if he wanted to use vaccines to implant microchips into people, the billionaire responded simply: "No." Indeed, in terms of tracking people and controlling their moods, the social media giants are already way ahead of the game. Gates went on to point out that building the system to identify and eliminate COVID-19 regardless of a nation's wealth will also give the world a running start when the next pandemic rolls around. "The self-interested thing and the altruistic thing," he said, "are one and the same." Source
  2. Llamas—Yes, Llamas—Could Help Us Fight Covid-19 These creatures have evolved special "nanobodies" that may have an edge over human antibodies when it comes to developing a new treatment. Photograph: Alamy Millions of years ago, some unknown common ancestor of today’s llamas, camels, and alpacas underwent an unusual genetic mutation. This evolutionary happenstance gave llamas and their kin a strange type of antibody that no other mammals have—which, surprisingly, could end up aiding in the fight against Covid-19. On Monday, in the journal Nature Structural & Molecular Biology, researchers from the Rosalind Franklin Institute and the University of Oxford reported the discovery of two llama antibodies, also called nanobodies, that could prevent the virus that causes Covid-19 from infecting human cells. “These [nanobodies] can block—do block quite potently—the interaction between the virus and the human cell,” says Ray Owens, a professor of molecular biology at the University of Oxford and one of the study’s senior authors. “They basically neutralize the virus.” Like all antibodies, the nanobodies that Owens and his team developed have the ability to recognize and attach to a specific spot on a specific protein—in this case, the so-called spike proteins that cover the surface of the novel coronavirus. When these spikes latch onto ACE2, a protein that sits on the outside of many human cells, the coronavirus can enter and infect those cells. If, however, the spike proteins are blocked from attaching to ACE2, the virus will float around harmlessly, unable to invade. Most species, including humans, make very similar antibodies. Typically, antibodies developed for medical treatments are first produced in lab animals such as rabbits, then isolated and genetically tweaked to more closely resemble human antibodies. But a few species, including llamas, their fellow camelids, and sharks, are antibody oddballs. These animals make nanobodies, so called because they are substantially smaller than their antibody cousins. These tiny molecules have their own particular benefits. “Sometimes there might be a particular pocket that forms on the surface of a protein that's recessed,” says Jason McLellan, an associate professor of molecular biosciences at the University of Texas at Austin who has also discovered a llama nanobody that blocks the spike protein from binding to ACE2. Larger antibodies, he says, “can't bind inside that pocket.” Even when they are used in exactly the same spots, nanobodies may have an edge over human antibodies. “They're very stable,” Owens says. Unlike most antibodies, they maintain their shape in extreme environments, like the human stomach. Given these advantages, nanobodies have been developed as treatments for diseases, and one has even been approved by the FDA as a cancer treatment. The tried-and-true method of developing nanobodies involves injecting a harmless chunk of the pathogen into a llama and waiting for the animal to mount an immune response. But inoculating a llama and extracting its nanobodies is a monthslong process, slow by the standards of Covid-19-era research. So Owens and his colleagues took a different tack. They started with an enormous set of nanobodies that had previously been isolated from llamas. “We have a whole collection of different sequences with different binding potentials,” says Owens. They then used the spike protein to “fish out” any nanobodies that would attach to it. This strategy allowed them to quickly identify a nanobody that had potential against SARS-CoV-2. Unfortunately, this nanobody didn’t attach to the protein tightly enough to effectively block the novel coronavirus from entering cells. So Owens and his team randomly mutated the region of the nanobody that connected with the spike protein, in hopes of creating a snugger fit. And they succeeded: In the presence of large enough quantities of one of these mutated nanobodies, SARS-CoV-2 was entirely incapable of entering human cells. “They literally can't develop infection,” Owens says. McLellan and his team, who published their nanobody discovery in Cell in May, leveraged a different strategy. They were already developing a nanobody against SARS-CoV-1, the virus that caused the 2002–04 SARS epidemic; fortuitously, they found that this same nanobody proved effective against SARS-CoV-2. While their nanobody has the advantage of being effective against multiple coronaviruses, the approach favored by Owens and his colleagues may have its own virtues. “Generally, in order to get breadth, you give up some potency or specificity against any one particular molecule,” McLellan says. “It’s a delicate balance.” Because Owens and his team optimized their nanobodies for use on SARS-CoV-2, they could prove more effective against it—though further research is needed. Regardless of which type of nanobody comes out on top, two may be better than one for Covid-19 treatment. “These two nanobodies could be used simultaneously, to maybe generate an additive or synergistic effect,” McLellan says. Since the nanobodies discovered by each group attach to the spike protein at different spots, when used in concert they could team up to make it even harder for the spike to connect with ACE2. These quick methods of adapting old nanobodies for new purposes are stopgap measures. Scientists are still waiting for the llamas that they have exposed to the spike protein to produce their own SARS-CoV-2 nanobodies from scratch: Both Owens and McLellan are currently working on such projects. “Using immunization, the natural immune system, to mature high affinity interactions obviously gives you the best binders,” Owens says. In the meantime, both researchers hope that their nanobodies might prove to be effective treatments for people who are severely ill with Covid-19. While a patient’s immune system struggles to mount an adequate immune response, nanobodies and other types of antibodies could function as an emergency measure to prevent SARS-CoV-2 from entering more of their cells. The same rationale is behind treatments that involve injecting a patient with plasma from a Covid-19 survivor, but transfusions come with a risk of infection and depend on donations. Until a vaccine becomes available, some researchers believe antibody treatments could be used as short-term protection for health care workers and the families of patients. One they reach the clinical stage, nanobodies might be more convenient to work with than other antibodies. Because they are so small, they can travel much more easily through body tissues, so they wouldn’t necessarily have to be injected into patients. “Potentially, they could be inhaled directly into the lung, where the respiratory infections are occurring,” says McLellan. “They’re also much easier to make,” Owens says. Their small size means that they can be produced in bacteria—much more cheaply and more quickly than standard antibodies, which must be made in animal cells. Jacob Glanville, president and CEO of Distributed Bio, a biotech company that is developing traditional antibodies for use against the novel coronavirus, believes that the ease of producing nanobodies is a material point in their favor. “I think that is a legitimate advantage,” he says. “I’m very concerned about the global capacity to produce CHO,” or Chinese hamster ovary cells, which are used to generate larger antibodies at scale. In the long run, McLellan hopes that llama antibodies can help to prevent a pandemic like Covid-19 from ever happening again. “I think one of the next steps is to start trying to identify antibodies and nanobodies that can broadly bind and neutralize diverse coronaviruses,” McLleland says. “In the event there's another coronavirus outbreak in the future, we might then already have the antibody immediately, from day one, that could work and neutralize the virus.” Llamas—Yes, Llamas—Could Help Us Fight Covid-19
  3. Google and Apple Reveal How Covid-19 Alert Apps Might Look As contact tracing plans firm up, the tech giants are sharing new details for their framework—and a potential app interface. Public health officials still have to make the actual apps. But Apple and Google have given them a reference interface—and strict guidelines on how much data they can collect.Illustration: Getty Images Finding out that you've been exposed to a serious disease through a push notification may still seem like something out of dystopian science fiction. But the ingredients for that exact scenario will be baked into Google and Apple's operating system in as soon as a matter of days. Now the two companies have shown not only how it will work, but how it could look—and how it'll let you know if you're at risk. On Monday, Apple and Google released a few new details about the Bluetooth system they're building into both Android and iOS that will let health care authorities track potential encounters with Covid-19. The companies have now made clear that only government agencies—preferably at the national level, Google and Apple say, though they note they're willing to work with state and regional authorities—will be granted permission to the feature's application programming interface. If those government-run apps want access to Apple and Google's Bluetooth-based system, they won't be allowed to collect location data, and must ask for consent before collecting information on a user's proximity to others. They'll need permission to upload any information from the phones of Covid-19 positive people as well. The two companies have published sample user interface screenshots for the first time as well. As Google and Apple first outlined last month, their Covid-19 exposure notification system transmits unique, rotating codes from phones via their Bluetooth radios based on cryptographic keys that change daily. They not only keep a log of the last two weeks of your codes, but also listen for the codes broadcast by others. If two people running the app spend a certain amount of time in proximity—say, 10 minutes within six feet, or whatever health care agencies dictate—their phones will both record each others' Bluetooth codes. If one of them later receives a positive Covid-19 diagnosis, they can choose to upload all of their keys from the last two weeks to the app's server, which will then send those keys out to the phones of all the other users in their region. Those phones will then check if the codes they've recorded from other nearby users can be generated from those keys. If you get a match, the app will show a message that you've potentially been exposed to Covid-19 and caution you to self-quarantine or get tested. Now Google and Apple are showing how some parts of that process might look. The two companies warn, however, that they're only releasing sample images as references, since health care agencies will build the final apps, not Apple and Google. Here, for instance, is how Google and Apple suggest the apps ask for user consent to transmit and record Bluetooth codes when the app is first installed: Courtesy of Apple In another series of screenshots, the companies show how the apps will likely work when a user is diagnosed as Covid-19 positive. As Apple and Google had suggested earlier, they'll require users to enter a unique code provided by health care providers or a Covid-19 testing lab before allowing them to declare themselves as infected, since otherwise trolls or mistaken self-diagnoses could flood the system with false positives: Courtesy of Apple Finally, Google and Apple have shown an example of what a notification of potential contact with an infected Covid-19-positive person could look like: Courtesy of Apple Those sample messages confirm that Google and Apple will make it possible to determine the exact day a contact event occurred. Some developers of contact-tracing apps have argued that offering too much information about the time when a contact event happened will make it too easy to identify Covid-19-positive people, and that apps should only tell the user they've been exposed at some indeterminate time in the last two weeks. But others have pointed out that users should know when a contact event occurred so that they can consider factors like whether they were wearing a face mask or other personal protective equipment at the time, whether they were behind a protective barrier, or some other situation that might creative a false positive. By choosing to tell users the day—but not the time—that they were potentially exposed, Google and Apple appear to have reached a compromise. But the system still leaves open the possibility that some people could have their Covid-19-positive status exposed to strangers without their consent. Someone who is sheltering in place might leave their home only once daily to get their mail, for instance, and come into contact with just a few people—or even just one person. If they're later alerted they were exposed to Covid-19 that day, they might be able to remember which of their neighbors they saw and learn who has likely been diagnosed with Covid-19. That's just one of the potential pitfalls of Google and Apple's system. Security researcher Ashkan Soltani has pointed out, for instance, that someone could set up cameras and bluetooth beacons to identify Covid-19 positive users. The Electronic Frontier Foundation has warned that hackers could record and rebroadcast users' contact codes to feed false information into the system willy-nilly, though it's not clear what they'd accomplish with that system other than nihilistic trolling. But when it comes to privacy preservation, Google and Apple's system is nonetheless one of the most conservative of all the schemes that developers have proposed to use smartphones for contact-tracing or exposure notification. By focusing on only Bluetooth-based proximity detection, it avoids the privacy peril of collecting location information. And it doesn't upload anything to the server at all for the vast majority of users who aren't diagnosed as Covid-19 positive. All of their information stays on their phone. Apple and Google's system will likely only work if it's part of a much larger picture, one that includes widespread testing, social distancing, and manual contact-tracing. But it could serve as one piece in that system, another tool to help the world return normalcy. Now that the companies are publishing samples of the warnings they'll give to users and the consent they'll ask from them, people can start to judge for themselves if they're willing to put that tool in their pocket. Source: Google and Apple Reveal How Covid-19 Alert Apps Might Look (Wired)
  4. The Ars COVID-19 vaccine primer: 100-plus in the works, 8 in clinical trials Here's where we are and what may lie ahead for a vaccine against COVID-19. Enlarge / HUBEI, CHINA - APRIL 15: (CHINA MAINLAND OUT)220 volunteers from Wuhan are vaccinated with the novel coronavirus vaccine, which is in a human clinical trial. Getty | TPG 99 with 61 posters participating The clearest way out of the COVID-19 crisis is to develop a safe, effective vaccine—and scientists have wasted no time in getting started. They have at least 102 vaccine candidates in development worldwide. Eight of those have already entered early clinical trials in people. At least two have protected a small number of monkeys from infection with the novel coronavirus, SARS-CoV-2, that causes COVID-19. Some optimistic vaccine developers say that, if all goes perfectly, we could see large-scale production and limited deployment of vaccines as early as this fall. If true, it would be an extraordinary achievement. Less than four months ago, SARS-CoV-2 was an unnamed, never-before-seen virus that abruptly emerged in the central Chinese city of Wuhan. Researchers there quickly identified it and, by late January, had deciphered and shared its genetic code, allowing researchers around the world to get to work on defeating it. By late February, researchers on multiple continents were working up clinical trials for vaccine candidates. By mid-March, two of them began, and volunteers began receiving the first jabs of candidate vaccines against COVID-19. It’s a record-setting feat. But, it’s unclear if researchers will be able to maintain this break-neck pace. Generally, vaccines must go through three progressively more stringent human trial phases before they are considered safe and effective. The phases assess the candidates’ safety profile, the strength of the immune responses they trigger, and how good they are at actually protecting people from infection and disease. Most vaccine candidates don’t make it. By some estimates, more than 90 percent fail. And, though a pandemic-propelled timeline could conceivably deliver a vaccine in as little as 18 months, most vaccines take years—often more than 10 years, in fact—to go from preclinical vetting to a syringe in a doctor’s office. Abridging that timeline can up the risk of failure. For instance, vaccine candidates usually enter the three phases of clinical trials only after being well tested in lab animals that can model the human disease. But, with such a new virus, there is no established animal model for COVID-19. And amid a devastating pandemic, there’s not enough time to thoroughly develop one. Some researchers are now doing that ground-level animal work in parallel with human trials—such as the small monkey trials mentioned above. Researchers already have reason to be a little anxious about the safety of any COVID-19 vaccine. When they tried in the past to make vaccines against some of SARS-CoV-2’s coronavirus relatives, they found a small number of instances when candidate vaccines seemed to make infections worse. That is, these candidate vaccines seemed to prompt berserk immune responses that caused lung damage in monkeys and liver damage in ferrets. Researchers still don’t fully understand the problem and don’t know if it could happen in humans, let alone if it will show up with the new candidate vaccines against SARS-CoV-2. But we may soon know the answers. As the pandemic tops the grim milestone of three million cases worldwide and well over 200,000 deaths, researchers are relentlessly moving forward with vaccine development. Here's where the scientific community currently stands in its frenetic effort. First, the basics Researchers are using a wide variety of tools and techniques to develop a vaccine—some are tried and tested, others are fresh and unproven. Regardless of the strategy, they all aim to do the same thing: train the immune system to identify SARS-CoV-2 (or some element of it) and destroy it before it establishes an infection and causes COVID-19. The way a vaccine can pull this off, typically, is by feeding immune cells a signature element of a disease-causing germ, such as a unique protein that coats the outside of a dangerous virus. From there, a type of white blood cell called B cells can generate antibodies that specifically recognize and glom onto those signature germ elements. Antibodies are Y-shaped proteins, which have their germ-specific detecting regions on their outstretched arms. The base of their “Y” shape is a generic region that can signal certain immune responses if they detect an invading germ. A strong, effective vaccine can generate so-called neutralizing antibodies. These antibodies circulate in the blood, surveilling the whole body after a vaccine is given. If the germ they’re trained to detect actually shows up, the antibodies can swarm and paralyze it. The base of the antibodies—now dangling off their smothered target germ—can then signal immune cells to help finish the job. In the case of COVID-19, the goal of candidate vaccines is to train our immune systems to make antibodies that specifically detect and destroy SARS-CoV-2 (which is, again, the novel coronavirus that causes COVID-19). Though there’s a lot we don’t know about SARS-CoV-2, we know enough of the basics to direct early vaccine development. We know that SARS-CoV-2 is a betacoronavirus related to two other notorious betacoronaviruses: SARS-CoV-1, which causes SARS (severe acute respiratory syndrome), and the Middle Eastern respiratory syndrome coronavirus (MERS-CoV), which causes MERS. Coronaviruses, generally, keep their genetic blueprints in the form of a large, single-stranded, positive-sense RNA genome, which is bundled into a round viral particle. That genetic code provides the molecular instructions to make all of the components of the virus, including enzymes required to make copies of the virus’s genome, and the virus’s famous spike protein. The spike protein is what the coronaviruses use to grab ahold of host cells—that is, human cells they infect or the cells of any other animal victim. Once the virus latches on with its spike protein, it gets into the cell and hijacks the cell's activities, forcing it to help manufacture viral clones, which then burst forth to infect more cells. There are many copies of the spike protein on the outer surface of coronaviruses, creating a spikey exterior—think a cartoon sea mine. The pointy adornments are actually what give coronaviruses their name. Under an electron microscope, the spikes give the viral particle a crown-like appearance, hence corona viruses. But more importantly, the spike proteins are a prime target for antibodies. And, because we have the whole genome sequence for SARS-CoV-2, researchers have a good start at figuring out effective ways to engineer vaccines to attack the spike proteins and other critical components of the virus. Vaccine platforms There are many ways to try to train the immune system to fight off a specific germ or specific elements of germs, such as SARS-CoV-2 or the SARS-CoV-2 spike proteins. Here are the general categories currently in play: Live-attenuated vaccine: These vaccines use whole viruses that are weakened so they can no longer cause disease. This is a well-established method for creating vaccines. In the past, researchers weakened viruses by growing them in lab conditions for long periods of time—which is a bit like domesticating germs. The cushy, all-inclusive petri-dish lifestyle can essentially allow viruses and bacteria to adapt to their tranquil surroundings and lose virulence over time. But, it can take a while. Scientists grew the measles virus in lab conditions for nearly 10 years before using it for a live-attenuated vaccine in the early 1960s. Nowadays, there are faster, more controlled approaches to engineer weakened viruses, such as targeted mutations and other manipulations of a virus’s genetic code. Live-attenuated virus vaccines have the advantage of generating the same variety of protective antibodies as a real infection—without causing a pesky, life-threatening disease, for the most part. But there are risks. Because the virus can still replicate, certain people (particularly those with immunodeficiencies) may have severe reactions. Though the newer strategies for weakening viruses may reduce these risks, they still require extensive safety testing before reaching the market. That said, this is a vaccine platform that has already proven successful. Several vaccines in use are live-attenuated vaccines, including vaccines for chickenpox and typhoid. If such a vaccine proved effective at preventing COVID-19, we already have the know-how and infrastructure to quickly scale up production to make these vaccines. Inactivated vaccine: This is another straightforward, old-school method that uses whole viruses. In this case, the viruses are effectively dead, though, usually inactivated by heat or chemicals. These corpse viruses can still prime the immune system to make neutralizing antibodies; they just do it less efficiently. The advantage of this strategy is that it is relatively simple to make these types of vaccines and, because the viruses don’t replicate, there is no risk of infection and less risk of severe reactions. Disadvantages include that inactivated, non-replicating viruses don’t elicit as strong of an immune response as a disease-causing or weakened virus. Inactivated vaccines always require multiple doses and may need periodic booster shots as well. Like weakened virus vaccines, using a whole viral particle gives the immune system many potential viral targets for antibodies. Some may be good targets to neutralize a real infection, and some may not. But, using an inactivated virus is a proven method. For instance, some existing vaccines against polio, hepatitis A, and rabies use this method. Viral vector-based vaccine: For these vaccines, researchers take a weakened or harmless virus and engineer it to contain an element of a dangerous virus they want to protect against. In the context of COVID-19, this might mean engineering a harmless virus to produce, say, the spike protein from SARS-CoV-2. This way you get the immune response to a live but benign virus, coupled with the likelihood of having antibodies that target a specific critical protein from the dangerous SARS-CoV-2. This, too, is a proven strategy for effective vaccines. The newly approved Ebola vaccine, for instance, uses this method. Subunit vaccines: These are bare-bones vaccines that include only a component of a dangerous virus to elicit immune responses. For COVID-19 vaccines, the spike protein is—no surprise—a popular candidate. Subunits can be delivered in formulations with adjuvants—accessory ingredients that can enhance immune responses. One common adjuvant is alum, an aluminum salt, long known to be useful for vaccines. Some newer subunit vaccines come in snappier packages, however. These include artificial “virus-like particles” (VLPs) and nanoparticles. Subunit vaccines are already an established vaccine platform. The HPV vaccine in use involves a VLP that feeds the immune system proteins from the HPV’s outer shell—which can then be targeted by antibodies. RNA and DNA vaccines: These are among the newest types of vaccines—and among the shakiest. There are currently no licensed vaccines that use this method. But researchers are optimistic about their potential. The basic idea is to deliver genetic material of a virus—either in the form of DNA or RNA—directly to human cells, which are then somehow compelled to translate that genetic code into viral proteins and then able to make antibodies against those. Some of the details of how these candidate vaccines work are proprietary and unproven, so it’s difficult to assess how likely they are to succeed or how easy it will be to scale up vaccine production if they are successful. Enlarge / Adapted from a review of candidate vaccines. This includes information about vaccine development that is not publicly available. It is a larger list of candidates than what is reported by the WHO. Ars Technica Potential pitfalls As mentioned earlier, in some previous work on developing a vaccine against SARS-CoV-1—the virus behind SARS—researchers came across a few instances where candidate vaccines seemed to make disease worse in animal models. This led to some instances of organ damage in a few animal models, namely monkeys, ferrets, and also mice. So far, it’s unclear what was going on there. Some researchers have speculated that it may be a form of Antibody-Dependent Enhancement (ADE). Very generally, this is a scenario in which the immune system makes antibodies against an invading germ, but those antibodies are not able to neutralize the germ completely. This can make the situation worse if the shoddy antibodies signal for immune cells to respond while the germ is still infectious. Basically, the antibodies are just recruiting immune cells to be the germ’s next victims. And this, in turn, can lead to additional—excessive—immune responses that end up damaging the body. One of the best understood examples of this occurs with dengue viruses. There are four types of dengue viruses that circulate (in people and mosquitoes), and research suggests that some antibodies to one type of dengue may sometimes generate ADE in subsequent infections or exposures with other types of dengue. This is why researchers think that some patients with dengue fever, which can be a mild disease, go on to develop dengue hemorrhagic fever. This is a rare but severe form of the disease in which immune cells release chemicals called inflammatory cytokines that end up damaging the circulatory system, leading to blood plasma leaking out of capillaries. From there, the patient can go into shock and die. But, many researchers are not convinced that ADE is behind some of the problems seen with early SARS vaccines—nor that ADE will necessarily be an issue with a COVID-19 vaccine. For one thing, the berserk immune responses seen in the animal models don’t seem to involve some of the same immune system components seen in well-understood cases of ADE, like dengue. “There’s no clear evidence that ADE is an issue,” microbiologist Maria Elena Bottazzi tells Ars. Bottazzi is the associate dean of the National School of Tropical Medicine at Baylor College of Medicine. Instead, Bottazzi and colleagues hypothesize that something about the coronaviruses and whole-virus vaccine candidates may induce an excessive, aberrant inflammatory response, potentially through the activity of specialized, pro-inflammatory immune cells called T helper 17 cells, which are linked to inflammatory autoimmune diseases. This may help explain why some patients with the most severe forms of COVID-19 seem to experience so-called “cytokine storms,” which are like a disastrous deluge of pro-inflammatory signals unleashed by the immune system that end up causing damage to the body—just like in the animal models. Much of this is still speculative, but Bottazzi says what we know so far may be helpful for directing vaccine development strategies. She notes that the excessive immune responses may mainly occur when the immune system is presented with a whole, intact coronavirus particle. Something about interacting with that whole particle may send our immune systems into a tailspin, the thinking goes. A safer strategy may be to use a subunit vaccine or another more targeted approach to train our immune systems—an approach that only shows the immune system what it needs to see to defeat the virus. Many vaccine developers are already on board with this thinking, it seems. Bottazzi notes that most of the candidates in development now do not involve the whole virus, but subunits, genetic material, or other targeted strategies. “Having the whole virus, of course it has higher risks, so the new platforms are actually selecting for better candidates,” she says. Bottazzi and her colleagues are themselves now working up such a subunit vaccine candidate for SARS-CoV-2, which follows up on their vaccine work for SARS-CoV-1. The vaccine includes just a portion of the SARS-CoV-2 spike protein—the precise segment that actually binds to human cells. She notes that further questions about potential ADE or excessive immune responses to any candidate vaccine might be more closely looked at further along in vaccine development, perhaps in phase II trials. But, right now, “it’s not a high-ranking concern,” she says. Timing Another potential problem vaccine developers should keep in mind is how long the antibody responses may last in the body. Past research has suggested that coronaviruses that cause just common colds—there are four strains of these that circulate in humans—don’t prompt long-lasting antibodies. A person may only be protected for a few years. Ideally, vaccines should be optimized to generate the strongest immune response possible that will, hopefully, offer long-lasting if not life-long protection. But, if immune responses to an otherwise effective vaccine wane over time, and SARS-CoV-2 becomes an endemic disease or comes in seasonal waves, we may have to look at periodic boosters until a more effective vaccine is developed. We already have annual vaccines for influenza, but this is because the influenza virus mutates so quickly that our immune system may not recognize strains from one year to the next. Also, there are different mixes of strains circulating from season to season. Both of these issues lead to the need for season-specific vaccine formulations. So far, SARS-CoV-2 does not seem to be mutating in a particularly fast or problematic fashion, suggesting that we may not need seasonal shots—at least not for these reasons. Early front-runners With all of this in mind, vaccine developers have charged ahead. There are currently at least 102 candidates, and eight of them are in clinical trials. One of the earliest was an RNA vaccine, called mRNA-1273, from biotechnology company Moderna. As we mentioned earlier, vaccines based on genetic material are unproven so far. Moreover, because the technology is so new, much of it is still proprietary, so outside researchers don’t know a lot about how these vaccines work. As such, they’re difficult to assess from the outside—and it’s difficult to know how easy it will be to scale up production for worldwide vaccination campaigns (if they work), Bottazzi says. Based on what we know about Moderna’s work, their vaccine contains the genetic blueprints for the SARS-CoV-2 spike proteins. The genetic code is modified to have artificial components—such as pseudouridine instead of RNA’s usual uridine—so that the immune system doesn’t automatically recognize the vaccine as foreign genetic material and try to destroy it. The genetic material is also packaged for cell delivery in a lipid nanoparticle. Moderna, working with the National Institutes of Health, got a clinical trial set up in February and gave its first doses to humans on March 16. If all goes to plan, the company has suggested that it could have a vaccine ready for frontline healthcare workers by this fall. Eight candidate vaccines in clinical evaluation Platform Type of candidate vaccine Developer Current stage of clinical evaluation/regulatory status—coronavirus candidate Same platform for non-coronavirus candidates Non-replicating viral vector Adenovirus Type 5 Vector CanSino Biological Inc./Beijing Institute of Biotechnology Phase 2: ChiCTR2000031781 Phase 1: ChiCTR2000030906 Ebola Non-replicating viral vector ChAdOx1 University of Oxford Phase 1/2: NCT04324606 MERS, Influenza, TB, Chikungunya, Zika, MenB, plague DNA DNA plasmid vaccine with electropolation Inovio Pharmaceuticals Phase 1: NCT04336410 Multiple candidates Inactivated Inactivated Wuhan Institute of Biological Products/Sinopharm Phase 1: ChiCTR2000031809 Inactivated Inactivated Beijing Institute of Biological Products/Sinopharm Phase 1 (regulatory approval) Inactivated Inactivated + alum Sinovac Phase 1: NCT04352608 SARS RNA mRNA BioNTech/Fosun Pharma/Pfizer Phase 1/2: 2020-001038-36 RNA LNP-encapsulated mRNA Moderna/NIAID Phase 1: NCT04283461 Multiple candidates Source: WHO Meanwhile, in China, biotechnology company CanSino Biologics began a trial March 17 for its viral vector-based vaccine candidate. The strategy packages genetic material from SARS-CoV-2 into a weakened adenovirus strain. The company has already gotten to work on a Phase II trial. Beijing-based Sinovac Biotech made headlines this month after its whole-virus inactivated SARS-CoV-2 vaccine candidate was shown to protect a small number of monkeys from COVID-19 in early lab tests. Its Phase I clinical trials in humans began on April 16. The results are positive, but some researchers are anxious to see more testing and safety data. Researchers at Oxford University are also off to a good start with their viral vector-based vaccine candidate. They have packaged the SARS-CoV-2 spike protein in a weakened adenovirus, similar to CanSino’s approach. And like Sinovac, their vaccine has protected a small number of monkeys in early lab experiments. Oxford researchers began dosing trial participants last week. The researchers told The New York Times that if the trials go to plan, they could produce millions of doses by September. The latest, ever-expanding and updating list of candidate vaccines assembled by the World Health Organization can be found here. Source: The Ars COVID-19 vaccine primer: 100-plus in the works, 8 in clinical trials (Ars Technica)
  5. Microsoft's New Coronavirus Map Lets You Track The Number Of COVID-19 Cases In Countries Around The World, And Every State In The US Microsoft's interactive map provides information about corona virus cases in every country .. Clicking on a particular country gives a break down of cases .. The map provides data on the number of active cases, recovered cases and fatal cases for every spot on the map .. Users can also click any country on the map for a list of related articles about the chosen region (although keep in mind they can be outdated, as The Verge noted .. The map also includes a breakdown of cases for every US state .. That includes the total number of active, recovered, and fatal cases .. Source
  6. Trump says he wants to ease up on coronavirus related shutdowns 'pretty soon' amid concerns about economy - updates WASHINGTON — President Donald Trump on Monday said his administration is looking at ways to ease economic restrictions it stressed just days earlier even as the U.S. braces for a jump in coronavirus cases and states tighten restrictions on people and businesses. "I'm not looking at months," Trump said of the duration of social distancing guidelines that have led to school and business closures. "We will be back in business as a country pretty soon." Trump’s suggestion comes as others are taking their most strict measures yet. On Monday, four U.S. states announced more rigid orders for residents and businesses, an International Olympic Committee member revealed this year's games would be postponed and U.S. deaths approached 600, according to the Johns Hopkins University data dashboard. The federal government, Trump said, will use data "to recommend new protocols” to allow local economies to “cautiously resume their activity at the appropriate time." Coronavirus:Trump signals growing impatience with coronavirus-related economic shutdowns He did not say when those protocols would be rolled out as the coronavirus spreads across the U.S. The remarks were a major departure from Trump's prediction just days ago that the guidelines could potentially be in place through the summer. Trump appeared to signal that parts of the country that are less hard hit could be placed under less strict guidelines than states like New York and California. At the same time, Trump admitted the outbreak will only get worse in the U.S. Trump said he agreed with his surgeon general’s prediction that the number of coronavirus cases would jump. “This is going to be bad,” Trump said. “We’re trying to make it so it’s much, much less bad.” - John Fritze and Sean Rossman Source: usatoday.com
  7. Lyft to deliver food and medical supplies during COVID-19 After the company's ride-hailing services were significantly impacted due to the COVID-19 pandemic, Lyft has now stated that it plans to start a new service to deliver food and medical supplies (via Engadget). The company noted the following reason for this initiative: This work helps create new opportunities for drivers, provides rides to those in need, and helps distribute essential goods. For now, the initiative, which consists of three parts, will have drivers delivering medical supplies and test kits to the elderly and people vulnerable to the virus along with transporting food to seniors, as well as students who depend on school meals. The company says that deliveries will be picked up from distribution centers and dropped off without contact. The plan will first launch in the Bay Area and gradually expand across California and the rest of the country. The company is also collaborating with eight Medicaid agencies to assist people requiring non-emergency transportation in getting to their medical appointments. To expand the access, it is working with states throughout the country, Lyft stated. Additionally, John Zimmer and Logan Green, the co-founders, informed Reuters that their salaries until June will be donated to assist the company's drivers. Meanwhile, they will also help the drivers in finding temporary employment opportunities. Source: Lyft to deliver food and medical supplies during COVID-19 (Neowin)
  8. We can do this — The doctor who helped defeat smallpox explains what’s coming We can beat the novel coronavirus—but first, we need lots more testing. Enlarge / Producer Larry Brilliant speaks onstage at the HBO Documentary "Open Your Eyes" Special Screening At The Rubin Museum at Rubin Museum of Art on July 13, 2016 in New York City. Paul Zimmerman | Getty Images 141 with 71 posters participating Larry Brilliant says he doesn’t have a crystal ball. But 14 years ago, Brilliant, the epidemiologist who helped eradicate smallpox, spoke to a TED audience and described what the next pandemic would look like. At the time, it sounded almost too horrible to take seriously. “A billion people would get sick," he said. “As many as 165 million people would die. There would be a global recession and depression, and the cost to our economy of $1 to $3 trillion would be far worse for everyone than merely 100 million people dying, because so many more people would lose their jobs and their health care benefits, that the consequences are almost unthinkable.” Now the unthinkable is here, and Brilliant, the Chairman of the board of Ending Pandemics, is sharing expertise with those on the front lines. We are a long way from 100 million deaths due to the novel coronavirus, but it has turned our world upside down. Brilliant is trying not to say “I told you so” too often. But he did tell us so, not only in talks and writings, but as the senior technical advisor for the pandemic horror film Contagion, now a top streaming selection for the homebound. Besides working with the World Health Organization in the effort to end smallpox, Brilliant, who is now 75, has fought flu, polio, and blindness; once led Google’s nonprofit wing, Google.org; co-founded the conferencing system the Well; and has traveled with the Grateful Dead. We talked by phone on Tuesday. At the time, President Donald Trump’s response to the crisis had started to change from “no worries at all” to finally taking more significant steps to stem the pandemic. Brilliant lives in one of the six Bay Area counties where residents were ordered to shelter in place. When we began the conversation, he’d just gotten off the phone with someone he described as high government official, who asked Brilliant “How the fuck did we get here?” I wanted to hear how we’ll get out of here. The conversation has been edited and condensed. Steven Levy: I was in the room in 2006 when you gave that TED talk. Your wish was “Help Me Stop Pandemics.” You didn't get your wish, did you? Larry Brilliant: No, I didn't get that wish at all, although the systems that I asked for have certainly been created and are being used. It's very funny because we did a movie, Contagion— We're all watching that movie now. People say Contagion is prescient. We just saw the science. The whole epidemiological community has been warning everybody for the past 10 or 15 years that it wasn't a question of whether we were going to have a pandemic like this. It was simply when. It's really hard to get people to listen. I mean, Trump pushed out the admiral on the National Security Council, who was the only person at that level who's responsible for pandemic defense. With him went his entire downline of employees and staff and relationships. And then Trump removed the [early warning] funding for countries around the world. I've heard you talk about the significance that this is a “novel” virus. It doesn't mean a fictitious virus. It’s not like a novel or a novella. Too bad. It means it's new. That there is no human being in the world that has immunity as a result of having had it before. That means it’s capable of infecting 7.8 billion of our brothers and sisters. Since it's novel, we’re still learning about it. Do you believe that if someone gets it and recovers, that person thereafter has immunity? So I don't see anything in this virus, even though it's novel, [that contradicts that]. There are cases where people think that they've gotten it again, [but] that's more likely to be a test failure than it is an actual reinfection. But there's going to be tens of millions of us or hundreds of millions of us or more who will get this virus before it's all over, and with large numbers like that, almost anything where you ask “Does this happen?” can happen. That doesn't mean that it is of public health or epidemiological importance. Is this the worst outbreak you’ve ever seen? It's the most dangerous pandemic in our lifetime. We are being asked to do things, certainly, that never happened in my lifetime—stay in the house, stay six feet away from other people, don’t go to group gatherings. Are we getting the right advice? Well, as you reach me, I'm pretending that I'm in a meditation retreat, but I'm actually being semi-quarantined in Marin County. Yes, this is very good advice. But did we get good advice from the president of the United States for the first 12 weeks? No. All we got were lies. Saying it’s fake, by saying this is a Democratic hoax. There are still people today who believe that, to their detriment. Speaking as a public health person, this is the most irresponsible act of an elected official that I've ever witnessed in my lifetime. But what you're hearing now [to self-isolate, close schools, cancel events] is right. Is it going to protect us completely? Is it going to make the world safe forever? No. It's a great thing because we want to spread out the disease over time. Flatten the curve. By slowing it down or flattening it, we're not going to decrease the total number of cases, we're going to postpone many cases, until we get a vaccine—which we will, because there's nothing in the virology that makes me frightened that we won’t get a vaccine in 12 to 18 months. Eventually, we will get to the epidemiologist gold ring. What’s that? That means, A, a large enough quantity of us have caught the disease and become immune. And B, we have a vaccine. The combination of A plus B is enough to create herd immunity, which is around 70 or 80 percent. I hold out hope that we get an antiviral for Covid-19 that is curative, but in addition is prophylactic. It's certainly unproven and it's certainly controversial, and certainly a lot of people are not going to agree with me. But I offer as evidence two papers in 2005, one in Nature and one in Science. They both did mathematical modeling with influenza, to see whether saturation with just Tamiflu of an area around a case of influenza could stop the outbreak. And in both cases, it worked. I also offer as evidence the fact that at one point we thought HIV/AIDS was incurable and a death sentence. Then, some wonderful scientists discovered antiviral drugs, and we've learned that some of those drugs can be given prior to exposure and prevent the disease. Because of the intense interest in getting [Covid-19] conquered, we will put the scientific clout and money and resources behind finding antivirals that have prophylactic or preventive characteristics that can be used in addition to [vaccines]. When will we be able to leave the house and go back to work? I have a very good retrospect-oscope, but what's needed right now as a prospecto-scope. If this were a tennis match, I would say advantage virus right now. But there's really good news from South Korea—they had less than 100 cases today. China had more cases imported than it had from continuous transmission from Wuhan today. The Chinese model will be very hard for us to follow. We're not going to be locking people up in their apartments, boarding them up. But the South Korea model is one that we could follow. Unfortunately, it requires doing the proportionate number of tests that they did—they did well over a quarter of a million tests. In fact, by the time South Korea had done 200,000 tests, we had probably done less than 1,000. Now that we've missed the opportunity for early testing, is it too late for testing to make a difference? Absolutely not. Tests would make a measurable difference. We should be doing a stochastic process random probability sample of the country to find out where the hell the virus really is. Because we don't know. Maybe Mississippi is reporting no cases because it's not looking. How would they know? Zimbabwe reports zero cases because they don't have testing capability, not because they don't have the virus. We need something that looks like a home pregnancy test, that you can do at home. If you were the president for one day, what would you say in the daily briefing? I would begin the press conference by saying "Ladies and gentlemen, let me introduce you to Ron Klain—he was the Ebola czar [under President Barack Obama], and now I’ve called him back and made him COVID czar. Everything will be centralized under one person who has the respect of both the public health community and the political community." We're a divided country right now. Right now, Tony Fauci [head of the National Institute of Allergy and Infectious Diseases] is the closest that we come to that. Are you scared? I'm in the age group that has a one in seven mortality rate if I get it. If you're not worried, you're not paying attention. But I'm not scared. I firmly believe that the steps that we're taking will extend the time that it takes for the virus to make the rounds. I think that, in turn, will increase the likelihood that we will have a vaccine or we will have a prophylactic antiviral in time to cut off, reduce, or truncate the spread. Everybody needs to remember: This is not a zombie apocalypse. It's not a mass extinction event. Should we be wearing masks? The N95 mask itself is extremely wonderful. The pores in the mask are three microns wide. The virus is one micron wide. So you get people who say, well, it's not going to work. But you try having three big, huge football players who are rushing for lunch through a door at lunchtime—they're not going to get through. In the latest data I saw, the mask provided 5x protection. That's really good. But we have to keep the hospitals going and we have to keep the health professionals able to come to work and be safe. So masks should go where they’re needed the most: in taking care of patients. How will we know when we’re through this? The world is not going to begin to look normal until three things have happened. One, we figure out whether the distribution of this virus looks like an iceberg, which is one-seventh above the water, or a pyramid, where we see everything. If we're only seeing right now one-seventh of the actual disease because we're not testing enough, and we're just blind to it, then we're in a world of hurt. Two, we have a treatment that works, a vaccine or antiviral. And three, maybe most important, we begin to see large numbers of people—in particular nurses, home health care providers, doctors, policemen, firemen, and teachers who have had the disease—are immune, and we have tested them to know that they are not infectious any longer. And we have a system that identifies them, either a concert wristband or a card with their photograph and some kind of a stamp on it. Then we can be comfortable sending our children back to school, because we know the teacher is not infectious. And instead of saying "No, you can't visit anybody in nursing home," we have a group of people who are certified that they work with elderly and vulnerable people, and nurses who can go back into the hospitals and dentists who can open your mouth and look in your mouth and not be giving you the virus. When those three things happen, that's when normalcy will return. Is there in any way a brighter side to this? Well, I'm a scientist, but I'm also a person of faith. And I can't ever look at something without asking the question of isn't there a higher power that in some way will help us to be the best version of ourselves that we could be? I thought we would see the equivalent of empty streets in the civic arena, but the amount of civic engagement is greater than I've ever seen. But I'm seeing young kids, millennials, who are volunteering to go take groceries to people who are homebound, elderly. I'm seeing an incredible influx of nurses, heroic nurses, who are coming and working many more hours than they worked before, doctors who fearlessly go into the hospital to work. I've never seen the kind of volunteerism I'm seeing. I don't want to pretend that this is an exercise worth going through in order to get to that state. This is a really unprecedented and difficult time that will test us. When we do get through it, maybe like the Second World War, it will cause us to reexamine what has caused the fractional division we have in this country. The virus is an equal opportunity infector. And it’s probably the way we would be better if we saw ourselves that way, which is much more alike than different. This story originally appeared on wired.com. Source: The doctor who helped defeat smallpox explains what’s coming (Ars Technica)
  9. [ Because this Ars Technica article will be regularly updated, I'm only posting the title and the link. ] Don’t Panic: The comprehensive Ars Technica guide to the coronavirus This is a fast-moving epidemic—we'll update this guide regularly. Source: Don’t Panic: The comprehensive Ars Technica guide to the coronavirus (Ars Technica)
  10. Kids Can Get Covid-19. They Just Don't Get That Sick New data suggests that children aren’t immune to the new coronavirus. That could have huge implications for efforts to contain local outbreaks. Photograph: Getty Images The outbreak of a new virus always breeds confusion. Where did it come from? How does it spread? How dangerous is it? Ten weeks into the Covid-19 epidemic, enough information has emerged to start filling in some of these gaps. Scientists believe the virus that causes the respiratory disease is likely to be transmitted in droplets through coughing. The available data suggests that a single contagious person will infect about 2.2 others, on average. Globally, 3.4 percent of reported Covid-19 patients have died, though that fatality rate is likely inflated, since people with mild symptoms are probably not being diagnosed and counted in the overall patient pool. But as the weeks have gone by, one mystery has remained: Where are all the kids? In a recent analysis by a team of researchers at Johns Hopkins and in China of more than 72,000 confirmed cases from China, children under the age of 10 accounted for less than 1 percent of all infections. Of the 1,023 deaths recorded in China at the time, not a single child was among them. “We see relatively few cases among children,” World Health Organization director general Tedros Adhanom Gheberyesus told reporters in mid-February. “More research is needed to understand why.” “It’s really very weird,” says Buddy Creech, an infectious disease pediatrician at the Vanderbilt University Medical Center. Mortality patterns associated with most respiratory pathogens traditionally form a U-shaped curve, reflecting more severe disease in the very young and the elderly, says Creech. Respiratory viruses flourish in bodies where the immune system is either still developing or has started to wear out. These include the four coronaviruses that cause the common cold, which tend to be way more common in children than adults. “The new virus that causes Covid-19 appears to flip that,” says Creech. Now, a detailed new study helps to explain what’s been going on. It turns out, it’s not that kids are somehow immune to SARS-CoV-2. They’re just not getting very sick. “Kids are just as likely to get infected as adults,” says Justin Lessler, an infectious disease epidemiologist at Johns Hopkins Bloomberg School of Public Health, who co-led the new study with epidemiologists at the Harbin Institute of Technology in Shenzhen and the Shenzhen Center for Disease Control and Prevention. “If you only have data on cases, which is most of what’s out there, you can’t figure out whether an exposed kid is more likely to get infected than an exposed adult. Nobody besides us has been able to look at data on groups of exposed people to see who got sick and who didn’t.” A few weeks ago, Lessler was contacted by a Johns Hopkins alumnus currently working in China about collaborating on disease modeling using data collected by the Shenzhen CDC. Once he got a look at the data, Lessler realized it could help answer this question about how the virus acts in different age groups. On January 8, the Shenzhen CDC identified its first local case of Covid-19 and began monitoring travelers from Hubei province, the center of the outbreak 700 miles to the north. Over the next few weeks, the agency expanded its surveillance, testing people with fevers in hospitals and local clinics. Altogether, public health officials identified 391 Covid-19 patients and 1,286 people who’d been in close enough contact to these patients to be exposed to the virus. They followed these contacts, testing them regularly to see whether they contracted the disease, even if they never showed symptoms. The team found that children ages 9 and younger who had been exposed to the virus were just as likely to be infected as other age groups—between 7 and 8 percent of the time. But they were much less likely to have the kinds of severe symptoms seen in older groups. In fact, many kids never showed symptoms at all. The researchers posted their analysis to the medRxiv preprint server on Wednesday. The data stops short of explaining why children develop a milder form of illness. But older research conducted on the SARS-CoV-2 virus’ genetic relative, the coronavirus that caused the 2002-2003 SARS outbreak, lends some clues. It also ravaged adults more than children. That global outbreak killed 774 people, or about one in 10 of those SARS infected. Not a single person under the age of 24 died. In severe cases of SARS, a patient would initially have a fever and cough while the virus was rapidly replicating in their lungs. About a week later, they’d spontaneously improve, as their immune system kicked in. But then a second phase of the disease would start, which would be much worse than the first. One study by researchers at the University of Hong Kong focusing on 75 SARS patients found that the second stage, the one that often led to death, wasn’t caused by the virus at all, but by patients’ runaway immune systems. For reasons that still aren’t clear, some people, especially the old and sick, weren’t able to turn off their inflammatory response, leading immune cells and inflammation-inducing molecules known as cytokines to flood into the lungs. This so-called “cytokine storm” caused the most severe symptoms of the disease: pneumonia, difficulty breathing, and organ damage. “These cytokines are supposed to help the immune system clear the virus, but in the people that did poorly the response was overly exuberant, causing more damage than the virus itself,” says Stanley Perlman, a virologist and pediatric infectious disease specialist at the University of Iowa. Covid-19 appears to have some similarities, so doctors have wondered if limiting this inflammation would be helpful. In one of the first studies of Covid-19 patients, doctors at the Zhongnan Hospital of Wuhan University in Hubei reported that nearly half received steroids, which tamp down an immune response. Though the study’s ability to assess outcomes was limited, the authors reported that no treatments proved effective. Perlman says scientists still don’t know exactly why some people respond this way. But in studies with mice, his lab discovered that as animals age, their lungs take on damage that leads to structural changes that make them more susceptible to coronavirus infections. With SARS in particular, the older the mice, the sicker they got. “We know the lung environment really matters with this class of respiratory viruses,” says Perlman. “As people age, that lung environment changes. It gets pelted with pollen and pollution and the body responds with inflammation. A history of inflammation may impact how well you do with coronaviruses.” More research is needed, but it’s a plausible explanation for Covid-19’s mild symptoms in children, says Creech. “The non-inflamed lung is a much less hospitable place for any virus to land,” he says. The next step would be to look at how children with less pristine lungs are faring in the outbreak—like kids with a history of asthma or babies who are born prematurely and lack a substance that helps keep open the tiny sacs in the lungs that exchange oxygen. If these kids experience severe Covid-19 symptoms too, then the “pristine lung” hypothesis holds up. Another (highly speculative) possibility, says Creech, is that somehow kids may be leveraging their previous immune responses to the cold-causing coronaviruses they’re constantly being assaulted with. “Each of us is a little different in how we can modify the tips of our antibodies to latch on to foreign invaders,” says Creech. “It’s possible that recent coronavirus exposure in kids has led to the emergence of antibodies that have some cross-reactivity with the virus that causes Covid-19.” But, he stresses, so far there’s no evidence that’s what’s going on. It may take years of careful experimentation before scientists figure out the mechanism behind why Covid-19 seems less damaging to kids. But Lessler’s research has clear implications for public health interventions now. If kids can get infected, they can likely play a role in further spreading the disease, because their milder symptoms may go undetected. “If we thought that kids weren’t getting infected, then closing schools might be creating undue hardship for people with no real upside,” says Lessler. “But the data suggests that closing schools might be an important thing to do to prevent onward transmission.” As case numbers continue to rise in the US, public health officials will soon be confronted with a choice over which kinds of social distancing strategies to deploy to contain local outbreaks. It may be time to keep the kids at home. Source: Kids Can Get Covid-19. They Just Don't Get That Sick (Wired)
  11. Covid-19: Firms scramble for laptops as work-from-home regulations take effect Some IT firms are keen to procure refurbished systems, thinking that this norm won’t last long But the trend is likely to stay and firms should brace for long-term shift, say experts Mumbai/New Delhi: The rush among companies to meet the new work-from-home norm amid the Covid-19 outbreak has led to a spike in demand for laptops, especially of refurbished leased ones of every kind. There was already a shortage of devices in the market due to the disruption in supplies from virus-hit China. Now, the additional demand has worsened the shortage, said Jaipal Singh, associate research manager (client devices) at IDC India. “The current demand that enterprises have is an immediate one, whereas normally they would place these orders over some time. Given that the supply side is also recovering, enterprises are certainly looking for refurbished devices as an option to maintain business continuity," said Singh. Smaller IT firms are keen to procure refurbished devices in the expectation that the current work-at-home norm won’t last long, which means using these products would keep expenses down. IDC’s Worldwide Quarterly Personal Computing Device Tracker, which covers everything from desktops and workstations to laptops and tablets, forecast a considerable decline in PC shipments in H1 2020. Its research was published in late February, after which the epidemic has expanded rapidly. Many critical components, such as panels, touch sensors and printed circuit boards, come from the badly-hit regions, which will cause a supply crunch heading into Q2 (April-June quarter). As a result, companies are reaching out to the refurbished computers market to meet demand. Nakul Kumar, co-founder and chief operating officer of Cashify, said dealers offering laptops on lease are running out of systems as there is a growing demand for laptops in Delhi by companies urging their employees to work from home. “If it is a long-term contract, they provide new laptops but in case of short-term requirements, they lease out refurbished laptops," added Kumar . Delhi-based SIG Systems which gives out laptops on lease has seen a surge in demand in last few weeks. “We are getting more than 1,000 requests every day from Delhi NCR [National Capital Region]. Earlier, we used to rent out 15 to 30 laptops on a daily basis, but now, we are doing 300-400 laptops every day. The duration of the lease is minimum one month," a SIG Systems spokesperson said. According to a personal computing (PC) industry person, demand for new laptops, including the cost-effective Chromebooks from leading vendors like HP, has spiked significantly in the last few weeks from both individual users as well as enterprise clients. To be sure, most IT companies have protocols on the extent to which teams are authorized to work from home and many client-specific projects would not allow it normally. On Monday, Brihanmumbai Municipal Corporation (BMC) commissioner Praveen Pardeshi asked private firms in Mumbai to function “only at 50% of their staff capacity or face action under section 188 of the IPC" following a large number of positive cases in Maharashtra. So, in addition to laptops, companies are also trying to procure interim digital collaboration tools to enable employees to work remotely, ensuring security controls and network support are in place, said research firm Gartner Inc. “We see remote working is likely to become a mainstream mode of working after the event, and organizations should expect this to be a permanent and persistent pattern in their workplace and prepare for this long-term shift. This would mean demand for remote working tools, laptops and network bandwidth over a period is going to grow," said D.D. Mishra, senior director analyst at Gartner. Source
  12. Viral weak spots — COVID-19: the biology of an effective therapy We already know lots about coronavirus biology. Enlarge Aurich Lawson / Getty 45 with 29 posters participating, including story author A coronavirus vaccine may not arrive for at least a year—so what are the chances of finding a useful therapy that could stave off the worst effects of the virus in the meantime? Earlier coronavirus outbreaks like SARS and MERS raised warning flags for public health officials. Fortunately, they also alerted the biological research community that this large family of viruses was worth studying in more detail. Recent research has built on a large body of knowledge about coronaviruses that have long caused significant diseases in livestock, and so SARS-CoV-2 does not arrive as a total unknown. Indeed, we are actually in a decent position to understand what might make a good potential therapy. While some of the therapies being tested may seem random—we're trying chloroquine, an antimalarial drug?—there's serious biology behind what's being done. Genes without DNA A basic challenge confronts all viral therapies: most viruses have just a handful of genes, and they rely on proteins in the cells they infect (host cells) to perform many of the functions needed to reproduce. But therapies that target host cell proteins run the risk of killing uninfected cells, making matters worse. So antiviral therapies usually target something unique about the virus—something important enough that a few mutations in the virus won't make the therapy ineffective. Those of you who didn't sleep through high school biology may remember that genetic information is carried by DNA. When a protein needs to be built, the relevant bit of DNA is read and the cell makes a temporary copy of the information using a very similar chemical called RNA. This piece of RNA is then translated into a sequence of amino acids, which form the protein. While there are some exceptions to this—many RNAs perform important functions without ever being translated into proteins—all RNA in our cells is made by transcribing a DNA sequence. But we've known for a long time that this process doesn't hold for viruses. Many viruses, including HIV and the influenza virus, use RNA for their basic genetic material. The coronavirus is also an RNA virus; it consists of a single, 30,000-base-long RNA molecule. This is a problem for the virus. The host cells it infects only have proteins that copy DNA, not RNA, so how can more copies of the virus get made? Target: reproduction It turns out that the virus carries its own solution with it. When virus' RNA genome first enters a cell, it interacts with the host's protein-making machinery, using it to make proteins that can copy RNA molecules. These RNA-copying proteins, called "polymerases," make an enticing target for therapies. Because host cells don't naturally have them, therapies that target these RNA-making proteins should have a lower chance of off-target effects. Block these RNA polymerases, and the virus can no longer reproduce, stopping an infection. That's the good news. The bad news is that DNA and RNA are so closely related that it can be difficult to make a drug that affects only one type of polymerase. We saw this with some of the first therapies against HIV, which targeted the enzymes that copied the virus' RNA genome: they did slow the virus down, but they also harmed any rapidly dividing cells in the host. Enlarge / The 30,000 base long coronavirus genome is used to produce a large variety of proteins. Sawicki, Sawicki, and Siddell/J. Virology So the work is tricky. But many such drugs have been developed that don't interact as well with our own DNA polymerases. Some have even been tested for safety in humans, since they were developed for earlier threats like HIV or Ebola. Now, several are being quickly tested against coronavirus. One such drug, remdesivir, was originally developed in the hope that it would limit Ebola virus and its relatives. While that hasn't worked out, the drug was safe for human use and showed promise in its ability to limit the spread of another coronavirus (MERS-CoV) in cultured cells. As a result, it was quickly tested against SARS-CoV-2, and the results were also positive. The National Institutes of Health started a clinical trial against COVID-19 in February. Vincent Racaniello is a faculty member at Columbia University and the host of the This Week in Virology podcast. He believes that RNA polymerases are so similar across a range of coronaviruses that we might find a single molecule that inhibits them all. To Racaniello, our response to SARS and MERS wasted a great opportunity. "We could have had a broadly acting antiviral that targeted RNA polymerase by now," he told Ars. "We could have had people isolating the gene from various bat coronaviruses and doing screens to see if we could find compounds that could have inhibited them all. That's the kind of thing that's doable and should have been done. And if we had such antivirals ready, they could have been used right at the onset in China." Target: processing RNA copying polymerases aren't the only potential therapeutic targets for a coronavirus. Their RNA polymerases are initially made in forms that aren't fully functional; instead, they must have small pieces snipped out in order to adopt their mature configuration. Coronavirus RNA therefore encodes two or three proteins that do this cutting. They belong to a class of proteins collectively termed "proteases" for their protein-cutting ability. Proteases typically have a very specific site where the cutting takes place, and any chemicals that can fit into this site might shut the protease down. Not surprisingly, such chemicals are called protease inhibitors. This approach has been used successfully against other viruses, notably including HIV. Scientists have now found that protease inhibitors targeted to HIV might have activity against coronavirus, despite the fact that these viruses are unrelated. Because proteases are present in small numbers in infected cells and have a catalytic activity that depends on a single, specific site, Racaniello views them as some of the most promising targets for therapies. We've also got large libraries of chemicals that are known to inhibit similar proteins, many of which are already approved for use in humans. So, while the news around protease inhibitors has been somewhat limited, expect it to pick up dramatically as more of these molecules are screened. Enlarge / The structure of a coronavirus protease. Protein Database Japan Target: packaging After replication, viral RNA can't continue an infection until it is packaged up into a mature virus and gets outside of the host cell. This requires special packaging proteins. (In coronavirus, these proteins do double duty by also helping the viral RNA link up with its copying enzymes.) This packaging step would seem to provide a great opportunity for targeted therapy, as disrupting it should limit the amount of functional virus that gets made and exported from any particular cell. But drugs that try to block viral packaging are rare—Racaniello can only think of one, a treatment for Hepatitis B that causes the mature virus particles to form without any genetic material inside. "That's been a very unusual antiviral," Racaniello said. "There's no other like it." Part of the problem, he said, is that structural proteins like this are present in high numbers, since they're part of every single virus particle that's produced. And you have to interfere with all these copies to be effective. Another problem is that the interactions among proteins and genetic material during packaging of a virus tend to involve extensive contacts between multiple molecules. These are a bit harder to disrupt specifically, and doing so may require large molecules that don't diffuse in and out of cells well. So, while we know which protein binds to the RNA and helps package it inside the virus particle, this protein is not an obvious target for therapies. It's also hard to disrupt newly packaged viruses as they are moved out of the cell. Once packaged, coronaviruses leave their host cell via an export system that's normally used to send material to the cell's surface (a process called exocytosis). This process is fairly generic—it works with a huge variety of proteins in addition to those encoded by coronaviruses—making it vital for cell survival. As a result, there are not many places where we can intervene without shutting down exocytosis in healthy cells as well. Target: the viral shell Once we have a mature virus particle, its behavior is controlled by the proteins that form the exterior structure of the virus. In the coronavirus, two of these proteins (called "membrane" and "envelope") combine with some of the cell's membrane to form the virus' shell. There's also the spike protein, which creates a halo (or "corona," meaning "crown") around the virus that gives it its name—and which serves to latch on to cells to enable infection. In some coronavirus strains, the envelope protein can be eliminated without blocking the virus from infecting cells, which means it's a lousy target for therapies. The membrane protein is the most abundant protein on the surface of the virus, but it's small and buried within the membrane (as its name implies). Not much of it is accessible to the outside world. Combine that with the fact that it doesn't appear to have an enzymatic function, and it's not an ideal target, either. That leaves the spike protein. Spike is a complicated protein that provides a wealth of targets for potential therapies. As the most prominent feature of the virus' exterior, spike is the main target of antibodies against the virus produced by the immune system. We've already got the structure of the coronavirus' primary surface protein. Wrapp et. al. This reality has already led to one option for therapies: purifying plasma from people who have fought off a coronavirus infection, on the assumption that the plasma contains antibodies that can neutralize the virus. This plasma can then be infused into sick people, where the antibodies should help the immune system clear the virus. While it's only a temporary fix—antibodies don't survive indefinitely in the blood stream—it may give a patient's own immune system sufficient time to develop its own antibodies. There are unknowns about whether infected individuals produce effective antibodies—more on that immediately below. But the big issue here is scaling, as plasma treatment relies on having enough healthy, formerly infected individuals who are willing to donate blood plasma. If used strategically—on the most at-risk patients, or to help infected health care professionals—it could be a helpful tool, but isn't likely an effective general therapy. A different approach to antibodies But antibodies therapies aren't limited to infusing blood plasma. Once the immune system generates cells that produce anti-coronavirus antibodies, we can pull out the genes that encode these antibodies, insert the genes into plant cells, and get those cells to pump out large quantities of the antibodies. With a bit of time, we might even produce a cocktail of several antibodies that all bind to coronavirus, and do so in quantities that could make this an effective therapy for those infected. (This approach was tried during an Ebola virus outbreak.) This approach will take longer to develop and vet for safety, so it won't be the quick fix provided by blood plasma. But it does offer the promise of scale, producing sufficient quantities of the therapy to treat entire populations. It also provides us with the ability to carefully select the antibodies we produce. While our immune systems produce antibodies to viruses like HIV and influenza, many of these bind to parts of the virus that can easily change through mutations. That makes them ineffective, since the virus has an opportunity to evolve. What we need are "broadly neutralizing" antibodies, which seem to bind to parts of the virus where mutational changes can't occur without compromising its basic function. In many cases, broadly neutralizing antibodies turn out to stick to the parts of the virus that latch on to human cells to start new infections, and thus they block the virus' ability to infect anything. At the moment, we simply don't know how much the proteins on the surface of SARS-CoV-2 can change while still retaining their function. We can make some inferences based on what we've seen in other coronaviruses, but experts have reached somewhat different conclusions. This is a research area to watch carefully, because the rate of change in the surface proteins will dictate how effective antibody-based therapies are—and how easy it will be to develop a vaccine. Fortunately, things are moving quickly, with one company announcing on Wednesday that it has identified hundreds of antibodies that target SARS-CoV-2. It estimates that it could have sufficient production for testing by the summer and be making hundreds of thousands of doses a month by the end of the summer. Target: new infections The final step in the virus' life cycle is infecting a new cell. Typically, what is taught here is a "lie of simplification," which goes: the virus latches on to a protein on the cell's surface, then uses that protein to gain entry into the cell. This is true as far as it goes, but for most viruses, things are considerably more complicated. Coronaviruses definitely fall into the "more complicated" category in this regard. SARS-CoV-2 does latch on to a protein on the surface of cells in the respiratory tract; we've already confirmed that it's the same protein as the one used by the original SARS-CoV. But that doesn't immediately result in viral contents entering the cell. Instead, the complex of virus and receptors stays on the outside of the cell membrane. That membrane, however, gets pulled into the cell and "pinched off" from the cell's surface, creating a sac within the cell that now contains "outside" material. Enlarge Aurich Lawson Once this occurs, the virus is technically inside the cell, but it's still on the wrong side of a membrane from everything it needs to reproduce. The cell takes over this compartment, lowering its pH and adding enzymes to break down its contents. Corona and other viruses actually take advantage of these changes to enable their infection. In the case of coronavirus, a protease made by the host cell cuts the viral spike protein. Once cut, the spike protein triggers a merger between the membrane in the virus' coat and the membrane of the compartment it is trapped in. This finally places the virus' genome inside the cell, where it can proceed with the infection. This series of events provides potential targets for therapies. One of these targets is the drop in pH. This is the step that's targeted by chloroquine, the antimalarial drug. Chloroquine can cross membranes and so can enter the sac containing the virus. Once there, it can neutralize the pH. That's significant, because many proteases are only active at lower pH. If the pH inside the sac doesn't change, it's possible that the coronavirus spike protein won't be cut and thus won't be activated. This appears to be the case in cultured cells infected by the virus, and there are anecdotal case reports of chloroquine helping COVID-19 patients. The host cell proteases themselves also make a tempting target. A paper we mentioned above identified a protease that appears to be essential for the coronavirus spike protein's activation. That team showed that an inhibitor of this protease blocked coronavirus infections in cultured cells. The inhibitor has been approved for use in humans by Japan, so this may be another promising avenue for tests. (Racaniello notes that this protease is also used to activate influenza viruses.) The risk here is that the protease in question might also play an essential role in healthy cells. Finally, it's tempting to directly target the interactions between the spike protein and the protein it binds. But Racaniello says that these interactions are extensive, and they can be difficult to disrupt with a single molecule. It's been tried with HIV but mostly came up short. The only thing that has worked is a 30-amino-acid-long protein that mimics part of the protein HIV binds to, but that can't be stored in water, and it needs to be mixed up and injected for use—not the sort of thing likely to be helpful when a pandemic is limiting healthcare resources. Beyond the obvious There are plenty of options for interfering with coronavirus based on what we already know about its biology. But there are still many things we don't know. A recent article in the New York Times described how scientists have identified hundreds of proteins made by host cells that interact with proteins encoded in the coronavirus genome. We don't know the significance of most of these interactions and whether or not they're important or coincidental, but any of them could potentially lead to a therapy. That would, however, probably take longer than a targeted therapy, since there are more steps involved in screening for effective drugs than there are in, say, screening a library of known protease inhibitors against the coronavirus' proteases. There's also the potential to intervene at the level of the body's response to the virus, rather than targeting the virus itself. The more damaging consequences of some infections come from an exaggerated immune response to the virus. Biotech giant Genentech, for example, announced on Thursday that it was starting clinical trials of an immune-dampening treatment on hospitalized coronavirus cases. The potential return for having any useful therapy is so large that it's worth following as many of these paths as we can at once. The easiest way to understand why is to return to the epidemiological model we covered earlier this week. The model indicated that any steps short of extreme isolation measures would likely allow the virus to overwhelm the healthcare system—and any easing off of restrictions could lead to a resurgence within weeks. Extreme restrictions, however, will probably cause severe economic problems, especially if the only hope is a vaccine that might be over a year off. But the model has an obvious gap: it doesn't account for an effective therapy. If any of the approaches described above—or one we didn't consider—is even moderately effective, it could radically change our circumstances. It could ensure that far fewer coronavirus cases need hospitalization, and that fewer of those that do require critical care. A country's healthcare system could then continue functioning in the presence of a higher rate of infection, which in turn could mean that less dramatic social restrictions are required. If carefully managed, this might even allow countries to allow enough infections so that they achieve herd immunity before the availability of a vaccine. We are just beginning clinical trials on a small subset of these ideas now, so we're still facing difficult times in the months to come. And it's important to emphasize that there's no guarantee that any of these approaches will work. But finding a therapy does offer hope that the difficult months of isolation in our immediate future might not stretch to the end of the year. Source: COVID-19: the biology of an effective therapy (Ars Technica)
  13. BEIJING (Reuters) - A Beijing district put itself on a “wartime” footing and the capital banned tourism and sports events on Saturday after a cluster of novel coronavirus infections centred around a major wholesale market sparked fears of a new wave of COVID-19. Forty-five people out of 517 tested with throat swabs at the Xinfadi market in the city’s southwestern Fengtai district had tested positive for the coronavirus, Chu Junwei, a district official, told a briefing. None were showing symptoms of COVID-19, he said, but added that 11 neighbourhoods in the vicinity of the market, which claims to be the largest agricultural wholesale market in Asia, had been locked down with 24-hour guards put in place. “In accordance with the principle of putting the safety of the masses and health first, we have adopted lockdown measures for the Xinfadi market and surrounding neighbourhoods,” Chu said. The district is in a “wartime emergency mode,” he added. The closure of the market and new restrictions come as concerns grow about a second wave of the pandemic, which has infected more than 7.66 million people worldwide and killed more than 420,000. They also underline how even in countries which have had great success in curbing the spread of the virus, clusters can sometimes easily arise. The entire Xinfadi market was shut down at 3 a.m. on Saturday (1900 GMT on Friday), after two men working at a meat research centre who had recently visited the market were reported to have the virus. It was not immediately clear how they had been infected. People are wearing face masks inside the Jingshen seafood market which has been closed for business after new coronavirus infections were detected, in Beijing, China, June 12, 2020. On Saturday, market entrances were blocked and police stood guard. Beijing authorities had earlier halted beef and mutton trading at the market and had closed other wholesale markets around the city. They plan for more than 10,000 people at the Xinfadi market to take nucleic acid tests to detect coronavirus infections. According to the Xinfadi website, more than 1,500 tonnes of seafood, 18,000 tonnes of vegetables and 20,000 tonnes of fruit are traded at the market daily. TOURIST SITES CLOSE A city spokesman told the briefing that all six COVID-19 patients confirmed in Beijing on Friday had visited the Xinfadi market. The capital will suspend sports events and tourists from other parts of China, effective immediately, he said. In Nanjing, capital of the eastern province of Jiangsu, a local association of restaurants said it would halt the serving of foods containing raw seafood or animal products. Some Beijing residents, including a man shopping at a Carrefour supermarket in Fengtai district, said they were confident authorities had the situation under control. “If I were worried, I wouldn’t come here to buy meat. I believe it has been quarantined,” said the man, who gave his surname as Zhang. Beijing’s Yonghe temple and National Theatre also announced they would close from Saturday, and the city government said it had dropped plans to reopen schools on Monday for students in grades one through three because of the new cases. One person at an agricultural market in the city’s northwestern Haidian district also tested positive for the coronavirus, Chu said. Highlighting the new sense of alarm within the city, health authorities visited the home of a Reuters reporter in Beijing’s Dongcheng district on Saturday to ask whether she had visited the Xinfadi market, which is 15 km (9 miles) away. They said the visit was part of patrols Dongcheng was conducting. And following reports in state-run newspapers that the coronavirus was discovered on chopping boards used for imported salmon at the market, major supermarkets in Beijing removed salmon from their shelves overnight. That concern also spread to other cities, with a major agricultural wholesale market in Chengdu, the capital of the southwestern province of Sichuan, saying it would remove salmon products from its shelves from Saturday. Slideshow of 8 images at the Source Source
  14. The COVID-19 pandemic has led to a significant drop in emergency room visits among patients with other ailments, the Centers for Disease Control and Prevention said. Visits to hospital U.S. emergency rooms have dropped by more than 40 percent so far in 2020, compared to the same period last year, according to figures released Wednesday by the U.S. Centers for Disease Control and Prevention. The statistics indicate that a significant number of Americans may have delayed or declined emergency care because of the COVID-19 pandemic, the agency said. In their analysis of ER visit trends, CDC researchers analyzed data from the National Syndromic Surveillance Program for the period of Jan. 1 through May 30. The program includes data from all U.S. states except Hawaii, South Dakota and Wyoming. Changes in how hospitals, and specifically ERs, are used could be a lasting legacy of the new coronavirus, according to some public health experts. Many patients who once addressed health concerns by heading to the ER could be managed remotely, using telemedicine, Dr. Paul Biddinger, during a conference call with reporters on May 26. Biddinger, vice chair for emergency preparedness in the Department of Emergency Medicine at Massachusetts General Hospital, was not part of the CDC analysis. "People have been working for years, probably really fair to say decades, on telemedicine, when it's appropriate for patients not to have to come to the hospital, but they can see their doctor remotely," Biddinger said. "And the pandemic forced a lot of that on us," he said. The CDC researchers compared total visits so far this year to the same five-month period in 2019. The number of ER visits declined from a mean of roughly 2.1 million per week between March 31, 2019, and April 27, 2019, to a mean of 1.22 million per week during the "early pandemic" period of March 29 to April 25 of this year, according to the CDC. ER visits declined for every age group, with the largest proportional declines in children 10 years old and younger at 72 percent and children 11 to 14 years old at 71 percent, the agency said. Researchers found the largest declines in ER visits occurred in the New England states at 49 percent, as well as in the mid-Atlantic region at 48 percent. That region includes New York and New Jersey, which has been the epicenter of the U.S. COVID-19 outbreak. ER visits related to abdominal pain and other digestive problems fell by more than 66,000 per week from year to year, while those among patients reporting musculoskeletal pain -- excluding low-back pain -- dropped by more than 52,000 per week, according to the CDC report. Visits for "sprains and strains" declined by nearly 34,000 per week, and those related to "superficial injuries" fell by nearly 31,000 per week, the researchers said. Conversely, ER visits for "exposure, encounters, screening or contact with infectious disease" increased by nearly 19,000 per week from 2019 to 2020, the analysis found. Specifically, some 18,000 ER visits occurred per week across the country for COVID-19 symptoms through the end of May, the researchers said. Still, additional research is needed to determine whether the decline in ER visits could be also attributed to "actual reductions in injuries or illness [due] to changing activity patterns during the pandemic" lockdown, the CDC researchers wrote. "The striking decline in [ER] visits nationwide, with the highest declines in regions where the pandemic was most severe, suggests that the pandemic has altered the use of the [ER] by the public," researchers said. Source
  15. COVID-19 vaccine must protect 50% of people for approval, FDA says FDA sets rules for vaccine approval amid concern of hastiness and political pressure. Enlarge / Stephen Hahn, Commissioner of Food and Drugs at the US Food and Drug Administration (FDA), speaks during a Senate Health, Education, Labor and Pensions Committee hearing on June 30, 2020, in Washington, DC. Getty | Al Drago 59 with 49 posters participating Any experimental COVID-19 vaccines aspiring to earn regulatory approval from the Food and Drug Administration will need to prevent or decrease the severity of disease in at least 50 percent of people, the agency announced Tuesday. The criterium is part of a larger set of guidelines released by the agency for developing a vaccine to halt the spread of pandemic coronavirus, SARS-CoV-2—which causes COVID-19 and is now accelerating in much of the country after months of sustained devastation. With the guidelines, the FDA tried to dispel fears that the rush to develop a COVID-19 vaccine may come at the expense of adequate safety testing. “We recognize the urgent need to develop a safe and effective vaccine to prevent COVID-19,” FDA Commissioner Stephen Hahn said in a statement. “While the FDA is committed to expediting this work, we will not cut corners in our decisions and are making clear through this guidance what data should be submitted to meet our regulatory standards.” Exceptions The agency also hopes to assuage concerns that it has succumbed to political pressure from the Trump administration in making regulatory decisions during the pandemic—eschewing its reliance on efficacy and safety data. Most notable is the case of hydroxychloroquine, a malaria drug known to have severe potential side effects, including triggering potentially fatal heart arrhythmias. Despite a lack of evidence for its efficacy against COVID-19, President Trump touted the drug as a “game changer” and even admitted to taking it himself. The FDA made the unusual decision to issue an Emergency Use Authorization (EUA) for hydroxychloroquine and the related drug, chloroquine, in late March. The EUA allowed doctors to use the drugs to treat COVID-19 patients outside of clinical trials, despite the lack of the evidence. As data piled up that the drugs are ineffective against COVID-19 and come with serious risks, the FDA revoked the EUA in mid-June. Though political leaders, health experts, and media reports have suggested the Trump administration influenced the FDA’s initial decision to issue an EUA, Hahn has denied this. In a Congressional hearing June 23, he testified that “I have not felt political pressure nor has the FDA to make any decision in any specific direction.” He echoed the point in today’s announcement of the vaccine guidelines, saying “We have not lost sight of our responsibility to the American people to maintain our regulatory independence and ensure our decisions related to all medical products, including COVID-19 vaccines, are based on science and the available data.” In the announcement, the FDA noted that, although the guidelines lay out what’s needed for full approval, the agency may still consider issuing an EUA to candidate COVID-19 vaccines on a “case-by-case” basis. The agency said it would consider an EUA based on “the target population, the characteristics of the product, and the totality of the relevant, available scientific evidence, including preclinical and human clinical study data on the product’s safety and effectiveness.” COVID-19 vaccine must protect 50% of people for approval, FDA says
  16. China moves forward with COVID-19 vaccine, approving it for use in military Early trial data suggests that vaccine is safe, but efficacy still unclear. Enlarge / Chinese President Xi Jinping learns about the progress on a COVID-19 vaccine during his visit to the Academy of Military Medical Sciences in Beijing on March 2, 2020. Getty | Xinhua News Agency 31 with 28 posters participating China has approved an experimental COVID-19 vaccine for use in its military after early clinical trial data suggested it was safe and spurred immune responses—but before larger trials that will test whether the vaccine can protect against SARS-CoV-2 infections. This marks the first time any country has approved a candidate vaccine for military use. China’s Central Military Commission made the approval June 25, which will last for a year, according to a filing reported by Reuters. The vaccine, developed by biotech company CanSino Biologics and the Chinese military, is a type of viral vector-based vaccine. That means researchers started with a viral vector, in this case a common strain of adenovirus (type-5), which typically causes mild upper respiratory infections. The researchers crippled the virus so that it doesn’t replicate in human cells and cause disease. Then, they engineered the virus to carry a signature feature of SARS-CoV-2—the coronavirus’s infamous spike protein, which juts out from the viral particle and allows the virus to get a hold on human cells. The idea is that, when the harmless vaccine virus is injected into the body, it will essentially present the SARS-CoV-2 spike protein to the immune system, which can then develop anti-SARS-CoV-2 responses. Those include antibodies, which are Y-shaped proteins that surveil the body and detect previously encountered germ invaders by key features. Once a germ is detected, neutralizing antibodies can glom onto the germ and prevent it from sparking an infection. In a Phase 1 safety trial involving 108 people, the vaccine—dubbed Ad5-nCoV—proved safe and was able to spur the production of neutralizing antibodies and other immune responses. However, the study, published in The Lancet, also detected a potential foil for the vaccine candidate: in people who had been infected with Ad5 in their past, the vaccine didn’t generate as strong of a response to SARS-CoV-2’s spike protein. This may be because their immune systems quickly recognized the adenovirus and focused their responses on the viral vector, rather than the nefarious spike. CanSino said it had since completed a larger Phase 2 trial, looking at safety and efficacy, but has yet to release results, according to the South China Morning Post. The paper also noted that CanSino has reached an agreement with the Canadian government to conduct Phase 3 trials there. Those trials will look at efficacy and potential side effects in an even larger group of people. In the meantime, CanSino declined to say if members of the Chinese military would be required to receive the experimental vaccine or if it would be optional, according to Reuters. According to the latest tally by the World Health Organization, there are 17 COVID-19 vaccine candidates in clinical trials and 132 others in pre-clinical development. Many vaccines are being developed in China, but with the now-limited spread of the coronavirus there, researchers are working to conduct vaccine trials elsewhere, in areas still seeing heavy transmission. China moves forward with COVID-19 vaccine, approving it for use in military
  17. Apple will battle COVID-19 by designing and making millions of medical face shields Company joins GM, Tesla, startups, and more to make supplies to battle COVID-19. Apple CEO Tim Cook took to a Twitter video to announce that the company will design and make face shields for medical workers battling the COVID-19 crisis, to the tune of one million shields per week. This announcement follows already publicized efforts to source face masks from the company's supply chains; Cook said that effort has produced 20 million face masks to date. "We've launched a company-wide effort bringing together product designers, engineering, operations, and packing teams and our suppliers, to design, produce, and ship face shields for health workers," Cook explained in the two-minute video. He added that one shipment has been delivered to Kaiser hospital facilities in the Santa Clara valley and that the company expects to make one million face masks by the end of the week and just as many each following week. Cook went on to explain that the shields "pack flat, one hundred to a box" and that each shield can be assembled in under two minutes. Both materials and manufacturing will be sourced from the United States and China, Apple's two primary countries of operation. For now, Apple is distributing the masks within the United States, but Cook said the company hopes to expand to other countries and regions in the future. He ended his statements by encouraging viewers to follow local guidelines to shelter in place and maintain social distancing to slow the spread of the virus. Apple is not the only company putting some resources toward producing critical supplies for the response to COVID-19. Tesla announced plans to work on ventilators, GM has worked at sourcing face masks, and many 3D printing startups have found their moment in this crisis, to name a few. Even some brewing companies have pivoted in full or in part to producing hand sanitizer. The range of corporate responses to the crisis ranges from positive efforts like this to negative ones like mass layoffs or even efforts to profit off of the crisis. Listing image by Justin Sullivan/Getty Images Source: Apple will battle COVID-19 by designing and making millions of medical face shields (Ars Technica)
  18. Plastic bags are making a comeback because of COVID-19 There’s no evidence of reusable bags spreading the novel coronavirus, but people are being cautious Photo by Fiona Goodall / Getty Images With grocery stores being one of the few places still open during COVID-19 lockdowns, disposable plastic bags are making a comeback as some people fear that reusable bags could spread the disease. Before the pandemic, a growing number of governments banned single-use plastic bags in an effort to cut down on waste. But as the novel coronavirus has spread around the globe, people have gotten leery about coming in close contact with other people and their possessions, including reusable bags. On March 31st, New Hampshire became the first state in the US to temporarily ban reusable bags during the pandemic. “For whatever reason, people seem to get very fired up about grocery bags,” says Meghan May, a professor of microbiology and infectious disease at the University of New England College of Osteopathic Medicine. “Ordinarily I use [reusable bags] all the time because I live in a beach town and a clean ocean is really important,” May tells The Verge. But now she and many others are thinking twice. Like pretty much everything else right now, reusable bags should probably be handled more carefully to minimize the risk of transmitting disease to other people. At the same time, there has been no evidence so far that using reusable grocery bags have been responsible for spreading the novel coronavirus. We don’t really know how long the novel coronavirus can persist on reusable bags. The best data experts have is from one study that found that the virus could stay viable on plastic for up to three days in lab conditions. (That means shoppers may want to be careful when handling disposable plastic bags, too, environmental advocates contend.) That research didn’t look into how the virus fares on fabric, so we can’t apply its findings directly to cloth bags, according to May. Shoppers should still take precautions with reusable bags, despite the lack of data, May advises. “One would want to err on the side of caution here because we know [the virus] can survive on many different types of surfaces,” she says. “We should probably assume that it can be transmitted that way until someone demonstrates that it can’t.” One way to stop the spread of germs is to wash reusable bags before and after each use. (That’s in addition to washing your hands before and after you go to the store, avoiding touching your face, wiping down baskets and carts, and bagging your own items.) Plastic and nylon bags can be cleaned with soap and water, then sprayed or wiped down with a diluted bleach solution or disinfectant, according to recommendations from North Carolina State University. Make sure to clean both the inside and outside of the bag and let them air dry before storing or using them, the university adds, and cloth bags can be washed like laundry, then they should be dried on the warmest setting. But the virus could transfer quickly from one person to an item they’ve been in close contact with, like a bag, reusable or otherwise, May points out. If an infected person hands the bag to someone else, they risk passing along the virus. The person who faces the most risk, according to May, is the grocery store worker interacting with many customers throughout his or her shift. “They have to touch [the reusable bag], handle it and pack things into it, and then they have to then turn around and do that with the next customer that comes in their line,” May says. “The person at least risk is the person who owns the bag.” That’s why some grocery stores and states are turning back to disposable bags: they simply aren’t handled quite as much, so there’s less uncertainty over where they’ve been. But protecting public health doesn’t have to be at odds with efforts to stem the flood of plastics filling landfills and collecting in the ocean, environmental advocates say. “If stores, particularly workers, want to keep themselves as safe as possible and limit the bags coming in because they don’t know if people wash them, certainly a temporary pause on that, I think that’s understandable,” Ivy Schlegel, a senior research specialist for Greenpeace USA, says. But that “pause” shouldn’t be permanent, says Schlegel. She has followed the plastics industry’s history of fighting environmental reforms by claiming that reusable bags are unsanitary. She sees the industry seizing the opportunity now to push its own agenda. A frequently cited 2011 study that found bacteria in seldom-washed reusable bags was actually underwritten by a fossil fuel and chemical industry group, the American Chemistry Council. It was cited in a March 18th letter that the Plastics Industry Association penned to the Department of Health and Human Services asking that the department “speak out against bans on [single-use plastic] products as a public safety risk.” “Some people will call it disaster capitalism,” says Schlegel. “Using this moment where everything is in chaos and people are legitimately concerned about public health to turn back the clock to go back to a world where plastic is the norm, rather than right now where reusables are becoming the norm in many places.” The plastic pollution problem isn’t going away anytime soon. A plastic grocery bag adrift in the ocean can take up to 20 years to decompose. A plastic bottle could stick around for up to 450 years, according to estimates from the National Oceanic and Atmospheric Administration. Less than 10 percent of all plastics have actually been recycled. The industry knew all along that recycling wouldn’t solve the environmental harms posed by plastic, but it continued to promote it as a viable solution anyway, according to a joint investigation by PBS Frontline and NPR published this week. There are ways to limit plastic waste during the COVID-19 pandemic. May recommends simply carrying groceries straight from the basket or cart to your car if that’s possible. Paper bags are another alternative; they are still single-use, but at least they’re compostable. And Schlegel tells The Verge that one way to make reusable bags cleaner and more convenient in the future could be to implement municipal programs that pick up residents’ reusable bags, sanitize them, and then return them to stores for reuse. Those solutions might not be available everywhere during this pandemic, but they’re worth thinking about as we prepare for what comes next. In the long run, protecting public health and the planet usually go hand in hand. Source: Plastic bags are making a comeback because of COVID-19 (The Verge)
  19. FDA authorizes first antibody-based test for COVID-19 Antibody tests aren’t great diagnostics Photo: Xinhua / Shen Bohan via Getty Images The Food and Drug Administration has issued its first authorization for a COVID-19 test that looks for antibodies in the blood, rather than for the virus in the nose or throat. While the antibody approach means this test will have limitations, it’s an important tool that could help in the response to the pandemic. The test is produced by the biotechnology company Cellex. Health care providers have to draw blood from a patient’s vein to run the test, and it can only be done in certified labs — not a doctor’s office. It takes 15 to 20 minutes to get a result. When someone is infected with a virus for the first time, their immune system begins producing antibodies specific to that virus. Checking to see if someone has coronavirus-specific antibodies is good evidence that they’ve been infected. However, the body doesn’t start to make these immediately, and they might not appear until someone’s illness has run its course. As a result, antibody-based tests can tell doctors whether someone has already had COVID-19, but they’re not as good at testing if the patient currently has it. Still, the FDA authorization indicates that the agency thinks the benefits of having the test available outweigh the risks. “It is reasonable to believe that your product may be effective in diagnosing COVID-19,” the agency wrote in the letter, which authorized the test for emergency use. The FDA was already allowing companies to make and distribute antibody tests for COVID-19 without formal authorization. However, without approval, they were not able to claim that their test could diagnose the disease. Even if they’re not great diagnostics, antibody tests are critical in the response to the pandemic. They’d help figure out who has already been sick — whether they had significant symptoms or not — and therefore, who is probably immune enough to the virus to safely move around the world normally. They’ll also help public health officials understand how much of the population has been infected by the coronavirus. Dozens of companies are working to develop antibody tests, as are researchers at the Centers for Disease Control and Prevention. The US struggled to ramp up COVID-19 testing, and it’s still hard for people to access tests. Though there have been over 1 million tests run in the US, a milestone President Trump highlighted earlier this week, the testing rate per capita is still far behind other countries. An easily available antibody test would give people who were not able to get tested when they were sick a chance to know if they actually had COVID-19. Source: FDA authorizes first antibody-based test for COVID-19 (The Verge)
  20. The world is in lockdown due to the spreading coronavirus COVID-19, with bars, pubs and clubs forced to close. Image: Covid-19 graffiti was sprayed onto a boarded up bar called Mocka Lounge in Cardiff, Wales, amid the coronavirus-induced lockdown that's been put into place in countries around the world The lockdown is hitting these drug-taking hotspots hard and having knock-on effects everywhere—including darknet drug dealers who accept bitcoin as payment. It's thought some $600 million worth of bitcoin was spent on darknet markets during the last three months of 2019, according to a recent report from bitcoin, crypto, and blockchain data research firm Chainalysis, with spending steadily rising over recent years. However, bitcoin spending on darknet markets, which allow users to buy everything from illegal drugs to guns and stolen goods, has dropped since the coronavirus COVID-19 began spreading out of China in late February, Chainalysis has found. "The effects of the COVID-19 [bitcoin] price drop on darknet markets is especially interesting," the Chainalysis team wrote in a blog post this week. The bitcoin price crashed in mid-March, losing almost half its value in the space of a week, as markets around the world went into free fall in anticipation of a global coronavirus-induced shutdown. "Darknet market revenue has fallen much more than we’d expect following bitcoin’s recent major price drop," Chainalysis reported, noting that supply problems for Mexican drug cartels and dealers in China’s Hubei province could be "hampering darknet market vendors’ ability to do business." "Perhaps darknet market customers aren’t buying as many drugs given the public health crisis," Chainalysis wrote. "It’s also possible that vendors slowed down sales during the price drop, out of fear that the bitcoin they accept one day could be worthless the next. But it’s also likely that COVID-19 itself is making it harder to sell drugs at the moment." Across the U.S. and Europe, bars, clubs, and pubs are settling into what some fear could be a long-term lockdown, designed to limit the spread of the coronavirus COVID-19. The White House coronavirus co-ordinator has said recent projections show between 100,000 and 200,000 Americans could die due to COVID-19, with over 181,000 confirmed coronavirus cases and 3,606 deaths in the country so far—more than in China, where the disease was first discovered. It's thought as many as three in every four Americans are now, or about to be, under some form of lockdown, only allowed out to get essential supplies and medicines or limited forms of exercise. The economic consequences of the mass lockdown have already spread to every corner of society, with millions of people losing their jobs and a global recession a near certainty despite extreme action from the U.S. government and central banks around the world to limit its impact. Image: The dollar value of bitcoin sent to darknet markets fell sharply March--something that usually remains steady despite fluctuations bitcoin price Chainalysis, which closely follows bitcoin and cryptocurrency spending, has previously found that darknet markets’ revenue has historically had a weak inverse correlation with the bitcoin price. "Darknet market activity is much less affected by the ebbs and flows of the market than other types of services, suggesting typical customers are willing to spend on drugs (and, to a lesser degree, other illicit stock such as stolen credit card data, firearms, and more) no matter how much their bitcoin is worth. However, the correlational relationship has now reversed." Source: Billy Bambrough @ Forbes
  21. COVID-19, Do you have it? Do you personally know anyone who has it? (friends, family etc...NOT TV stars and people in the news.)
  22. Apple launches COVID-19 screening app and website You can ask Siri for resources as well Image: Apple Apple today launched a website and a new app dedicated to COVID-19 screening. The resources offer an online screening tool, information about the disease, and some guidance on when to seek testing or emergency care. Apple developed the site and app in collaboration with the Centers for Disease Control and Prevention (CDC), Federal Emergency Management Agency (FEMA), and the White House. The screening tool asks you questions about your symptoms, recent travel, and contact you may have had with people who have had or been exposed to the virus. After completing the screening process, you’ll be taken to a page with recommended next steps that will also suggest whether you need to be tested for COVID-19. Apple noted in a press release that the screening tool “does not replace instructions from healthcare providers or guidance from state and local health authorities.” If your screening results indicate that you may need to take a COVID-19 test, Apple doesn’t provide direct advice on where to get tested. It merely suggests that you “talk to someone about testing.” That’s likely because testing in the US is inconsistent and limited right now, and the CDC has urged people to contact their primary doctor before heading to a hospital in hopes of a test. However, Apple urges anyone experiencing difficulty breathing to immediately dial 911. Apple says it doesn’t collect or share data from the screening tool, nor does it require logging in with your Apple ID or any other account. “To help improve the site, Apple collects some information about how you use it. The information collected will not personally identify you.” It also doesn’t ask for location access, so the app won’t give you any localized recommendations. In addition to these tools, you can also now ask Siri “How do I know if I have coronavirus?” and Siri will have you respond to a few screening questions and point you toward information from the CDC. Apple is not the first to offer online screening resources. Amazon’s Alexa can now help US users diagnose COVID-19, and the CDC offers an online assessment chatbot built on Microsoft’s Healthcare Bot service. Google sister company Verily has also launched a COVID-19 screening and testing website. Source: Apple launches COVID-19 screening app and website (The Verge)
  23. FDA approves the emergency use of chloroquine for COVID-19 Move comes despite worries about lack of evidence, shortage for existing users. Enlarge / Medical staff at the IHU Mediterranee Infection Institute in Marseille shows packets of a Nivaquine (tablets containing chloroquine) and Plaqueril (tablets containing hydroxychloroquine) on February 26, 2020,. Gerard Julien/Getty Images 114 with 61 posters participating On Saturday, the Food and Drug Administration issued an Emergency Use Authorization that will allow patients suffering from COVID-19 to be treated using drugs without clear evidence of the drugs' efficacy. The move comes after President Donald Trump has touted the drugs' potential several times on the basis of tiny, anecdotal trials. There have also been reports of hoarding of the drugs, which are needed by people with some autoimmune disorders. Potential or hype? The drugs in question are relatives of chloroquine, specifically chloroquine phosphate and hydroxychloroquine sulfate. Originally developed as an antimalarial, chloroquine has a variety of effects, including the ability to reduce immune activity. That has made it useful for the treatment of autoimmune disorders such as lupus and rheumatoid arthritis. Given its multiple effects, it's not surprising that the drug also has a variety of side effects, the most significant probably being a slowing of the heart's rhythm that can potentially lead to fatal complications. (Technically, the drug extends the QT interval.) What does any of this have to do with a coronavirus? As we discussed when exploring potential treatments for SARS-CoV-2, chloroquine can also alter the pH of the compartment in which some viruses are brought into the cell. This can interfere with the process of depositing the virus' genome inside the cell and thus block the virus' ability to reproduce. Experiments in cultured cells infected by SARS-CoV-2 indicated that chloroquine treatments can keep the virus from spreading within the culture. But cultured cells are very different from the environments the drugs would encounter in the human body, and SARS-CoV-2 obviously behaves differently from earlier coronaviruses. So ideally, we would want evidence that it works in humans against the source of the current pandemic. Unfortunately, all we have at present is anecdotal evidence. One small trial indicated that the drug was somewhat effective on its own, with its effectiveness enhanced by an antibiotic. But a recent perspective on the drugs' use noted that the trial had "serious methodological flaws," and follow-up work lacked any negative controls to compare with the treated group. There are also indications that the trial was rushed through peer review at a journal edited by one of its authors, who has been involved with research that contains fabricated data. Meanwhile, a small study performed in China saw no indication that the drug was effective on its own. And it's not clear why an antibiotic, which normally targets bacteria, would enhance the effect of an antiviral treatment. Larger, properly controlled clinical trials are already in progress, but it may be months before they produce enough data for us to make evidence-based decisions here. Wait for evidence? But the absence of any other known treatments for this highly infectious disease has led to a number of people latching on to the anecdotal reports about chloroquine drugs, most prominently including President Trump. This has led to a nationwide shortage as doctors and even dentists have handed out unjustified prescriptions or attempted to hoard the drugs for themselves. This has made the drugs difficult to obtain for those who use them to treat immune disorders, raising the prospect that some of the people with those autoimmune disorders will need extensive care from our overstretched medical system. And at least two people attempting to self-medicate have ended up dead. As a result, some scientists have been harshly critical of Trump's promotion of the drug. But now the FDA has stepped in. In a letter released on Saturday, the FDA's Chief Scientist, Denise Hinton, responded positively to a request from the Department of Health and Human Services to provide an Emergency Use Authorization for chloroquine-based drugs. According to the law that governs Emergency Use, authorizations can be made after the Secretary of Health and Human Services declares a public health emergency, which has already happened. At that point, the judgement about whether an authorization should be granted is "based on the totality of scientific evidence available to the secretary, including data from adequate and well-controlled clinical trials, if available, it is reasonable to believe that the product may be effective in diagnosing, treating, or preventing" the cause of the emergency. Obviously, "reasonable to believe" can mean different things to different people. Hinton specifically refers to what she terms the "limited" studies mentioned above and notes that a handful of other countries have recommended the use of chloroquine. For her, this constitutes "reasonable." For others, it almost certainly will not, ensuring that the decision will be controversial. Who gets it? The perspective we linked to above recommends that any use of chloroquine attempt to prioritize availability for those in clinical trials, as well as those who need it to treat other conditions. The FDA's Authorization will be specifically for those who cannot enroll in a clinical trial and will attempt to fulfill their needs using the Strategic National Stockpile, with distribution from there to regional health authorities. According to The Washington Post, two pharmaceutical giants have already agreed to supply the stockpile with additional doses. Use will be limited to hospitals, which should avoid issues with public hoarding, although the distribution of any materials to health care providers has been very chaotic in the United States. The guidance to patients and doctors on the use of the drug emphasizes our uncertainty. "Chloroquine phosphate is experimental because we do not know if it works for COVID-19," the guidance for patients notes, before going on to say that "There is limited information known about the safety and effectiveness (whether this will make you better) of using chloroquine phosphate for hospitalized patients with COVID-19." Doctors are warned that [t]he optimal dosing and duration of treatment for COVID-19 is unknown" and instructed to carefully monitor heart activity for indications of problems caused by the drugs' side effects. Given that we probably have weeks to months to go before properly controlled clinical-trial data allows us to make conclusions about any drug's effectiveness, it's likely that chloroquine will remain the standard treatment for the peak of several regional epidemics in the US. The one thing that this decision does ensure is that we'll have lots of anecdotal reports on its use to complicate the public's understanding of treatment options. Source: FDA approves the emergency use of chloroquine for COVID-19 (Ars Technica)
  24. The CDC Now Recommends Americans Wear Face Masks Staying home is still the best way to protect yourself from the coronavirus. But the CDC now says that masks are effective as an additional measure. Photograph: ISAAC LAWRENCE/Getty Images On Friday, the US Centers for Disease Control and Prevention recommended that citizens should wear "non-medical, cloth masks" to help prevent the spread of the coronavirus. Previously, the CDC had recommended that only those with Covid-19 symptoms wear masks. The agency now recommends that those who aren't feeling sick should still wear a mask, though compliance is voluntary. In a statement on its website, the CDC says: "Cloth face coverings fashioned from household items or made at home from common materials at low cost can be used as an additional, voluntary public health measure." The word "additional" is key here; sheltering in place is still the most effective way to protect yourself and those in your community, and the agency recommends maintaining 6-fot social distancing as the primary method of reducing exposure. This new policy comes on the heels of new research about how the virus is transmitted, and with cases on the rise across the US, there's some evidence that people who aren't showing any symptoms can still be spreading the virus as they move about in public. This week, cities like New York and Los Angeles have also recommended that all residents wear face coverings in public, whether they're showing signs of sickness or not. Specific guidance has been issued for Los Angeles (and California as a whole) and New York City. These policy recommendations are happening at a time when surgical face masks and N95 masks are already in critically short supply. This scarcity of protective equipment has been devastating for health care workers busy treating patients, and many fear that a nationwide decree to wear a mask could strain supplies even more. If you live in a community where masks are recommended, or if you are caring for a loved one who's currently sick, you should make your own mask. Do not buy N95 masks, and absolutely do not hoard supplies that medical professionals need. It's important to remember that cloth face coverings like those recommended by California's Department of Public Heath may help unknowingly infected people from transmitting the virus, but there is no guarantee they can prevent a healthy person from becoming infected. Staying Home Is Still Most Important Wearing a mask is a last-resort measure. A mask is not a virus-blocking solution that will allow you to return to normal social interactions. We all still need to stay home as much as possible until shelter-in-place orders have lifted. If you do have to go outside for supplies, stay 6 feet away from other people, and continue washing your hands and disinfecting your home. So what should you wear? According to the CDC, a well-made mask that is snugly secured around the ears is best. Alternatively, any type of face covering like a bandana or scarf is better than nothing if you have to go out, although the CDC cautions that these are not considered proper protective gear and should only be used as a last resort. In either case, you want to be sure your nose and mouth are securely covered from all sides so droplets can't escape. Some health care workers have taken to wearing homemade masks over their N95 masks to lengthen its lifespan. A few hospitals have put out calls asking for home-sewn donations, like University Hospitals in Ohio, or Deaconess Hospital in Evansville, Indiana, which has also set up a nationwide database to connect heath care facilities in need with those who can make masks and donate them. If you can sew, consider making and donating face masks to your local hospital. The online marketplace Etsy has also asked its sellers to switch to making masks, but has offered crafters a number of precautions, like forbidding them to resell medical equipment and telling them not to make medical claims about home-sewn masks. WIRED is providing free access to stories about public health and how to protect yourself during the coronavirus pandemic. Sign up for our Coronavirus Update newsletter for the latest updates, and subscribe to support our journalism. Source: The CDC Now Recommends Americans Wear Face Masks (Wired)
  25. Face masks for COVID-19: A deep dive into the data With all the talk of masks, here's what the data really says. Enlarge / Self-sewn protective face masks in a fabric store on April 3, 2020 in Jena, Germany. Getty | Jens Schlueter 256 with 131 posters participating, including story author As COVID-19 cases increase sharply nationwide, some health experts are now recommending that seemingly healthy members of the public wear cloth masks when they’re out and about. On April 3, President Trump announced a new federal recommendation urging the public to wear cloth masks to prevent people who are infected, but may not have symptoms, from unknowingly spreading the disease. The recommendation is an about-face from previous guidance on mask usage. Until now, officials at the World Health Organization, the US Centers for Disease Control and Prevention, and other agencies worldwide have discouraged the public from wearing masks unless they are sick or caring for someone who is sick. They noted that there is little evidence to support mass masking and that the limited data we do have suggests it may reduce disease transmission only marginally at best. With evidence of benefits in short supply, experts also raised concerns about potential harms. Mask wearing may give people a false sense of security, some experts said. This may lead some members of the public to be lax about other, far more critical precautions, such as staying two meters apart from others, limiting outings, and washing their hands frequently and thoroughly. Moreover, donning an uncomfortable, awkward mask may lead some people to touch their faces more, some argued. Any face touching has the potential to transfer virus particles from contaminated hands to entry points, such as the eyes, nose, and mouth. And even if a mask-wearer’s hands are clean to begin with, simply touching their mask could contaminate their hands if there are viral particles caught on the outside. If that’s the case, a mask wearer could then transfer virus particles from their mask to their face unwittingly—negating any benefit of having the mask. They might also transfer the virus from their mask to their environment by touching surfaces, where the virus particles could get picked up by other people. Last, they argued, the masks that would be most effective at stopping the new coronavirus—SARS-CoV-2—are things like N95 respirators and surgical masks, which are in short supply worldwide. Without question, these should be preserved for the heroic frontline health workers, who are putting their lives at risk every day to treat patients with COVID-19 during this overwhelming pandemic. While experts unanimously agree on that last point—that proper medical masks should go to healthcare workers first—the other points are now up for debate. With SARS-CoV-2 now spreading widely and unchecked through communities nationwide, experts are taking a more favorable look at the limited data behind masks preventing disease spread among the public. In a recent a commentary in The Lancet, a group of UK and Hong Kong researchers argue that “there is an essential distinction between absence of evidence and evidence of absence.” And though there are no large, high-quality studies looking at public mask usage, there is some data to support mask usage. As for potential harms of mask wearing—such as fraught face fussing and wearers relaxing other precautions—experts are now dismissing the concerns. Wearing a mask in public could keep people alert to current health risks in public, some experts say. A conspicuous mask strapped to your head is a constant reminder right over one’s nose to be mindful of possible viral transmission. And—as a bonus—if everyone wears a mask, it could lessen the chances of stigma of those who wear them because they are sick. Of course, wearing a mask does not replace other interventions, like staying two meters apart or practicing good hand hygiene, says Joseph Allen, an expert of exposure assessment science in the Department of Environmental Health at Harvard T.H. Chan School of Public Health. “It’s just one more layer of protection.” “The scale and scope of what we’re facing requires or mandates taking every precaution we can,” he says. As such, some experts—Dr. Allen included—are now in favor of having the healthy public wear home-made cotton masks or other face coverings that could act as a basic physical barrier. “It’s not as good [as medical masks], but it’s better than nothing,” Dr. Allen argues. So with the conflicting reasoning and logic, what does the data on masks actually show? How were they dismissed before but embraced now? Here’s a rundown of pertinent data. Transmission First, to understand why masks could be helpful at blocking SARS-CoV-2 transmission, it’s important to understand how the coronavirus is transmitted. And, frankly, we still don’t know all the answers to this question. So far, SARS-CoV-2 mainly appears to move from one human to another by being launched in relatively large respiratory droplets. These are unleashed when an infected person breathes, talks, coughs, or sneezes. These droplets are relatively heavy, they generally don’t travel much farther than two meters away from their launch site, and they follow a ballistic trajectory, that is, they fall toward the ground after blast off. But if they land on a person’s face before that or fall to a surface a person will soon touch, they could cause a new infection. There’s also the possibility that SARS-CoV-2 can spread in smaller respiratory droplets called aerosols (less than 5 micrometers). These are droplets we exhale that are so small they can hang in the air for minutes to hours. Experts at the WHO and elsewhere say that the data so far suggests aerosol transmission is not the primary way the virus spreads, though it is still possible. So far, it appears aerosol transmission is mainly a concern for healthcare workers while they’re performing certain medical procedures on COVID-19 patients, such as placing a tube in their airway to aid breathing (intubation). This may create circumstances for the virus to aerosolize and linger in the air in hospital rooms. Whether SARS-CoV-2 is aerosolized in everyday settings is still unknown and up for debate. Some experts, such as Dr. Allen, believe that it could be happening. Others are more skeptical of the idea given that infected people only infect two to three other people on average. If each COVID-19 patient were creating infectious clouds of SARS-CoV-2 wherever they went, some experts would expect the patients would infect far more people on average. Measles, for instance, has been associated with airborne transmission for decades and each measles patient, on average, may infect 12 to 18 people—or more. There’s even evidence the measles virus can disperse through ventilation systems. Though that doesn’t appear to be the case for SARS-CoV-2, experts like Allen caution that the size of virus-containing respiratory droplets is a continuum, not subject to clear cut-offs or strict rules. There is evidence that if SARS-CoV-2 does make it into aerosols, the virus can survive in the air for hours in laboratory conditions. Last, there’s evidence that SARS-CoV-2 particles that land on surfaces or objects can loiter and potentially be picked up by others. These contaminated surfaces and objects that can then transfer the infectious virus particles are called fomites. Masks may keep a wearer from putting a fomite-contaminated hand to their face, but masks may also act as fomites. Enlarge Aurich Lawson / Getty Filtration by N95 respirators, surgical masks, and homemade masks N95 respirators get their name from their National Institute for Occupational Safety and Health (NIOSH) designation. They contain filter material that uses electrostatic attraction to thwart particles of all sizes. The N in the name means the masks are not resistant to oil and the 95 refers to their efficiency. To get a 95 designation, a mask has to filter out at least 95 percent of all particles. Specifically, the designation is granted if the mask proves to filter out at least 95 percent of particles in the size range it is least efficient at filtering out in standard conditions. This is considered “worst case” testing. In one 2014 study, researchers compared the effectiveness of 44 masks, including N95 equivalent respirators, surgical and dental masks, general cotton masks, and handkerchiefs. They used particle penetration tests similar to those used by NIOSH and the European Union. They found that the N95 equivalent mask blocked more than 95 percent of all particles, as expected. The surgical mask was around 40 percent effective, with the dental masks coming in at around 60 percent. Cotton masks were around 30 percent effective and cotton handkerchiefs ranged from 2 percent (one layer) to 13 percent (four layers). A similar study in 2010 by NIOSH researchers looked at masks made of different types of fabrics. They found that masks made from t-shirts blocked about 10 percent of particles in a wide range, masks made from sweatshirt fabric blocked 20 to 40 percent, masks made from towels blocked around 40 percent, and scarves blocked 10 to 20 percent. In a study published April 3, 2020 in Nature Medicine, researchers found that surgical masks reduced the detection of respiratory viruses in aerosols generated by infected people breathing or coughing in a breath-collecting machine. Masks in the real world Overall, the body of research on mask efficacy in real-world settings is small and scattershot. And because SARS-CoV-2 was completely unknown to humanity just five (extremely long) months ago, there is no data on the efficacy of any type of mask wearing in any setting (healthcare or home) for this virus. As such, any relevant data has to be gleaned from studies looking at other respiratory illnesses and how various masks in various settings play a role. Masks on healthy people In a 2011 randomized clinical trial, researchers monitored 1,441 healthcare workers in 15 Beijing hospitals to compare the rates of respiratory infections if they wore either a surgical mask or an N95 respirator during their shifts. They compared infection rates in the two masked groups to a convenience sample of 481 healthcare workers who didn’t wear masks. Overall, both masked groups had fewer respiratory symptoms, influenza-like illnesses, and confirmed viral infections than the control group. The rates of illness were approximately double in those who wore surgical masks compared with those who wore N95 respirators, though. For instance, about 9 percent of non-mask wearers reported respiratory symptoms compared with about 7 percent of surgical mask wearers and 4 percent of N95 wearers. But with such small infection rates overall, there was limited power to detect differences, and the authors note that the findings may not hold up in other settings. Enlarge / Dawn Canova, clinical manager for outpatient wound care at Carroll Hospital, takes samples from people to test them for the coronavirus at a drive-thru station in the hospital's parking garage while wearing a medical grade mask. Chip Somodevilla Masks on sick people The push to preserve medical-grade masks for healthcare workers is intended to try to protect them from contracting illnesses from their patients. But the push for public face mask use is powered by the desire to prevent sick people from spraying respiratory droplets around and potentially sicken others. This has become a greater concern as more evidence has pointed to apparent symptomless spread of COVID-19. That is, people who don’t show symptoms (either asymptomatic or pre-symptomatic) may be able to pass on the infection without knowing it. While there is evidence that this is happening in some cases, it’s still very unclear how often it happens. Estimates of how many cases are spreading stealthily like this have ranged from between 25 percent of cases to over 60 percent. Experts at the WHO, though, continue to say that people who are coughing or sneezing are still most likely to be the ones passing on the virus. In a 2016 randomized controlled trial, researchers examined whether wearing a surgical mask could keep people with influenza-like illnesses (ILI) from passing the infection on to members of their household. Those household members were not asked to wear masks and the researchers didn’t collect data on it. The study included 123 ILI patients who were instructed to wear masks at home around other household members and 122 ILI patients who didn’t wear masks. The masked and unmasked ILI patients were in households with, on average, 2.5 or 2.4 members, respectively. While the infection rates in home of masks-wearing patients were consistently lower than those in the homes of unmasked patients, the numbers were too small to be statistically significant. “The study indicates a potential benefit of medical masks for source control but is limited by small sample size and low secondary attack rates [subsequent infections],” the authors concluded. “Larger trials are needed to confirm efficacy of medical masks as source control.” Masks on everyone With the new recommendations, everyone may be wearing masks, which has also been examined in a number of studies. In 2008, a randomized controlled trial led by researchers in Hong Kong looked at the effect of blanket mask wearing on the spread of flu within households. They started with 198 households with one confirmed case at the beginning. Of those households, 127 were told that all household members should wear masks around each other. In 35 households, members were instructed to adhere to hand hygiene protocols and the remaining 36 households were controls.The researchers found little difference in infection spread among all three groups. In 2009, researchers led by a group in Australia followed up with a similar randomized controlled study. The group looked at the spread of influenza-like illness to 286 adults in 143 households with a sick child. Participants were either assorted into a control group, a surgical mask group, or a more protective mask. Overall, they detected no difference in infection rates among the three groups. They noted that at least half of masked participants didn’t adhere to wearing the mask. Another randomized controlled trial in 2009 followed people in 259 households in Hong Kong. Collectively, the households started with 407 household members with flu and 794 uninfected contacts. The households were randomly assorted to either all wear surgical masks, practice hand hygiene, or act as controls. Overall, the interventions didn’t lead to statistically significant differences in the spread of infections within the households. But when they looked at households that started using masks quickly (within 36 hours) after the onset of flu symptoms in a member, they did see a statistically significant reduction in infection spread. Likewise, in a 2012 randomized controlled trial involving 84 households in Germany, researchers again found no difference in disease spread among household members that used masks, masks and hand hygiene, or were in a control group. However, when they did a separate analysis just looking at the households who fully implemented mask wearing or mask wearing and hygiene within 36 hours of onset of symptoms in their first case, they did note a lower chance of transmission than what was seen in controls. Cloth masks While most studies have looked at the effectiveness of surgical masks and other medical-grade masks, a few have ventured to look at cloth and homemade masks. In a 2015 randomized controlled trial involving 1,607 healthcare workers, researchers compared the rate of influenza-like illness in healthcare workers wearing cloth masks or medical masks to those in a control group (which sometimes used masks). Wearing cloth masks resulted in significantly higher rates of infection, the authors found. They also noted that in their test, the cloth masks were only 3 percent effective at blocking particles. Potential risks of masks There is evidence that virus particles hang out on the outside of masks—particularly among healthcare workers who likely have high exposure. Among 59 healthcare workers who had their protective gear, clothes, and skin sampled in a 2019 study, many were contaminated with virus. Overall, 31 percent of gloves, 21 percent of gowns, and 12 percent of face masks were positive for virus. Moreover, 11 percent had viral particles on their scrubs and 7 percent had them on their bare faces. A similar study, also in 2019, confirmed that respiratory viruses are often found on the outside surface of medical masks and can be a source of self-contamination. In yet another study from last year, researchers in Chicago observed healthcare workers taking off their person protective equipment (masks, gloves, gowns, etc)—the removal is called doffing. This is a time when healthcare workers can easily self-contaminate by taking gear off incorrectly. The researchers found that healthcare workers incorrectly removed their protective gear 90 percent of the time. If you do wear a mask, be sure to remove it from behind your head. Don’t touch the surface of the mask. If you do touch the surface, immediately wash your hands or use hand sanitizer. Update 4/3/2020, 6:20pm ET: This post was updated to include the new federal recommendation for the public to wear cloth masks. Source: Face masks for COVID-19: A deep dive into the data (Ars Technica)
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