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Rockefeller plan details government takeover through pandemic martial law

sorce

 

Scenarios for the Future of Technology and International Development   .pdf        Plandemic  p18

 

"In 2012, the pandemic that the world had been anticipating for years finally hit. Unlike 2009’s H1N1, this new influenza strain—originating from wild geese—was extremely virulent and deadly. Even the most pandemic-prepared nations were quickly overwhelmed when the virus streaked around the world, infecting nearly 20 percent of the global population and killing 8 million in just seven months, the majority of them healthy young adults. The pandemic also had a deadly effect on economies: international mobility of both people and goods screeched to a halt, debilitating industries like tourism and breaking global supply chains. Even locally, normally bustling shops and office buildings sat empty for months, devoid of both employees and customers.

The pandemic blanketed the planet—though disproportionate numbers died in Africa, Southeast Asia, and Central America, where the virus spread like wildfire in the absence of official containment protocols. But even in developed countries, containment was a challenge. The United States’ initial policy of “strongly discouraging” citizens from flying proved deadly in its leniency, accelerating the spread of the virus not just within the U.S. but across borders. However, a few countries did fare better—China in particular. The Chinese government’s quick imposition and enforcement of mandatory quarantine for all citizens, as well as its instant and near-hermetic sealing off of all borders, saved millions of lives, stopping the spread of the virus far earlier than in other countries and enabling a swifter post-pandemic recovery."

 

 

Frederick T. Gates AMERICAN PHILANTHROPIST

 

"Frederick.T.Gates then went to work for Rockefeller and was entrusted with directing the oilman’s vast philanthropic contributions. He also served as an astute business and financial adviser to many of Rockefeller’s businesses, including railroads, mines, and manufacturing plants. Gates was the organizer and director of the Lake Superior Consolidated Iron Mine until it was sold to United States Steel in 1900 for $75,000,000. He organized and served as president of the Rockefeller Institute for Medical Research and also played an important role in the creation of the Rockefeller Foundation."

 

 

Bill Gates may say he has nothing in common with John D. Rockefeller, but the author of a new biography begs to differ.

 

A tale of two titans: Gates and John D. Rockefeller

 

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https://www.wired.co.uk/article/coronavirus-immunity-passports

Immunity passports aren’t a good way out of the coronavirus crisis

 

On April 2, health secretary Matt Hancock offered a glimmer of hope for members of the public already beleaguered after weeks of lockdown. If people could take tests that prove they were immune to the virus, they might be able to return to normal life sooner, he said.

The inspiration for this plan likely comes from Germany, where researchers at the Helmholtz Centre for Infection Researchers plan to send out hundreds of thousands of antibody tests over the coming weeks. In a scheme identical to Hancock’s proposal, those who test positive could receive an “immunity certificate” allowing them to return to work and some elements of normal life.

 

But the government’s plan is far from straightforward. First off, it would have to procure a working test, which is still not on the immediate horizon. Even if we did have a functional test – and that’s a big if – making immunity passports work is fraught with difficulties.

Ostensibly, it’s clear why the idea is being explored. It’s obvious that with each day we stay in lockdown the economic repercussions grow worse. (Though this says nothing about the repercussions of lifting the lockdown too early.) “There clearly is an urgent need to get people back to functioning, and if it’s the case that a number of people who would be safe then we need to take that really seriously,” says Robert West, a professor of health psychology at University College London.

Yet there are serious reasons why splitting society along the lines of immune and not-immune people might not be a good idea. It’s not hard to imagine how the split might generate resentment – imagine being locked indoors while your immune neighbours galavant around the park. Social cohesion will suffer. “There’s so much evidence on ‘in group’ and ‘out group’ work that, even when you set up arbitrary ‘in groups’ and ‘out groups’, people become quite tribal,” says West

“The whole approach might also undermine the message that we are all in this together, which is crucial if we are going to get through this relatively quickly,” says Adam Oliver, a behavioural economist at the London School of Economics.

 

It’s also hard to imagine how this divide would be enforced. Police have struggled to contain a blanket ban on picnics and sunbathers. “If somebody feels that they can go to the pub and meet with their friends, and then they claim they’ve got a positive test, which they did at home, how do we know whether that’s true or not?” says Martin Hibberd, a professor at the London School of Hygiene and Tropical Medicine

 

Employers might also run into legal issues if they require employees to carry out immunity testing or return to work prior to the general workplace restrictions being lifted, particularly if they provide non-essential services or can carry out their work from home. The private health data in an immunity passport is also likely to be a sticking point, explains Collier-Wright. This data is subject to enhanced processing obligations and restrictions, which will likely complicate its collection.

Employers would possibly be better off avoiding any immunity passport scheme entirely. “From a practical standpoint, employers who are able to keep their business open using remote working or who are receiving grants from HMRC under the furlough leave scheme may prefer to stick to the status quo until such time as all restrictions are lifted, rather than re-integrating employees on a case-by-case basis once they have obtained immunity passports,” he says.

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that ,s  the creatures were dealing with .........i think not to immunity passports !

 

Theranos was a privately held health technology corporation. It was initially touted as a breakthrough technology company, with claims of having devised blood tests that needed only very small amounts of blood and could be performed very rapidly using small automated devices the company had developed. However, the claims later proved to be false.

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New model looks at what might happen if SARS-CoV-2 is here to stay

If it’s like related viruses, it could cause seasonal outbreaks for years.

Image of two people walking a dog wearing face protection.
Enlarge / Face masks may be a regular feature in our near-term future.

Most of the optimistic ideas about what to do about SARS-CoV-2 involve engineering the virus's extinction. We could ramp up testing and isolate anyone who has been in contact with an infected individual. We could carefully manage infections to build up herd immunity without exceeding our hospital capacity. Or, in an ideal world, we could develop herd immunity using an effective vaccine.

 

Unfortunately, there are reasons to be worried that none of these will work. Tracing the contacts of infected individuals may be impossible with a virus that spreads as easily as SARS-CoV-2. And some of the virus's closest relatives don't build up the long-lasting immune response that's needed for persistent herd immunity. All of which raises a disturbing question: what happens then?

 

A group of Harvard epidemiologists attempted to answer the question by trying out models that tested the impacts of different assumptions about the virus's behavior and the immune system's response to it. The researchers find that there's a risk that it could become a seasonal menace, and we might have to be socially isolating every winter.

Unwanted family

The study is based on what we know about SARS-CoV-2's closest evolutionary relatives. Coronaviruses are a family-level designation, two steps up from species. One step up from species is genus, and there are four coronavirus genera (alpha, beta, gamma, and delta). SARS-CoV-2 is a member of the beta coronaviruses, a genus that includes subjects of prior pandemic fears like SARS-CoV-1 and MERS. But it also includes two species that are less threatening and more annoying: HCoV-OC43 and HCoV-HKU1, which are collectively the second-most common cause of cold-like symptoms.

 

The reason these cold viruses cause so much annoyance is because they fail to generate long-term immunity. By a year after infection, people's immune systems seem to have forgotten they've ever seen the virus.

 

But there are complicated relationships among the responses generated by these betacoronaviruses. SARS-CoV-1 generates a long-lasting immune response, which can include antibodies that block HCoV-OC43 and HCoV-HKU1, the cold viruses. And, while the immune response to the cold viruses is weak, the antibodies generated against them do react to SARS-CoV-1.

 

To find out what these interactions might mean, the researchers took test results for these two viruses and built an epidemiological model that matched their prevalence. As expected, the model showed a seasonal pattern of infections, with rates peaking between October and May. The model also suggests that the arrival of fall causes the start of this peak, but its decline is largely driven by the lack of susceptible individuals, as a large chunk of the population has already been infected by spring. In addition, the results indicate that infection by one of the viruses provides a degree of protection against the second, leading to only one being common in most years.

Now, add a pandemic

Layered on top of that this year, we have SARS-CoV-2. The basic properties of the virus—how long it takes to become infectious, how long it's infectious for, and so on—were based on the properties we're seeing in various countries. But the key questions here can't be extracted from known data: how long-lasting the immune response is and whether it provides protection against related coronaviruses. Another open question is whether the virus might display seasonal behavior like we see in its relatives.

 

So, the researchers simply tried different values for these properties to see what would happen.

 

In any case where immunity to SARS-CoV-2 isn't permanent, the virus is capable of producing sporadic outbreaks. If the duration of the immunity is less than a year, the outbreaks will be annual. If it's longer, we could see bi-annual outbreaks of COVID-19 cases. The model indicates that we'd need to develop long-term immunity to actually have a chance of suppressing future outbreaks.

 

Cross-immunity has some interesting effects. If the cold viruses provide even a weak immunity to SARS-CoV-2 (in the area of 30 percent), it's enough to delay future outbreaks of COVID-19; for example, if SARS-CoV-2 would have its next outbreak in 2022, this cross immunity would push that back to 2023. If SARS-CoV-2 induces immunity to the cold viruses, the impact could be dramatic. A 70-percent cross immunity would be enough to effectively eliminate the circulation of the cold viruses.

Doing the distance

Of course, we're not simply allowing SARS-CoV-2 to circulate unimpeded. When the researchers added social-distancing efforts, they saw what had been seen in other models: infections were suppressed, but the virus returned with a vengeance after they were lifted. And, because the isolation is so effective at suppressing the virus's circulation, there was little immunity built up in the population. As a result, the ensuing outbreak is roughly as large as one in which no social distancing is ever attempted. Adding a seasonal influence on the virus's behavior would simply ensure that the post-distancing outbreak would occur in winter.

 

If they assumed that distancing rules were put in place once infections reached a certain level, the authors' model suggested that the current outbreak could last until 2022, with social-distancing rules in place for anywhere between 25 and 75 percent of the time. During these years, we'd see increasing gaps between the times when distancing is enforced, as the percentage of the population with some immunity would steadily rise.

 

The researchers also examined two things that could reduce the societal impact of the ongoing outbreak: increasing critical care capacity and a partially effective therapy. Either could have a large impact, as they'd allow us to avoid social distancing for longer without the health care system being overloaded. And that, in turn, would mean we'd tolerate more infected individuals, and the immunity that would ensue would also be a benefit.

 

While there's a lot of information here, there's a couple of key takeaways. The key ideas for controlling SARS-CoV-2 involves generating herd immunity, either by controlled infections or through a vaccine. But these suppose a long-lasting immunity that is anything but guaranteed. This doesn't mean a vaccine won't work, but it does mean that we may have to plan on annual boosters—maybe it could be rolled into a flu vaccine. In fact, even without a vaccine, the model suggests that SARS-CoV-2 could settle into behavior that resembles our annual flu outbreaks.

 

The other big takeaway is that, to really understand what's coming next, we need to know how long-lasting the immunity is and whether there's any cross-immunity with the other betacoronavirus strains. Differences in these properties lead to very different behavior on a population level. And that means figuring out the actual values of those properties should be a priority if we're to do intelligent planning.

 

Of course, like any other model, there are limits to this one. Like all other models in operation now, it depends on our imperfect knowledge of things like the infectivity and frequency of asymptomatic cases. This particular model is also limited by its treatment of the population, which doesn't include any details of the geographic distribution of that population or its modes of interaction.

 

And, more generally, it's important to emphasize that no single model is ever going to be an exact recapitulation of reality. Instead, these models simply show the rough outlines of what we should expect if a given list of assumptions turns out to be accurate. And, ideally, as more models tackle an overlapping set of questions, we'll get a stronger consensus about what our near-term future is going to look like.

 

Science, 2020. DOI: 10.1126/science.abb5793  (About DOIs).

 

 

Source: New model looks at what might happen if SARS-CoV-2 is here to stay (Ars Technica) 

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What Does Covid-19 Do to Your Brain?

Scientists are racing to figure out why some patients also develop neurological ailments like confusion, stroke, seizure, or loss of smell.
Science_brain_covid19_1178748409.jpg
By now, you're familiar with the typical hallmarks of Covid-19. But stories of other, stranger symptoms—headaches, confusion, seizures, tingling and numbness, the loss of smell or taste—have been bubbling up from the frontlines for weeks.SCIENCE PHOTO LIBRARY

During the third week of March, as the pandemic coronavirus that causes Covid-19 was beginning to grip the city of Detroit, an ambulance sped through its streets to Henry Ford Hospital. Inside, a 58-year-old airline worker struggled to understand what was happening to her. Like hundreds of other Covid-19 patients flooding the city’s emergency rooms, the woman had a fever, cough, and aching muscles. But something else was happening too—something that had made her suddenly disoriented, unable to remember anything but her name.

 

Doctors at Henry Ford tested the woman for Covid-19, and she came back positive. They also ordered CT and MRI scans. The images showed a brain aflame, its folds swelling against the patient’s skull. On the computer screen, white lesions dotted the gray cross-sectioned landscape—each one filled with dead and dying neurons in regions that normally relay sensory signals, regulate alertness, and access memories. On the screen they appeared white. But in the electrical grid of the patient’s brain, those areas had gone dark.

 

Her doctors diagnosed a dangerous condition called acute necrotizing hemorrhagic encephalopathy, or ANE, which they detailed in the journal Radiology last month. It’s a rare complication known to occasionally accompany influenza and other viral infections, though usually in children. With the flu, scientists believe such brain damage is caused not so much by the virus itself but by squalls of inflammation-inducing molecules called cytokines, which are sometimes produced in excess by the body’s immune system during an infection. Scientists are still trying to figure out if the same is true for Covid-19, or if the coronavirus called SARS-CoV-2 is actually invading the nervous system directly. It’s an open question, the answer to which could have wide-ranging implications for how doctors diagnose and treat Covid-19 patients.

 

By now you’re probably familiar with the typical hallmarks of Covid-19, the disease that has so far killed more than 125,000 people around the world: fever, cough, difficulty breathing. But stories of other, stranger symptoms—headaches, confusion, seizures, tingling and numbness, the loss of smell or taste—have been bubbling up from the frontlines for weeks. Published data on how frequently the disease manifests in these types of neurological symptoms is still sparse, and experts say they likely occur in a minority of the 2 million officially tallied Covid-19 infections worldwide. But for physicians, they are important because some of these new symptoms may require a different line of treatment, one designed for the brain rather than the body.

 

“The medicines we use to treat any infection have very different penetrations into the central nervous system,” says S. Andrew Josephson, a neurologist at UC San Francisco. Most drugs can’t pass through the blood-brain barrier, a living border wall around the brain. If the coronavirus is breaching the blood-brain barrier and infecting neurons, that could make it harder to find effective treatments.

 

Right now, many doctors are trying a two-pronged approach. The first is finding antiviral drugs that can knock back how fast SARS-CoV-2 replicates. They often combine that with steroids, to prevent the immune system from going overboard and producing inflammation that can be damaging on its own. If doctors knew people had coronavirus in their brains, that would alter the equation. Unlike the lungs, the brain can’t be put on a ventilator.

 

The first reports of Covid-19 affecting the central nervous system appeared on the preprint server medRxiv in late February, posted by neurologists in Wuhan, China, where the outbreak started. Analyzing health records from 214 patients admitted to the Union Hospital of Huazhong University of Science and Technology, the team found that 36.4 percent of those patients showed signs of nervous-system-related issues.

 

The most common symptoms they observed were muscle pain, headaches, dizziness, or confusion—which tend to manifest during any viral infection, especially in older people. A few patients experienced more distinct neurological syndromes, including strokes, prolonged seizure, and a disappearing sense of smell. In at least some of the patients, especially the ones with headaches, the neurological symptoms started days before a cough and fever set in.

 

The upshot? Doctors need to consider altered brain function as cause to test for SARS-CoV-2, in order to “avoid delayed diagnosis or misdiagnosis and prevention of transmission,” the authors wrote in a peer-reviewed version of the study published Friday in the journal JAMA Neurology. Failure to recognize these early warning signs could result in patients being discharged and unknowingly exposing others to the virus, they wrote.

 

“We’ve been telling people that the major complications of this new disease are pulmonary, but it appears there are a fair number of neurologic complications that patients and their physicians should be aware of,” says Josephson, who co-authored a commentary about the study that appeared alongside it in JAMA Neurology. Still, it shouldn’t come as a complete surprise that SARS-CoV-2 causes some neurological impairment, he says. Any serious viral infection is likely to affect the central nervous system, either through a direct infection or indirectly through inflammation caused by an immune system response. One of the study’s biggest limitations is that it can’t distinguish between those two possibilities.

 

That’s in part due to the realities of trying to document a new disease while being buried beneath the first wave of the outbreak. With hospitals in Wuhan overwhelmed by a crush of Covid-19 patients during the first half of February, doctors often had to rely on patients’ own descriptions of their symptoms. There was a lot they couldn’t do, like imaging people’s brains, measuring their nervous system activity, or looking for copies of the coronavirus in their spinal fluid. But that’s the kind of data that would help pinpoint what’s disrupting brain function for some Covid-19 patients.

 

In its absence, researchers are left to ponder the scant, incomplete, and conflicting evidence in case reports. Like this one, published March 21 in Cureus, a publishing platform modeled on Turbotax and aimed at making it easier for doctors to share notable patient profiles. A 74-year-old Dutch man with a history of chronic lung disease, Parkinson’s, and stroke shows up in a Boca Raton emergency room complaining of a cough and slight fever. Chest X-rays rule out pneumonia, and he gets sent home. Twenty-four hours later he’s back—only now he can no longer speak or make eye contact. Nose swabs prove he’s positive for Covid-19. Brain scans and a battery of tests on his spinal fluid come back clear, with no sign of infection. His doctors conclude that SARS-CoV-2 does not cross the blood-brain barrier to prey upon neurons.

 

Or this one, published April 3 in the International Journal of Infectious Diseases: A 24-year-old man living in central Japan with no travel history goes to the doctor with a headache, fever, and fatigue. He tests negative for the flu and goes home. Three days later he visits another clinic, looking for relief from his worsening headache and sore throat. Chest X-rays and blood tests don’t turn up anything. Four days later he is found unconscious, lying on the floor in his own vomit. In the ambulance on the way to the hospital he has seizures. CT scans show swelling in his brain. Health care workers swab the inside of his nose and throat, but tests for SARS-CoV-2 come back negative. They try again, this time with spinal fluid, and that’s where they find the virus. SARS-CoV-2 can invade the central nervous system, his doctors conclude.

 

If you were hoping the Detroit case would turn out to be some kind of anecdotal tie-breaker, prepare to be disappointed. Doctors at Henry Ford weren’t able to test the airline worker’s spinal fluid for SARS-CoV-2 because a botched lumbar puncture introduced blood into the sample. Despite not having proof of the virus in the patient’s central nervous system, the woman’s doctors concluded that her pattern of inflammation was consistent with a viral infection. “This may indicate the virus can invade the brain directly in rare circumstances,” Elissa Fory, a Ford Health neurologist who was involved with the patient’s diagnosis, told The New York Times.

 

Doctors in Baton Rouge also weren’t able to administer the test, but for a different reason. According to Asia Filatov, a neurology resident who was part of the team that treated the Dutch patient, there aren’t any good guidelines for detecting the virus in spinal fluid, which has to be handled differently than blood or nasal swabs. “We attempted to contact multiple labs and institutions across the US,” Filatov wrote in an email to WIRED. “Unfortunately, there is a lack of protocols and reagents available to run the test and most labs don’t have the capability.”

 

Josephson says that might change in the coming weeks and months as testing capacity continues to expand and demand for nasal swab testing goes down, especially in cities like San Francisco where Covid-19 cases are expected to peak this week. Wider availability of spinal fluid testing would enable doctors to more accurately document what’s going on inside Covid-19 patients’ bodies when they present with neurological symptoms. Without those kinds of datasets, there’s no way to know how to interpret reports on patients like the ones in Japan, Michigan, and Florida. “Single cases are tantalizing, but they can be fraught with coincidence,” says Josephson.

 

But if SARS-CoV-2 turns out to be a brain-invader, it wouldn’t shock Stanley Perlman, a microbiologist and infectious disease physician at the University of Iowa. During the 2003 SARS epidemic that killed 774 people, only a few dozen autopsies were ever performed. But in at least eight of them, pathologists found bits of the virus and its genome in the brain, in addition to the lungs, kidneys, digestive tract, and spleen. Perlman wanted to understand how that might happen. So he zoomed in on a receptor called ACE2, which SARS-CoV—the coronavirus that causes SARS—uses to enter human cells. In a 2008 study, Perlman and his colleagues genetically engineered mice to express that human receptor and then squirted a small dose of SARS-CoV into their noses. Rather than descending into their lungs, the virus climbed out of the nasal cavity and into their brains using olfactory neurons like rungs on a ladder.

 

Once in the brain, SARS-CoV spread rapidly, causing widespread nerve damage that led to the animals’ death. A few years later the scientists replicated the work with the coronavirus that causes MERS. In both studies, the virus showed a preference for neurons in certain areas, including the brainstem, which is involved in regulating involuntary respiration. And like it its genetic cousin, SARS-CoV-2 also uses ACE2 as a molecular doorway into human cells.

 

Despite Covid-19’s far more devastating death toll, not many autopsies are being done. And the few published examples have so far primarily examined victims’ lungs. But according to Perlman, researchers in China have peered inside the skulls of deceased Covid-19 patients, and discovered the coronavirus lurking in brain tissues. Those autopsy studies are not yet published, but Perlman says it’s the strongest data he’s seen to support the possibility that at least in severe cases, SARS-Cov-2 crosses the blood-brain barrier. “At this point, I’d say there’s a good chance that there’s some viral invasion of the brain,” he says.

 

But what intrigues Perlman most isn’t these severe cases in which the virus seems able to penetrate deep into the brain. It’s the mild cases in which it seems like it doesn’t; specifically, the cases in which people lose their sense of smell. Preliminary data suggests that this sudden olfactory deprivation happens in 30 to 50 percent of Covid-19 infections. Often, it’s one of the first symptoms to appear, suggesting SARS-CoV-2 might be latching onto and damaging smell-sensing cells inside the nose. These neurons reside in the olfactory bulbs, each one extending a branching, odorant receptor-covered arm into the nasal cavity, like the tentacles of a smell-hunting jellyfish. “Here you have this virus tugging away at the only central nervous system cells exposed to the exterior world. If there was going to be SARS-CoV-2 brain disease, you’d think this would be the group that has it,” says Perlman. “But there’s no evidence of that. These people lose their sense of smell and not much else. It’s very curious.”

 

No one yet knows exactly why this happens; why the virus seems to stop in the nose rather than climbing into their brains like in Perlman’s mice. But clues are emerging. New research has shown that in people that might not be possible, because human olfactory neurons don’t appear to express ACE2 at all, unlike Perlman’s lab-engineered animals.

 

In two unrelated preprints posted earlier this month, researchers from the US, Switzerland, Italy, Belgium, and the UK mapped where in the respiratory tract and nasal passages the ACE2 receptor could be found. Both teams of scientists independently discovered these receptors on lots of different cell types, but importantly, not olfactory neurons. Their analyses suggest the virus could instead be infecting other cells in the nose. The group led by Harvard neurologists hypothesized that the point of invasion could be the cells that line capillaries and are involved in maintaining the blood-brain barrier. A team from the University of Geneva speculated that the virus could be targeting specialized life-support cells that surround olfactory neurons and help them survive. If either of those cell types got infected, it could temporarily impair or prevent olfactory neurons from interacting with odor molecules.

 

Verifying either mechanism will require studies of the living tissues inside Covid-19 patients’ noses. But, as Perlman points out, it will be hard to get people with otherwise mild symptoms to let doctors snip out little bits of their nasal passages for science. For most people, the swab used to test for the virus is more than enough nasal discomfort for one pandemic. Until more large-scale studies are conducted, doctors are still mostly on their own to figure out how to treat Covid-19 patients with neurological symptoms. For now, the best they can do is share their experiences to help others learn and adapt.

 

In Detroit, the Covid-19 patient who developed a rare form of encephalitis is now recovering in a rehabilitation facility. She was discharged last week. “I’m very cautiously optimistic that she will recover,” Fory said in a statement released by the hospital. The patient’s case, she said, highlights the need for physicians to expand the list of symptoms that should set off Covid-19 alarm bells. Look in the lungs, but don’t forget the brain.

 


 

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: What Does Covid-19 Do to Your Brain? (Wired)

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Global Vaccine Action Plan: 2011-2020

The Global Vaccine Action Plan (GVAP)—endorsed by the 194 Member States of the World Health Assembly in May 2012—is a roadmap to prevent millions of deaths by 2020 through more equitable access to vaccines for people in all communities. The GVAP aims to strengthen routine immunization, introduce new and improved vaccines, and advance research and development for the next generation of vaccines and technologies.

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Global Vaccine Action Plan: 2011-2020     pdf

 

 

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Sorry, Immunity to Covid-19 Won't Be Like a Superpower 

It's nice to think that recovery will give you absolute protection, but that's not really how this works. 
Sorry,-Immunity-to-Covid-19-Won't-Be-Lik
Despite the many unanswered questions about how our bodies fight off SARS-CoV-2 infection, one point is clear: adaptive immunity is not an on/off switch.Photo-Illustration: Sam Whitney; Getty Images

There are signs that the pandemic peak has passed in New York City, and maybe in other hot spots of infection too. While there will be much more suffering to come, both in these places and elsewhere, talk has turned in recent days to how we’re going to get people back out into society. Central to these discussions has been the notion of immunity. Which of us is safe from Covid-19, and how might that be measured? Are existing antibody tests good enough to clear people for going back to work? Should we put in place a nationwide system of immunity passports or certificates? What about raising an army of the recovered to lead the nation’s fight against the virus?

 

The answers to these questions come with considerable caveats. As many have pointed out, we can’t assume that any prior exposure to the virus will make it so a person can’t get sick again. Even if our bodies learn to fight off the illness, we don’t know how long this protection might endure. “Immunity after any infection can range from lifelong and complete to nearly nonexistent,” the epidemiologist Marc Lipsitch said in The New York Times on Sunday. “So far, however, only the first glimmers of data are available about immunity to SARS-CoV-2, the coronavirus that causes Covid-19.”

 

But public debates about immunity to Covid-19 could still be subject to a treacherous misapprehension, even once the caveats above have been acknowledged. The problem starts with just the word, immunity. It tends to conjure something binary: Either you have it or you don’t; either you’re a member of the superpowered legion of recovered, or you’re a vulnerable normie like the rest of us. The wisest commentators point to all the factors that remain unknown; they warn us that it’s possible that protection from Covid-19 will be short-lived or that it will go only to some of those who get infected. Yet a crude assumption can still be hiding in this miasma of uncertainty: that at any given point in time, people are perfectly immune to Covid-19—or else they’re not.

 

The truth is far less black and white. There may be many unanswered questions about how our bodies fight off SARS-CoV-2 infection, but one broader point is very clear: Adaptive immunity is not an on/off switch. Instead of treating it as such, we should learn to think in terms of an immunity continuum. At one end is what’s called sterilizing immunity, in which exposure to a pathogen tends to induce a lifelong, fail-safe protection from it. (That’s the case with measles.) At the other end is no immunity at all, where a history of prior illness doesn’t seem to matter—or, indeed, where it could even make things worse. Having an immune response to one strain of the virus causing dengue fever, for example, can worsen your reaction to the other types.

 

Experts say that SARS-CoV-2 likely falls somewhere in the middle, such that people who get exposed are neither sterilized against further illness nor left utterly defenseless. Instead, they enter into a state you might think of as “immunishness,” an intermediate level of protection that dwindles over time. The robustness of this immunish state—whether it prevents all reinfection or merely makes a second round of sickness less intense—and the period of time for which it lasts will depend on multiple factors, such as a patient’s genetics and sex (women tend to have stronger immune reactions than men), the strength of their initial immune response, and the characteristics of the virus itself as it continues to evolve.

 

Where, exactly, might responses to the new coronavirus fall on this continuum of induced immunishness? That’s still unknown. We don’t even know which types of antibodies are most crucial for preventing SARS-CoV-2 from infecting cells. Without that information, it will be very hard to design blood tests that deliver reasonable estimates of the strength of someone’s immunity, in the sense of how likely they are to become infected or how severe their symptoms might be.

 

If we want to know the duration of this immunity, whatever its strength, we’ll need to learn more about how the most relevant antibody levels change in the months or years post-infection. Previous studies of older, less dangerous coronaviruses seem to suggest that protection is short-lived: Antibody levels fall off significantly within a few months and continue to decline. A small study from 1990 re-exposed nine patients who had developed a mild cold to the same coronavirus a year later. Two-thirds of them developed a new bout of the infection, though they were contagious for a shorter period the second time around. The pattern may well be very different for SARS-CoV-2. Other research finds that decay rates for immunity can vary quite a bit from person to person, even in response to the same pathogen (or vaccine) exposure.

 

How sick you get with Covid-19 the first time may also make a difference. Those who recover from severe cases could end up with stronger immunity than those who were asymptomatic. Research from pathologist and immunology researcher Scott Boyd’s group at Stanford suggests that people in this category make higher levels of antibodies to the virus. There’s also a bit of preliminary evidence suggesting that at least some people may not develop much immunity at all on first exposure. Data from 175 patients in China who had only mild symptoms showed that about one-quarter of them developed only a weak immune response, as measured by antibody levels, while about 5 percent showed no measurable response at all. (That study is preliminary and not yet peer-reviewed.)

 

A report from South Korea found that 91 patients who’d recovered from SARS-CoV-2 tested positive later, suggesting either that they’d been reinfected or that the first infection was reactivated. There have also been reports of possible reinfection in China and Japan. One explanation for these incidents is that they’re not a sign that people are being infected, recovering, and then becoming infected again, but rather that the testing had been problematic. For instance, tests might be turning up false negatives and then later picking up signs of the initial infection.

 

One intriguing possibility is that previous exposure to other coronaviruses offers a smidgen of protection. (An old study of milder coronaviruses suggests this could be true.) Tulane University virologist Robert Garry and his research group have seen some patients with Covid-19 mount the sort of immune response you’d expect from someone experiencing a second exposure to the same pathogen. “Obviously they weren’t infected with SARS-CoV-2 before,” Garry says, but it may be that the new virus is similar enough to the seasonal coronaviruses that cause the common cold that it triggers a memory response. This could explain why Covid-19 cases seem to be less severe in children than adults: Maybe kids are more likely to have had recent exposure to the other coronaviruses.

 

With time and further research, these uncertainties will fade. Eventually we’ll have a better sense of how immunity to SARS-CoV-2 is formed and how long it tends to last. But even then, when all the data have come in, we may never get the clarity we crave. More and better science can elucidate the facts, but that doesn’t always make them any less bewildering. In all the talk about issuing certificates or concert wristbands so that people who recover can be sent into our schools and nursing homes and shelters, we tend to overlook the often squishy meaning of immunity. The truth is, our immune responses to this virus aren’t likely to be permanent or perfect. It’s nice to imagine that once someone’s been infected they become a knight in antibody armor, but that’s not really how it works.

 

Photographs: Steve Pfost/Getty Images; NIH/Science Source

 


 

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: Sorry, Immunity to Covid-19 Won't Be Like a Superpower (Wired)

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How the anti-vaccine community is responding to COVID-19

It's the old, familiar path of conspiratorial thinking and government mistrust.

A nurse prepares to administer the measles, mumps, and rubella (MMR) vaccine as well as a vaccine used to help prevent the diseases of diphtheria, pertussis, tetanus, and polio at Children's Primary Care Clinic in Minneapolis, Minnesota.
Enlarge / A nurse prepares to administer the measles, mumps, and rubella (MMR) vaccine as well as a vaccine used to help prevent the diseases of diphtheria, pertussis, tetanus, and polio at Children's Primary Care Clinic in Minneapolis, Minnesota.

In early March, Melissa Floyd, a self-described health freedom educator who co-hosts "The Vaccine Conversation" podcast, was forced to abruptly change plans. She and her co-host were supposed to pack up for a live multi-city tour. But the public health crisis born from COVID-19 delayed the start of their tour for months.

 

Floyd and her cohost, Bob Sears, a California-based pediatrician who advocates a delayed vaccine schedule and skipping some vaccines, addressed the cancellation in a podcast episode, noting that they don't have any personal fear of the virus. Our government agencies, Floyd said, “are talking about washing your hands, but why aren't they talking about things you can do to boost your immune system like vitamin D? Why aren't they talking about reducing sugar? Why aren’t they talking about eating fruits and vegetables and staying away from processed foods?

 

“I've not heard any footage,” Floyd continued, “that talks about how to make your body strong—it's just wash your hands, use a mask and hopefully that vaccine will come out sooner rather than later.” (Floyd did not respond to an interview request from Undark.)

 

Views like Floyd’s and Sears’ are influential—"The Vaccine Conversation" podcast has reportedly been downloaded nearly 400,000 times in 92 countries—and have been making gains in recent years, which has likely contributed to disease outbreaks like measles and whooping-cough. The beliefs and messaging vary: health and medical freedom advocates tend to oppose any mandated medical intervention, while vaccine skeptics question the need for medical immunizations. Those who are anti-vaccine may oppose them entirely. Approaches to the COVID-19 public health crisis also vary, but so far, while some in the community are rethinking their views, many of the responses from major influencers continue to wear down a familiar path of conspiratorial thinking and government mistrust, says Dorit Reiss, a law professor at the University of California Hastings who studies the anti-vaccination movement.

 

Experts say the trend doesn’t show much promise for changing entrenched skeptics’ minds about vaccines, even in the face of a global pandemic that has already cost more than 138,000 lives. On March 31, the White House coronavirus task force projected that 100,000 to 240,000 may die in the United States alone—and that’s with efforts to curb the virus’s spread. Public health officials agree that a vaccine is the only endgame that would allow people to resume all normal activities without periods of restricted movement or gatherings.

 

“I’m seeing a very similar pattern that I see when outbreaks of measles happen,” says Karen Ernst, executive director of Voices for Vaccines, a parent-led organization that advocates for vaccines. “That there is a certain amount of denial, blame, and conspiratorial thinking.” Anti-vaccine sentiment also ties into identity as much as belief. “These are people who make this part of their self-identity: I’m a mother, I have a natural lifestyle, I refuse vaccines. It’s important to deny things in order for that identity to be protected.”

 

But now that the world is remembering the horrors of viral disease—more than 1.9 million people have been infected worldwide—public health experts see an opportunity to convince people who are on the fence about the benefits of vaccination. “It’s a moment of opportunity” for vaccine support, says Reiss, adding that there may be a strong desire for a vaccine when it does arrive.

 

To be anti-vaccine in today’s world, says Reiss, you have to subscribe to some conspiracy theories, because there is so much data on the other side. That’s not to say anything about people's intelligence, she adds. “You can be very intelligent and very grounded and still believe in conspiracy theories.”

Anti-vaccine activist Del Bigtree hosting his YouTube show.
Enlarge / Anti-vaccine activist Del Bigtree hosting his YouTube show.
YouTube

The first way that those who are against or hesitant about vaccination are responding to the newest health crisis is by denying that it even exists or by saying it’s not that bad and people are not actually dying, says Reiss. For example, last month Del Bigtree—producer of the documentary "Vaxxed" and host of the popular online show "The Highwire"—told his audience that China’s numbers didn’t add up.

 

“It's not as deadly as we've been told,” he said, adding later in the show: “This is really only a tragic situation for a small group of people that are immune-suppressed or elderly.” Similarly, on March 28, Sears posted on Facebook: “Elderly are vulnerable and need protection AND Covid is harmless to almost everyone else.”

 

Both statements are incorrect—there are numerous reports of young, healthy people in intensive care and on ventilators. But it’s a common tactic, says Reiss. “They focus on death, and they ignore hospitalization, and they're going to say: look, it's not going to kill you, you shouldn't get the vaccine,” she says. “They do that with other diseases as well.” A recent Washington Post analysis found that hundreds of people under the age of 50 have also died from the coronavirus.

 

Other popular anti-vaccine COVID-19 theories suggest technology is to blame. Keri Hilson, an American singer with 4.2 million Twitter followers, posted now-deleted tweets attempting to link the coronavirus to 5G mobile networks. "People have been trying to warn us about 5G for YEARS,” she wrote, adding that 5G launched in China in November of 2019, and then people started dying. Joshua Coleman, an anti-vaccine activist who claims a vaccine injury caused his son to need a wheelchair, claimed on Facebook that coronavirus is in fact caused by 5G. In the United Kingdom, authorities say the conspiracy theory has led to the damage of dozens of wireless towers and other telecommunications equipment.

 

Meanwhile, Larry Cook, an anti-vaccine influencer who runs the popular Facebook page “Stop Mandatory Vaccination,” has claimed—without evidence—on his personal page that lockdowns and social distancing are a way to make it easier for the government to track people and require them to be tested for the virus. That way, he has said, the government would mandate vaccinations for everyone. “This lockdown and ‘social distancing’ is psychological and economic warfare against us so we will accept mandatory vaccination,” he wrote on April 12.

(Cook did not respond to an interview request from Undark.)

 

Still other anti-vaccine advocates focus on ongoing efforts to create and test a COVID-19 vaccine. The Children’s Health Defense, a nonprofit founded by Robert F. Kennedy, Jr. that links conditions like autism and diabetes to vaccines, pesticides, and other exposures, said the rush to find a vaccine—instead of focusing on treatments—is a looming problem that is driven by profit. A blog post on the group’s website claims: “For the moment, our government is prioritizing vaccine development (with the enticing promise of lucrative patents) over existing therapeutics (such as vitamin C and already-FDA-approved drugs) that do not offer comparable financial windfalls.” The post goes on to claim, without citing evidence, that “fast-tracked vaccines are a sweetheart deal for both biopharma and government.”

A screenshot from the now-private Stop Mandatory Vaccination Facebook group.
A screenshot from the now-private Stop Mandatory Vaccination Facebook group.
Facebook

Of course, even with COVID-19 treatments—which have not yet been rigorously studied—many health experts agree that life is never going to be normal without a vaccine, including former FDA Commissioner Scott Gottlieb and White House infectious disease adviser Anthony Fauci.

 

And another common thread in anti-vaccine groups focuses on the belief that natural immunity—the kind you get from actually having a disease—is better than immunity from a vaccine. The logic, they argue, is that if natural disease is a healthy and normal process, people should just go ahead and get infected with a disease, which will eventually give them immunity and protect more people. “It's an inferior immunity that vaccines provide, which is why we've seen second, third, fourth, fifth doses of vaccines, why everyone has to get a flu shot every single year,” Bigtree said on his March 26 show.

 

In an interview, Bigtree elaborated, saying he’s not anti-vaccine for the right people. “I would never have a problem with any product if it was designed for the people that need it,” he said. “I do not agree with the principle that perfectly healthy people need to take a product to protect a very small percentage of sick people.”

 

He added that he would probably not get the vaccine when it becomes available, and that he is willing to take certain calculated risks with his own family.

 

And it’s not just anti-vaccine groups promoting the idea that people should get sick. The Federalist, an American conservative online magazine, published a story on March 25 advocating a voluntary infection approach for COVID-19.

 

While it’s true that, in most cases, natural immunity can last longer than vaccine-induced immunity, public health experts say the risks of the former outweigh the risks of the latter for every recommended vaccine. Natural immunity, Ernst says, “protects people after a whole bunch of people get sick, and that’s not good.” Reiss adds that none of these denials or conspiracy theories is new—they’re classic beats in the anti-vaccination world: “They've been circulating around, but they're just applying old beliefs to new contexts.” The new context matters, though—COVID-19 is a public health crisis on a level that hasn’t been seen in 100 years.

 

Despite the common anti-vaccination themes that are cropping up in the COVID-19 pandemic, there are some signs of change. According to the experts Undark interviewed, the current crisis could usher in an era of increased interest in vaccines—or at least in taking responsibility for the health of others. That would be a welcome trend for public health advocates. In 2019, a global survey from The Wellcome Group of people in more than 140 countries found 79 percent of respondents think vaccines are safe and effective. Still, those living in Western Europe reported the lowest confidence in vaccines, which potentially endangers herd immunity.

 

Catherine Flores Martin, executive director for the California Immunization Coalition, says she is seeing a shift in people reacting to anti-vaccine posts on social media. And she thinks people are going to be a lot less forgiving of anti-vaccination beliefs in the future. “There will still be the believers, but I think other people are going to be a lot less tolerant of it now that people have seen how disease can impact their life. We have their attention.”

 

Flores Martin also sees a shift in the way people talk about their personal and societal responsibilities: “It’s not just about social responsibility or environmental responsibility, but public health responsibility.”

 

Ernst worries about a different downstream effect of the current crisis: With social distancing guidelines in place, fewer parents may bring babies under two years old to receive routine vaccinations. “That’s related because at the downward side of this pandemic, we don’t want to deal with measles outbreaks everywhere, or mumps on college campuses,” she says. “We don’t want meningitis at high schools. We don’t want to follow one crisis with a whole bunch of other preventable crises.”

 

The vaccine-skeptic communities haven’t ignored that possibility, either. On the “Your Baby, Your Way” Facebook page, a group that advocates a vaccine schedule that omits or delays routine vaccines, a post from March 27 extolled the virtues of skipping doctor’s visits.

 

“People in America are staying home because of Coronavirus,” the post read. “Even the most conventional parents are skipping some well-baby checks. You know what that means, right?! The less often you take a baby to ‘routine’ doctors’ appointments, the more likely you are to keep breastfeeding, avoid Tylenol, avoid antibiotics, and delay vaccines."

 

“Here’s to hoping every parent of a newborn, two-month-old, four-month-old, and six-month-old decides to SKIP the well-baby visits that are making so many of our babies sick,” the post concluded.

 

Jennifer Margulis, who authored the “Your Baby, Your Way” book and is one of nine moderators of the corresponding Facebook page, which has more than 40,000 followers, said that the page’s followers are worried about coronavirus—but they are equally concerned that the vaccines in development are being rushed to market without safety testing.

 

“Experts are saying that it will be very difficult to develop a safe vaccine against a respiratory illness like COVID-19,” she told Undark in an email. “An effective vaccine against SARS was never successfully implemented.” (A SARS vaccine was developed in the early 2000s but never brought to market as public health measures curbed the disease before it was ready.) Margulis also pointed to a dengue vaccine rolled out in the Philippines that has been shown to pose a risk of severe illness in people who have not been previously infected. Public health officials have since implemented restrictions and issued additional caution on the use of the vaccine.

 

William Schaffner, medical director of the National Foundation for Infectious Diseases and a professor of preventive medicine at Vanderbilt University sees a relevant historical lesson. During the run-up to the Iraq War, the government touted a smallpox vaccine. Smallpox had been eradicated globally in 1980, but Saddam Hussein had allegedly retained a small supply, and military leaders warned that he may use it against Americans. The vaccine never would be licensed today, Schaffner says, because it was linked to so many adverse events. “But the anti-vax movement was totally silent when that vaccine came out,” he adds. “The reason they were silent was evident—they were smart. Politically, it would be damaging to them if they had gone against something that the president of the US was in favor of, so they just kept quiet.”

 

“I suspect that if coronavirus continues to be a public health problem and if we get a vaccine, and if the leadership of this country defines it as a public health problem, and the nation’s focus is on getting as many people vaccinated as possible, my prediction is they will keep themselves very quiet about that. They will not come out against it,” he adds. “They are very media-savvy.”

 

This article originally appeared on Undark.

 

 

Source: How the anti-vaccine community is responding to COVID-19 (Ars Technica)  

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Covid-19 Does Not Discriminate by Body Weight

This-Pandemic-Does-Not-Discriminate-By-B

Photo-illustration: Sam Whitney; Getty Images

 

 

The claim that those with higher BMIs are at special risk of dying from the coronavirus is grossly overstated.

 

At this point it’s been made to seem like common sense: Larger-bodied people are at higher risk from this pandemic. “Those who are overweight really need to be careful,” France’s chief epidemiologist declared last week. “That is why we're worried about our friends in America.”

 

In recent weeks, many news outlets—and a few scientific journals—have sent the same frightening message. A study posted on a preprint server last weekend by researchers at New York University provided fodder for the latest round of this reporting: “Obesity appears to be one of the biggest risk factors related to Covid-19 hospitalizations and critical illness,” Newsweek claimed on Tuesday. Yet this rhetoric is based on flawed and limited evidence, which only exacerbates the stigma that larger-bodied people already face in society and our health care system. That stigma is what truly jeopardizes their health, not weight itself—a fact that’s only more important to consider in the midst of this pandemic.

 

To date, the most plausible research pointing to higher BMI as a risk factor includes three preliminary reports that have been released since April 8: a Centers for Disease Control and Prevention report with descriptive statistics on people who’ve been hospitalized for Covid-19, showing that 48 percent of those with available BMI data are in the “obese” category (a slightly higher percentage than the 42 percent in the US as a whole); a small French study that found people with a BMI of 35 and above are at higher risk of being put on a ventilator; and a letter to the editor of the journal Clinical Infectious Diseases from researchers at NYU’s School of Medicine (including one of the authors of last week’s preprint), sharing a preliminary finding that people with a BMI of 30 or above appear to be at higher risk for hospitalization and intensive-care admission, if they’re less than 60 years old. (Among people who are 60 or older, weight status did not seem to be important.)

 

All of these reports are flawed in similar ways. Most important, none of them control for race, socioeconomic status, or quality of care—social determinants of health that we know explain the lion’s share of health disparities between groups of people. Structural racism and other forms of inequality in our society have long been linked to worse health outcomes, including higher rates of diabetes and hypertension (two likely Covid-19 risk factors) among people in oppressed groups. Now, those health disparities are on full display in the Covid-19 pandemic, which is disproportionately impacting black communities—not because of biology, but because of systemic inequalities like higher rates of exposure to the virus and less access to medical care.

As it happens, that recent preprint from NYU did take race into account, in its finding that having a very high BMI was a major risk factor for hospitalization. But the same analysis also found that BMI was only marginally important at predicting which hospitalized patients would go on to have “critical” illness. It also seemed to indicate that being African American was in some way significantly protective against Covid-19: Black patients admitted to the hospital were only half as likely as white patients to develop the most serious symptoms, according to the study. Needless to say, few if any outlets touted this dubious result.

 

Another glaring issue with the three published reports about BMI and Covid-19: They don’t control for known individual health risks that may be associated with worse outcomes for this virus, including asthma and other chronic respiratory conditions, cancer, and immunosuppressive medication use. The CDC report and NYU letter to the editor don’t control for diabetes or cardiovascular conditions, either, although these two likely risk factors for Covid-19 happen to be associated with higher BMI. The French study of 124 patients does control for diabetes and hypertension, as well as dyslipidemia, but not for other risk factors—even though in the study’s introduction, the authors themselves acknowledge that cardiovascular disease, chronic respiratory disease, and cancer are also likely to raise the risk of Covid-19.

 

Moreover, these reports all fail to control for the particular ways in which clinicians’ biases and beliefs about body size are likely to be influencing Covid-19 care decisions for higher-weight people. In 2013, the American Medical Association labeled “obesity” as a disease (against the recommendation of the AMA’s internal committee devoted to studying the matter), and the CDC has included a BMI of 40 or above on its list of risk factors for severe Covid-19 illness since mid-March. So higher-weight people may be more likely to get hospitalized simply because they’re viewed as unhealthy and deemed higher-risk patients. The April 8 CDC report only includes BMI measurements for 10 percent of the patients in the sample, and while it’s understandable that they’d have so much missing data amid the chaos of a global pandemic, it’s also possible that higher-weight people are more likely to be weighed because their weight is assumed to be clinically relevant. Thus, people with a high BMI could just be overrepresented in the data.

 

Where did the CDC get the idea that people with a BMI of 40 or above are at greater risk in the first place? It’s unclear. A CDC press contact didn’t respond to a request for comment, but the peer-reviewed evidence that was available at the time the agency made that pronouncement generally indicated weight was not a risk factor. Nearly all published data from China (where Covid-19 has been studied since first being discovered in December 2019) shows that high BMI alone isn’t associated with developing the disease or with having a critical outcome. In most Chinese studies, high BMI doesn’t even make the list of preexisting conditions among Covid-19 patients—despite the fact that one-third of China’s population has a BMI in the “overweight” or “obese" categories, and that China considers weight management a public-health priority. Early US reports from public health departments also seemed to indicate that higher BMI isn’t a risk factor: In New York State, for example, “obesity” hasn’t been on the state’s list of the top 10 preexisting conditions associated with Covid-19 fatality as of this writing. The “obesity” rate documented among some of the earliest Covid-19 cases in Washington’s King County matched that of the county as a whole.

 

What’s more, the (limited) data available on deaths and BMI so far suggest we could end up seeing a lower risk of death among higher-weight people. For example, the Louisiana health department is reporting as of April 16 that 22 percent of the people who’ve died of Covid-19 in Louisiana were in the “obese” BMI category, but nearly 37 percent of the state’s overall population falls into that category, according to the CDC.

 

Some of that could be an artifact of differences in age or sex. Age is clearly the biggest factor affecting the case fatality rate of Covid-19, and in general elderly adults tend to be smaller-bodied because of age-related losses in both fat and muscle mass. Another confounding factor could be that women are more likely to have BMIs in the “obese” category than men, and yet female sex seems to be a protective factor against Covid-19.

 

Still, the early numbers suggest it’s possible that being in that BMI category could actually be protective against Covid-19 death. That might sound outrageous, given the conventional wisdom that “obesity kills,” but there’s evidence to indicate that heavier people may have some protection against at least one of the major sources of Covid-19 mortality: acute respiratory distress syndrome (ARDS). A 2017 meta-analysis found that having a BMI of 30 or above was associated with a significantly lower risk of dying from ARDS, compared to those in the “normal” category. And ARDS isn’t the only condition where we see this pattern; higher BMI is associated with a lower risk of adverse outcomes in many diseases and clinical situations, such as pneumonia survival, sepsis, heart failure, and diabetes hospitalization and survival—the so-called “obesity paradox.”

 

Yet all of that early evidence didn’t stop researchers and editors of medical journals from speculating that high BMI was going to emerge as a risk factor. These groups were extrapolating from the evidence on H1N1 influenza (aka swine flu), where some data suggested this was true. But a 2016 meta-analysis of studies on H1N1 and weight points to different conclusions: For one, there’s no increased risk of death from swine flu for people with BMIs of 25 and above. And though it first appeared that people in this group did have an increased risk of having severe, nonfatal complications, those associations disappeared after the researchers adjusted for an important confounding variable: Smaller-bodied H1N1 patients were more likely to get early antiviral treatment. It turned out that lower-quality health care, not high BMI, was responsible for the increased risk seen in people with BMIs in the “obese” category.

 

That’s weight stigma, and it’s the real issue here. Anti-fat bias has been linked to sub-par health care in a variety of ways, including providers spending less time with larger-bodied patients; speaking more curtly and less compassionately to them; and misattributing symptoms to their weight instead of referring them for testing or offering evidence-based, non-weight-related treatment options. Discrimination against higher-weight people is a known, independent risk factor for all kinds of health problems that typically get blamed on weight, including diabetes and heart disease. And Covid-19 is only amplifying this preexisting disparity. “When you take that and then you throw a pandemic on top, it’s like adding water to a grease fire,” says Joy Cox, a researcher at Rutgers New Jersey Medical School. “Health disparities that weren’t addressed when there was an opportunity to address them have been magnified.”

 

The fact that researchers have been pointing to body size as a risk factor for weeks now, even in the absence of much evidence, is a clear example of how weight stigma gets enacted in science. “Consider the questions of whether high-BMI folks are at increased risk for contracting Covid-19—and if they do contract it, whether they have poorer outcomes,” says Lindo Bacon, a weight-science researcher and author of the books Health at Every Size and Body Respect. “First, notice the bias built into the questions. There is some indication that opposing hypotheses are better supported by current research—whether they are at lower risk, and have better outcomes—but I haven’t seen anyone frame their questions that way yet.”

 

Indeed, multiple studies have found that simply reading a news article about the so-called “obesity epidemic” induces weight stigma and increases the expression of anti-fat attitudes among participants. Reports about the pandemic that name body size as a risk factor likely do the same. “I suspect that this news coverage constantly linking weight to Covid-19 risk is also heightening anti-fat bias,” says Jeffrey Hunger, a researcher who studies the effects of weight stigma and other forms of discrimination at Miami University of Ohio. “This constant barrage of media coverage linking weight to Covid-19 might lead to blaming individuals for actually contracting it.” And from my interactions with dozens of higher-weight clients, readers, and podcast listeners, it’s clear that many people are feeling blamed and shamed right now. “In a lot of ways it does make you feel like it’s your fault,” says Cox, who is at a higher weight. That feeling of self-blame just worsens the already difficult situation of living through a global pandemic. “There's an extra mental and emotional toll that it takes,” Cox says.

 

Instead of trumpeting the supposed risks of high BMI and adding to the already damaging impact of weight stigma, researchers need to be asking deeper questions, and public health officials and journalists need to report on the science in more nuanced and sensitive ways. To do otherwise is to create the very outcomes that we want to avoid.

 

Photographs: Nathan Laine/Bloomberg/Getty Images; Ludovic Marin/AFP/Getty Images

 

 

Source: Covid-19 Does Not Discriminate by Body Weight (Wired)

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Coronavirus: China's Wuhan city revises up death toll by 1,290 - a 50% increase

 

The city, which was the epicentre of the outbreak, says the dramatic increase is due to previous omissions, delays and mistakes.

 

2372002280998394907_4933470.jpg?bypass-s

Patients at an exhibition centre converted into a hospital in Wuhan

The total number of coronavirus deaths in Wuhan has been revised up by 1,290 - a 50% increase.

According to the latest figures, 3,869 people are known to have died from COVID-19 in the Chinese city - the epicentre of the outbreak.

 

skynews-coronavirus-model-illustration_4

An illustration of the coronavirus structure

 

 

Earlier this month, Wuhan lifted a lockdown that had paralysed the city of 11 million for more than two months in a drastic effort to contain the virus.

However, over two million cases of the disease have now been reported across the world and dozens of countries are in lockdown.

More than 137,000 people have died, according to a tally by Johns Hopkins University.

 

Wuhan's revised death toll of 3,869 is the most in China. Numbers of total cases in the city were also raised by 325 to 50,333, accounting for about two-thirds of China's total 82,367 announced cases.

The official Xinhua News Agency quoted an unidentified official with Wuhan's epidemic and prevention and control headquarters as saying that during the early stages of the outbreak, "due to the insufficiency in admission and treatment capability, a few medical institutions failed to connect with the disease prevention and control system in time, while hospitals were overloaded and medics were overwhelmed with patients".

 

"As a result, belated, missed and mistaken reporting occurred," the official was quoted as saying.

China has strongly denied claims it delayed reporting on the virus outbreak in Wuhan late last year and underreported case numbers, worsening the impact on the US and other countries.

 

It comes as figures show China suffered its worst economic contraction since since at least the 1970s in the first quarter as it fought the coronavirus.

Weak consumer spending and factory activity also suggest the country faces a longer, harder recovery than initially expected.

The world's second-largest economy shrank 6.8% from a year ago in the three months ending in March after factories, shops and travel were shut down to contain the infection, official data showed.

 

2372002280998418707_4933496.jpg?bypass-s

Motorcyclists ride in an almost empty street in Wuhan in February

That was stronger than some forecasts that predicted a contraction of up to 16% but was still China's worst performance since before market-style economic reforms started in 1979.

skynews-wuhan-china-open_4965347.jpg?byp

A celebration was held earlier this month as Wuhan city reopen

 

The ruling Communist Party declared victory over the virus in early March and started reopening factories and offices even as the United States and Europe tightened controls.

 

But cinemas, hair salons and other businesses deemed non-essential but employ millions of people are still closed. Tourism is struggling to recover.

 

source: 

https://news.sky.com/story/coronavirus-chinas-wuhan-city-revises-up-death-toll-by-1-290-a-50-increase-11974466

 

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Why COVID-19 may attack the body differently than we think

Kidney, heart may be at particular risk due to exaggerated immune system response

 
adam-miller.JPG
Adam Miller · CBC News · Posted: Apr 18, 2020 4:00 AM ET | Last Updated: 42 minutes ago
 
aptopix-virus-outbreak-italy.jpg
A medical staffer holds the hand of a patient in the ICU of the Bassini Hospital near Milan, Italy, on Tuesday. One key thing to understand about the deadliness of the coronavirus is how it infects the body and how our body responds to fight it. (Claudio Furlan/LaPresse via AP)

This is an excerpt from Second Opinion, a weekly roundup of eclectic and under-the-radar health and medical science news emailed to subscribers every Saturday morning. If you haven't subscribed yet, you can do that by clicking here.


Understanding how COVID-19 attacks the human body is essential to developing an effective treatment or vaccine to stop the global pandemic — but there's still so much we don't know about how it can kill us.

 

As researchers around the world race to understand the illness, they are compiling and sharing their early observations of patients hit by a virus that has sickened more than two million people. The findings are preliminary, but they can help point researchers in the right directions.

They have seen that in severe cases, COVID-19 invades our respiratory cells and triggers an immune system response that targets those infected cells, destroys lung tissue and ultimately clogs our airways, cutting off our oxygen supply. 

That's when organ failure can also occur, causing severe damage to the kidneys, liver and heart, similar to other conditions like sepsis. 

But they will look to determine whether the virus is targeting and shutting down organs in a new way or just behaving like other infections that cause such common complications.

Why COVID-19 can be so deadly

One key thing to understand about the deadliness of the coronavirus is how it infects the body and how our body responds to fight it. 

Cytokines are small molecules released by the immune system that travel throughout the body to co-ordinate an immune response against an infection or injury — even with something as common as a mild fever. 

But if the immune system overproduces them in response to the infection, they can cause "cytokine storms" that can rampage through the bloodstream and severely damage the body. 

Dr. Douglas Fraser, an ICU doctor at London Health Sciences Centre and a researcher at Western University in London, Ont., has been studying that exaggerated immune response by collecting blood from critically ill COVID-19 patients in an effort to find new ways to treat the disease. 

"The immune response to this particular disease is very different than what we've seen in other infected patients that end up in the ICU," he said. "It's a unique response and it's going to require unique therapies." 

Fraser said his research shows there are different types of cytokines released in the body at unusual times and levels in response to COVID-19 compared with those that are typically found in critically ill patients from more common diseases. 

"What we're seeing seems to be occurring in all of the very sick patients: those who are requiring the ICU admissions, those who are requiring assistance with their breathing and those that are ultimately dying," he said.

Kidneys tied to severe complications

Kidney damage was an "important complication" in a preliminary publication of a recent observational study of 287 COVID-19 patients in China, which found almost one in five had some stage of sudden or "acute" kidney injury, putting them at "substantially higher" risk of death.

While it's not yet known what rate of Canadian COVID-19 patients have acute kidney damage, the majority occurs in severely ill patients, said Dr. Jeffrey Perl, a nephrologist at St Michael's Hospital in Toronto and an assistant medical professor at the University of Toronto. 

"As people's blood pressure gets very low from a very massive, overwhelming inflammatory immune response, the kidneys are starved of blood," he said, adding that it can often lead to the need for a dialysis machine to clean the patient's blood.

To give an idea of how serious a complication it can be, Perl said the mortality rate for patients who had developed acute kidney injury from SARS in 2003 was 92 per cent, compared to just eight per cent in those who didn't. 

 
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Toronto General Hospital employee Maria Tanta, left, a recovery room nurse, has her temperature checked by nurse Callie Dunne during the SARS epidemic on April 2, 2003. (J.P. Moczulski/Canadian Press)

Chronic kidney patients are also at higher risk of death with COVID-19 compared to those without pre-existing conditions who are otherwise well, he added. 

"We're very worried about those patients getting a COVID-19 infection," he said. "Similar to the elderly population that we're very concerned about, I would consider these patients another high-risk group." 

Heart may be 'directly' targeted by virus

One essential organ that may be at direct risk from the virus is the heart.

A cohort study published in JAMA last month found almost 20 per cent of 416 hospitalized COVID-19 patients in China had heart damage during hospitalization, putting them at a higher risk for death. 

While recent research from the American College of Cardiology found arrhythmia, or irregular heartbeat, in 16 per cent of patients and acute cardiac injury in 7.2 per cent.

"There's the possibility and the likelihood that some of the virus might actually get taken directly up into the heart muscle cells and cause that heart injury," said Dr. Patrick Lawler, a cardiologist and clinician scientist at the Peter Munk Cardiac Centre in Toronto. 

"We hear anecdotes from other people that have had a little bit more experience, unfortunately, with this that really are consistent with the heart suddenly starting to become weak." 

An observational study of 187 patients hospitalized with COVID-19 published in the New England Journal of Medicine last month found high levels of troponin, which can indicate problems with the heart, in 28 per cent of hospitalized COVID-19 patients in Wuhan, China, which concluded they were at risk of "much higher mortality." 

 
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A medical worker checks on a patient's condition at Jinyintan Hospital in Wuhan in central China's Hubei province on Feb. 16. Emerging research shows the heart may be at direct risk from the virus. One study in China found almost 20 per cent of 416 patients had cardiac issues. (Chinatopix/The Associated Press)

Lawler said the outcomes for COVID-19 patients with cardiac issues are "dramatically worse," and even though the virus enters through the respiratory system, it can take root in other areas of the body. 

"The heart is really a critical, critical part of what determines whether or not patients are going to recover from this or not," he said.

Can it help us find a cure?

Lawler is currently looking at the use of blood thinners as a possible treatment for COVID-19 patients, which may prevent the virus from binding to ACE2 receptors — enzymes found in cells throughout the human body that can act as an entryway for coronaviruses. 

He said research suggests blood clots may play a role in organ failure in critically ill patients, so different doses of anticoagulants may prevent that from happening. 

Fraser is also using his research on the "cytokine storm" immune response to COVID-19 to find "targets" to further efforts toward an effective treatment. 

He said there could be multiple components to why different people are susceptible to the virus that range from genetics, to pre-existing conditions to age.

"Once we have an understanding of what's going on, we can develop therapies, we can develop vaccines," he said. 

"Then we can get back to a normal life."

 

CBC

 

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Why The WHO Faked A Pandemic

 

 

The World Health Organization has suddenly gone from crying "The sky is falling!" like a cackling Chicken Little to squealing like a stuck pig. The reason: charges that the agency deliberately fomented swine flu hysteria. "The world is going through a real pandemic. The description of it as a fake is wrong and irresponsible," the agency claims on its Web site. A WHO spokesman declined to specify who or what gave this "description," but the primary accuser is hard to ignore.

 

The Parliamentary Assembly of the Council of Europe (PACE), a human rights watchdog, is publicly investigating the WHO's motives in declaring a pandemic. Indeed, the chairman of its influential health committee, epidemiologist Wolfgang Wodarg, has declared that the "false pandemic" is "one of the greatest medicine scandals of the century."

 

 

Even within the agency, the director of the WHO Collaborating Center for Epidemiology in Munster, Germany, Dr. Ulrich Kiel, has essentially labeled the pandemic a hoax. "We are witnessing a gigantic misallocation of resources [$18 billion so far] in terms of public health," he said.

 

They're right. This wasn't merely overcautiousness or simple misjudgment. The pandemic declaration and all the Klaxon-ringing since reflect sheer dishonesty motivated not by medical concerns but political ones.

 

Unquestionably, swine flu has proved to be vastly milder than ordinary seasonal flu. It kills at a third to a tenth the rate, according to U.S. Centers for Disease Control and Prevention estimates. Data from other countries like France and Japan indicate it's far tamer than that.

 

Indeed, judging by what we've seen in New Zealand and Australia (where the epidemics have ended), and by what we're seeing elsewhere in the world, we'll have considerably fewer flu deaths this season than normal. That's because swine flu muscles aside seasonal flu, acting as a sort of inoculation against the far deadlier strain.

 

Did the WHO have any indicators of this mildness when it declared the pandemic in June?

 

Absolutely, as I wrote at the time. We were then fully 11 weeks into the outbreak and swine flu had only killed 144 people worldwide--the same number who die of seasonal flu worldwide every few hours. (An estimated 250,000 to 500,000 per year by the WHO's own numbers.) The mildest pandemics of the 20th century killed at least a million people.

 

But how could the organization declare a pandemic when its own official definition required "simultaneous epidemics worldwide with enormous numbers of deaths and illness." Severity--that is, the number of deaths--is crucial, because every year flu causes "a global spread of disease."

 

Easy. In May, in what it admitted was a direct response to the outbreak of swine flu the month before, WHO promulgated a new definition matched to swine flu that simply eliminated severity as a factor. You could now have a pandemic with zero deaths.

 

Under fire, the organization is boldly lying about the change, to which anybody with an Internet connection can attest. In a mid-January virtual conference WHO swine flu chief Keiji Fukuda stated: "Did WHO change its definition of a pandemic? The answer is no: WHO did not change its definition." Two weeks later at a PACE conference he insisted: "Having severe deaths has never been part of the WHO definition."

 

They did it; but why?

 

In part, it was CYA for the WHO. The agency was losing credibility over the refusal of avian flu H5N1 to go pandemic and kill as many as 150 million people worldwide, as its "flu czar" had predicted in 2005.

 

Around the world nations heeded the warnings and spent vast sums developing vaccines and making other preparations. So when swine flu conveniently trotted in, the WHO essentially crossed out "avian," inserted "swine," and WHO Director-General Margaret Chan arrogantly boasted, "The world can now reap the benefits of investments over the last five years in pandemic preparedness."

 

But there's more than bureaucratic self-interest at work here. Bizarrely enough, the WHO has also exploited its phony pandemic to push a hard left political agenda.

 

In a September speech WHO Director-General Chan said "ministers of health" should take advantage of the "devastating impact" swine flu will have on poorer nations to get out the message that "changes in the functioning of the global economy" are needed to "distribute wealth on the basis of" values "like community, solidarity, equity and social justice." She further declared it should be used as a weapon against "international policies and systems that govern financial markets, economies, commerce, trade and foreign affairs."

 

Chan's dream now lies in tatters. All the WHO has done, says PACE's Wodart, is to destroy "much of the credibility that they should have, which is invaluable to us if there's a future scare that might turn out to be a killer on a large scale."

 

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The trial of Elizabeth Holmes has been pushed back due to the pandemic

 

Elizabeth Holmes is accused of federal wire fraud charges.

 

"The criminal trial of Elizabeth Holmes, founder of the failed blood-testing company Theranos, has been delayed due to the coronavirus pandemic.

Initially set to begin on July 28, the trial will now start on October 27, said Judge Edward Davila of the US District Court for the Northern District of California.

Davila, who presides over the case, announced the change during a status conference held by telephone Wednesday.

Holmes is charged with two counts of conspiracy to commit wire fraud and nine counts of wire fraud and faces up to 20 years in prison."

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she will get very very depressed !

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Institute of Virology: Man-made coronavirus beyond human intelligence

 

The Wuhan Institute of Virology of the Chinese Academy of Sciences is working on an inactivated vaccine for COVID-19. It houses the Wuhan National Biosafety Laboratory. As China's first level-four biosafety lab, it has been the focus of suspicion and conspiracy theories since the outbreak began in the city. CGTN's reporter talked to the director of the lab about its work.

 

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Eisenhower's Less Famous Warning: Government-Controlled Science

 

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From Dr. Strangelove. Credit: Columbia Pictures

 

A few times per year we have a meeting of the Trustees of the American Council on Science and Health, to discuss issues like finances (1), to discuss nominees for our Board of Scientific Advisors, and our general direction.

 

Among our Trustees is Fred Smith, the founder of Competitive Enterprise Institute (CEI), which promotes the benefits of free markets. I certainly agree with them on that (2). At our November meeting Fred asked for a spot on the agenda to talk about how we can better talk about science policy without getting into politics.

 

That is obviously tricky. Science is both corporate and political, when it comes to basic research the private sector and government fund about half each, so if you defend science you are implicitly defending corporations and engaging in politics. 

 

It wasn't always that way. Ernest Lawrence, whose name is now on both Lawrence Berkeley National Lab and Lawrence Livermore National Lab, ushered in the era of academic Big Science. He found that if you did what government wanted, they would throw money at you. And then you could use some of that money to do what you wanted. It really caught on after the Manhattan Project, which was the ultimate use of government guiding academic research to create applied science. People whose entire labs were funded with less than $20,000 per year saw Lawrence getting hundreds of thousands, and then millions, from Uncle Sam and the race was on: Government was firmly in the science business and academics wanted to be in business with politicians. (3) 

 

Not everyone was pleased by that. Most famous of the concerned about this new control of basic research by the government was President Dwight David Eisenhower - "Ike." Ike was someone so concerned about keeping politics out of strategic resources he refused to vote while he was a military officer. To him, it was a conflict of interest because he was paid by the government. His concern only grew while he was president during the bulk of the 1950s and government took more and more control of science funding. As politicians funded more of it, he believed, academia was going to self-select for those who also believed in big government and it would no longer be non-partisan. And corporations were going to control academic science by controlling politicians. Academics who "play the game" were going to get more funding and head up grant committees and panels. (4)

 

The concern about the growing "military-industrial complex" from Ike's 1961 farewell address - most alarming because he was a career military man who won War World II in Europe before he became President partly thanks to the military-industrial complex - became part of the cultural lexicon. But less well known is his second warning, about manipulation of academia by political interests, which Fred discussed in 2011 and passed around at our meeting.

 

President Eisenhower surrounded himself with brilliant academics, he knew that science ended World War II without costing another million American lives, but by 1961 he also knew "we must also be alert to the equal and opposite danger that public policy could itself become the captive of a scientific-technological elite.”

 

He worried about that government control over funding would change the nature of the “free university, historically the fountainhead of free ideas and scientific discovery.” And it has. If you want to find happiness in academia, find a humanities professor at a small college. If you want to find pressure, go to a biology lab at Johns Hopkins, which needs $300 million a year from the NIH if it's going to put up new buildings and recruit key names who can then raise more money from NIH.

 

Ike was right about culture as well. A decade after his speech, academia was still politically balanced and conservatives had the most trust in academic science, but by the 1980s they had begun to self-select for people who liked government funding. They even began to suggest that corporate science - the companies who put men on the moon and develop the vaccines and antibiotics and the GMO insulin that have saved hundreds of millions of lives - meant less independence. Academia meant freedom.

 

And then it became that to be an academic you had to be a liberal because liberals are just smarter. (5) That lurch into partisan politics has had repercussions. It's reality that when people know you are partisan, they trust your objectivity less even if you are on their side. Today, only liberals retain historical high levels of trust in the impartial nature of academic science. Conservatives, libertarians, and progressives do not. And so even the people on the political side of academics don't trust them on food, energy, medicine and chemicals any more than they trust corporate scientists or the government.

 

As a result of seeing science subtly manipulated by government and trust among the public declining, that tide is turning again. A new generation of science academics, who are starting on their third post-doc position and questioning the Old Guard's claims that corporate funding is wrong and only government is right, are critical of the claim that you can't be a scientist unless you are a liberal. And that corporate funding is bad. They realize that taxes are finite and that billions of dollars in federal government marketing about STEM careers in academia have led to a glut in Ph.D. supply, there are academic jobs for just 16 percent of graduating scientists. They have become pawns for scientific-technological elites with little chance of getting a seat at the table, just as President Eisenhower warned.

 

Given that milieu, how can we discuss policy without getting into partisan politics? It isn't easy. Virtually 100 percent of health and two-thirds of science policy are dictated by politicians. And it shows. For example, Syngenta makes an herbicide known as atrazine and when the Obama administration came into office, they convened two separate assessments on it to see if it was an endocrine disruptor in frogs. That was not based on science concern, the EPA during the Bush administration had already checked that claim in 2002 and debunked it.

 

Yet EPA was again forced to revisit the same product twice in just President Obama's first term, which certainly smacked of politicization of science. In early 2016, our CDC began promoting a condition termed "prediabetes", which other countries claim is ridiculous, especially at the arbitrary blood sugar level our government chose. The CDC also declared that nicotine replacement won't stop smoking - unless it's in a patch or gum sold by pharmaceutical giants - and that the opioid epidemic was caused by the medical community and pain patients rather than recreational users.

 

EPA declared that small micron particulate matter was causing acute deaths even though there were none, not even during the entire history of EPA. US Fish and Wildlife Service told a landowner in Louisiana to tear down their forest and build a new one for a frog they declared endangered - in Mississippi. We have to talk about those bad policy decisions if we are going to honor our mandate to be trusted guides for the American public on complex science and health issues.

 

Government-controlled science may be here to stay but that doesn't mean we have to accept rule by a scientific-technological elite that thrives on social authoritarianism. Standing in its way are 300 members of the American Council on Science and Health Board of Scientific Advisors, and a scientist or doctor who wants to put politics first is not participating in our work exposing merchants of doubt who manufacture fears about trace chemicals, food, energy, and medicine. 

So you can trust them, and going into our 40th year of separating health scares from health threats, you can be certain we'll continue to earn your trust as well.

 

(1) Never good - environmentalism is 1000X more lucrative because people send money when they are petrified, but 'your food is safe' is a terrible call to action.

 

(2) I was in the nascent physics software business when Japan was heavily subsidizing the semiconductor industry. Academics insisted our government needed to also subsidize it or we would "lose leadership" to Japan. I argued that the moment government got involved, RAM was going to cost $1 a MB because historically that was true. In that same vein, delivering a brutal hit against the government mentality at the National Institutes of Health, Samuel Broder, former Director of the National Cancer Institute, once said, "If it was up to the NIH to cure polio through a centrally directed program instead of independent investigator driven discovery, you'd have the best iron lung in the world, but not a polio vaccine." 

 

It has gotten no better today. We are funding a ridiculous "cancer moonshot" without using what made the Apollo program successful - corporations who competed to create the lowest price. The federal government had little to do with it. If you look at the spec for the original Mercury program from the government, it was laughable. Companies made it happen.

 

(3) And the private sector happily gave way where they could. Why fund expensive basic research, where only 1 in 1,000 things may work out, and put your shareholders at risk when you can get hundreds of millions of taxpayers to do it? Bonus: academics will believe they are more independent if we get government to approve the grant lobbyists said should be the direction of science funding.

 

(4) He seems to have been right. Look at the outrage when EPA declared that EPA-funded scholars could not be on panels determining EPA policy. Outraged academics did not see it as mitigating an obvious conflict of interest, they ridiculed that EPA did not even want research it funded. Do these same academics also insist corporate scientists be on government committees approving their drugs and chemicals? 

 

(5) At SUNY-Albany Ron McClamrock summed up the common belief, which reached its apex in the mid-2000s. "We outnumber them because academic institutions select for smart people who think their views through; and if you're smart, open-minded, and look into it carefully, you're just more likely to end up with views in the left half of contemporary America. Which is just to say: Lefties are overrepresented in academia because on average, we're just f-ing smarter." 

 

That sentiment is now considered laughable because "lefties" deny the science behind medicine, food, energy and chemicals so reliably you can predict someone's voting habits based on if they buy organic food, supplements, think fracking will cause the earth to deflate, and that BPA is an endocrine disruptor.

 

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again not just a us problem , we all have the same more or less ...

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France says no evidence Covid-19 linked to Wuhan research lab set up with French help

 

 

France on Friday said there was no factual evidence so far of a link between the Covid-19 outbreak and the work of the P4 research laboratory in the Chinese city of Wuhan, which France helped set up and where the current pandemic started.

 

"We would like to make it clear that there is to this day no factual evidence corroborating recent reports in the US press linking the origins of Covid-19 and the work of the P4 laboratory of Wuhan, China," an official at President Emmanuel Macron's office said.

 

The broad scientific consensus holds that SARS-CoV-2, the official name of the coronavirus, originated in bats.

 

In 2004, France signed an agreement with China to establish a research lab on infectious diseases of biosafety level 4, the highest level, in Wuhan, according to a French decree signed by then-foreign minister Michel Barnier.

 

US trying to determine if virus originated in lab

 

US President Donald Trump said on Wednesday his government was trying to determine whether the coronavirus emanated from a lab in Wuhan, and Secretary of State Mike Pompeo said Beijing "needs to come clean" on what they know.

 

General Mark Milley, chairman of the US Joint Chiefs of Staff, said on Tuesday that US intelligence indicates that the coronavirus likely occurred naturally, as opposed to being created in a laboratory in China, but there is no certainty either way.

 

The Washington Post said this week that national security officials in the Trump administration have long suspected research facilities in Wuhan to be the source of the novel coronavirus outbreak.

 

As far back as February, the Chinese state-backed Wuhan Institute of Virology dismissed rumours that the virus may have been artificially synthesised at one of its laboratories or perhaps escaped from such a facility.

 

The allegations came amid mounting international criticism of China’s initial cover-up of the virus and suspicions that Beijing had not revealed the extent of the public health crisis due to economic concerns.

 

China on Friday revised its pandemic toll again, this time by a major 50 percent increase in the total death toll. But Chinese authorities denied it was due to a cover-up, maintaining the revision was due to insufficient capacity during the peak of the pandemic.

 

The lab at the heart of the controversy

 

The Wuhan research laboratory at the heart of the controversy is home to the China Centre for Virus Culture Collection, the largest virus bank in Asia which, preserves more than 1,500 strains, according to its website.

 

The complex contains Asia's first maximum security lab equipped to handle Class 4 pathogens (P4) -- dangerous viruses that pose a high risk of person-to-person transmission, such as Ebola.

 

The 300 million yuan ($42 million) lab was completed in 2015, and finally opened in 2018, with the founder of a French bio-industrial firm, Alain Merieux, acting as a consultant in its construction. The institute also has a P3 laboratory that has been in operation since 2012.

 

The 3,000-square-metre P4 lab, located in a square building with a cylindrical annex, lies near a pond at the foot of a forested hill in Wuhan's remote outskirts.

 

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Let the blame games begin: Missouri sues China, including WUHAN LAB, over coronavirus outbreak

 

 

The state of Missouri has sued China - plus its Communist Party and a handful of other entities - for “causing a global pandemic that was unnecessary and preventable.” It’s the first state to take the dubious accusation to court.

 

Missouri Attorney General Eric Schmitt filed suit on Tuesday against the entire nation of China, its national, provincial and city governments, and a smattering of government agencies and research institutes, blaming the lot for allowing the coronavirus epidemic to go global. Laying the sum total of suffering that has resulted from the epidemic at China’s feet might sound like an overly ambitious gambit for little old Missouri, but the lawsuit reads less like a legal document and more like a manifesto.

 

 

“Defendants are responsible for the enormous death, suffering, and economic losses they inflicted on the world, including Missourians, and they should be held accountable,” Schmitt declares in the 47-page complaint. The specific parties being sued are the People’s Republic of China; the Chinese Communist Party; the local governments of Hubei Province and Wuhan; China’s National Health Commission, Ministry of Emergency Management, and Ministry of Civil Affairs; the Wuhan Institute of Virology; and the Chinese Academy of Sciences.

 

The lawsuit alleges that “during the critical weeks of the initial outbreak,” Chinese authorities kept it quiet by arresting whistleblowers, destroying research, “refusing cooperation with the global community,” and lying about person-to-person transmission - supposedly handicapping the global response. It’s a narrative that Americans have heard repeatedly from the Trump administration and western media - including the dozens of articles from US outlets that Schmitt cites to make his case.

 

“Literally every Missourian” was harmed physically and economically by China’s alleged actions and inactions, Schmitt claims, insisting this gives him grounds to sue - along with some legal gymnastics suggesting that China’s alleged “hoarding” of personal protective equipment constitutes international commerce. A group of Republican senators introduced a bill last week that would make it even easier to bleed China over coronavirus damages, potentially opening up a pressure release valve for Americans upset about being laid off and looking for someone to blame. 

 

 

While Schmitt is far from the first lawyer to salivate at the thought of extracting billions of dollars in restitution payments from China, any attempt to blame the country’s government for the epidemic is likely to boomerang. Multiple reports (and a few insider stock trades) indicate Washington was aware of the looming epidemic for months before taking action to protect the American people, and all the unfounded rumors about lab accidents in the world won’t protect the Trump administration or Congress if those facts come out.

 

 

Proving China forced local US governments’ hands in shutting down their economies and putting over 22 million Americans out of work is next to impossible, as is laying the blame for thousands of sick Missourians at the feet of a foreign government and not the local government whose policies kept quality healthcare out of the financial reach of millions. While the Missouri lawsuit attempts to draw a direct causal line between the actions of the Chinese government and the infringement on Missourians’ “common rights,” it’s just as likely that a court will see the actions of the state government that enacted the unprecedented shutdown as infringing on those rights.

 

Schmitt might think twice about opening that particular can of worms lest a wave of class-action lawsuits result - his is the first state to sue the Chinese for the coronavirus, but it likely won’t be the last.

 

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Coronavirus: behind the Chinese laboratory theory

The World Health Organization (WHO) has denied a growing number of allegations that the new coronavirus originated in a Chinese laboratory.

 

 

WHO spokesperson Fadela Chaib said that “it is probable, likely, that the virus is of animal origin”. The comment followed Donald Trump’s confirmation that his administration is investigating whether the new virus originated in a lab in the Chinese city of Wuhan.

 

Speculation that the new coronavirus, which causes Covid-19, may have escaped from the Wuhan Institute of Virology (WIV) has circulated “among right-wing bloggers and conservative media pundits”, says USA Today.

 

So is it fact or fiction?

 

According to Deutsche Welle, the theory “began making the rounds on social media sites as early as January”.

 

DW adds that the first posts suggesting that the virus came from the Wuhan lab originated “in connection to conspiracy theories referencing secret Chinese military labs developing bioweapons”. 

 

While there is no evidence for the link to bioweapons, the BBC reports that US State Department cables leaked to The Washington Post columnist Josh Rogin do show that US officials were in fact worried about biosecurity at a virus lab in Wuhan, China.

 

Rogin reports that in 2018 US science diplomats were sent on repeated visits to WIV, which had in 2015 become China’s first laboratory to achieve the highest level of international bioresearch safety.

 

One of the State Department cables reportedly said: “During interactions with scientists at the WIV laboratory, they noted the new lab has a serious shortage of appropriately trained technicians and investigators needed to safely operate this high-containment laboratory.”

 

Rogin says that the officials then sent two warnings to Washington about inadequate safety at the lab.

 

Chinese researchers at WIV were receiving financial assistance from the Galveston National Laboratory at the University of Texas Medical Branch and other US organisations, but the Chinese had requested additional help. “The cables argued that the United States should give the Wuhan lab further support, mainly because its research on bat coronaviruses was important but also dangerous,” Rogin says.

 

He concludes that “there is no evidence that the virus now plaguing the world was engineered” and that “scientists largely agree it came from animals”.

 

However, Xiao Qiang, a research scientist at the School of Information at the University of California at Berkeley, suggests this does not mean it definitely did not come from the lab, which had spent years testing bat coronaviruses in animals.

 

“The cable tells us that there have long been concerns about the possibility of the threat to public health that came from this lab’s research, if it was not being adequately conducted and protected,” he said.

 

Lack of evidence

 

According to Rogin, many national security officials inside the Trump administration have “long suspected either the WIV or the Wuhan Center for Disease Control and Prevention lab” was the behind the outbreak of the new coronavirus. But, the paper adds, “the intelligence community has provided no evidence to confirm this”.

 

Despite reports to the contrary by news outlets such as Fox News, the BBC notes that “there is no evidence of any kind that the Sars-CoV-2 virus (which causes Covid-19) was released accidentally from a lab”.

 

And as DW reports, researchers have “brushed off theories that the virus was manmade”, adding that it has characteristics that suggest it is “a naturally occurring virus and not a manmade mutation”. 

 

This assessment was backed up by a team of researchers who published their findings last month in the journal Nature Medicine. “Our analyses clearly show that SARS-CoV-2 is not a laboratory construct or a purposefully manipulated virus,” they concluded.

 

In another article, published in the journal Emerging Microbes & Infections in February, researchers led by Shan-Lu Liu at the Ohio State University found that there was “no credible evidence supporting claims of the laboratory engineering of SARS-CoV-2”.

 

“The virus’s genome has been sequenced, and if it had been altered, we would expect to see signs of inserted gene sequences. But we now know the points that differ from bat viruses are scattered in a fairly random way, just as they would be if the new virus had evolved naturally,” explains New Scientist.

 

DW also points to “the fact that the lab’s work is not secret” and that WIV published its findings in professional journals as evidence that the virus is unlikely to have been created by its researchers.

 

Shi Zhengli, the head of the WIV research project, has denied that the lab was the origin for the new coronavirus. In February this year, it was Zhengli and her team who first publicly reported that the virus was a bat-derived coronavirus.

 

However, Xiao tells Rogin that he does not think it is a “conspiracy theory” to ask questions about the research being carried out at the WIV lab.

“I think it’s a legitimate question that needs to be investigated and answered,” he said. “To understand exactly how this originated is critical knowledge for preventing this from happening in the future.”

 

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"Chinese companies and Chinese money are lining up for what they expect to be a fire sale of British businesses...Germany recently enacted protections against foreign takeovers of their companies during the COVID-19 crisis"

 

https://www.thenewamerican.com/world-news/europe/item/35401-nigel-farage-china-using-coronavirus-crisis-to-buy-up-british-companies

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