U.S. government gave $3.7 million grant to Wuhan lab at cent

Re: U.S. government gave $3.7 million grant to Wuhan lab at

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Dr. Michael Osterholm on Covid-19
May 2, 2020

Steve Skrovan: It's the Ralph Nader Radio Hour.

Steve Skrovan: Welcome to the Ralph Nader Radio Hour. My name is Steve Skrovan, along with my co-host, David Feldman. Hello there, David.

David Feldman: Hello there, Steve.

Steve Skrovan: And the man of the hour, Ralph Nader. Hello, Ralph.

Ralph Nader: Hello. Please listen carefully to this one, listeners.

Steve Skrovan: That's right. This week, some states have ended their lockdowns and some are easing restrictions. President Trump has suggested that some schools could reopen before the end of this school year. Just this week, he also said that COVID-19 will not return after this, or if it does, it will be small and contained. This is not what the experts are saying, and it should be disregarded, just like his suggestion last week that ingesting disinfectants might kill the virus. To be clear, do not ever drink bleach. First up, we welcome Dr. Michael Osterholm, one of the foremost experts in infectious diseases. He wrote a book in 2017 called Deadliest Enemy: Our War Against Killer Germs, in which he predicted a global pandemic. We first spoke with Dr. Osterholm more than two years ago after he wrote what is turning out to be a scarily prescient op ed for the New York Times entitled “We're Not Ready for a Flu Pandemic”. That warning was ignored by the Trump administration and Congress, and everything Dr. Osterholm wrote in January of 2018, 100 years after the so-called Spanish Flu Pandemic, and two years before COVID-19, has unfortunately come true.

Now, he predicts that the second peak of COVID-19 will be bigger than the first. We'll hear about what he means by that and how he thinks the country can reopen by "threading the rope through the needle", as he calls it, which means finding a balance between resuming some parts of life and keeping people safe.

That's the first part of the show. The second part of the show, we're going to talk about schools, because the future of schools is uncertain. Schools have switched to online learning with no end in sight. The inequalities already present in our education system have become even more apparent. 17% of students in the United States don't have a computer at home. These differences put low-income students at a disadvantage compared to their wealthier peers.

Our second guest, Naila Bolus, is the president and CEO of Jumpstart. Jumpstart is a national early-education organization that provides language, literacy, and social- emotional programming for preschoolers from underserved communities, and she's here to talk about educational inequality and Jumpstart's role in addressing it. As always, somewhere in between, we'll take a short break and check in with our corporate crime reporter, Russell Mokhiber, and if we have some time left over, we'll try to answer some listener questions. First, let's start by talking about what our new normal in the age of COVID might look like. David?

David Feldman: Dr. Michael Osterholm is a professor and director of the Center for Infectious Disease Research and Policy at the University of Minnesota. He is the author of the 2017 book, Deadliest Enemy: Our War Against Killer Germs. From 2018 through May of 2019, Dr. Osterholm served as a science envoy for health security on behalf of the U.S. Department of State. Welcome back to the Ralph Nader Radio Hour, Dr. Michael Osterholm.

Dr. Michael Osterholm: Thank you. It's great to be with you. I appreciate it. Ralph Nader: Mike, I'm going to ask you a question that a lot of people who have been asking you questions probably haven't. You've been very prophetic in warning the country year after year after year about the probability of these epidemics and pandemics coming from various places of the world quite apart from in this country. What would you suggest that this country should have done--let's go back, in its relations with China, its collaboration with specialists, epidemiologists, its treaties with countries--in order to have prevented this, detected it early, in this case, China, and prevented it? What kind of system should our country have put in place years ago, and what kind of resources should have been allocated. Because, this is going to happen again and again. This is not the last virus that's going to come from somewhere else.

Dr. Michael Osterholm: That's absolutely correct, and I think the best way for me to summarize this is in the book, Deadliest Enemies, that I wrote in 2017 [where] I laid out a battle plan, actually, for what we need to do, and it's extensive. But, the bottom line is that we can't prevent many of these infectious diseases from entering into the human race. It's going to happen. What we can do, though, however to stop them quickly, or at least more quickly than we have, and when we do stop them, we can then, also, for those individuals who will be at future risk, prevent that from happening again. What I mean by that is, for example, the tools we have; when we look at what we invest in military defense, what we invest in public health pales in comparison. Vaccine development, the idea that we knew that coronaviruses were going to be a problem again. In my 2017 book, the chapter on coronaviruses was entitled “SARS and MERS, a harbinger of things to come”. If we'd had creative imagination and said we need to invest heavily in platforms for the types of vaccines that could be used against coronaviruses, we would have been much further along in this situation.

We need to have a much more capable system for responding for testing so that we could pick up, very early, this virus and how can we elevate, quickly, the testing capability that we need to have, rather than almost piecemeal on a global basis. How do we communicate information? We do have a challenge today where countries, governments don't want bad news out, because it'll adversely impact them. What can we do to incentivize actually getting information out quickly? Stopping news is not just about being a good citizen, but you won't be punished financially.

There's a number of things I think that we can do for these acute big events. On the other hand, we have ones, and Ralph, you and I have talked about this before about antibiotic resistance, the idea that we're losing the gift that we've had for the last century of antibiotics because, as we use them, the bacteria, the viruses even, and the parasites mutate in a way that the antibiotic no longer kills them the way it once did. We're investing very little in that, yet we are very quickly sliding back into, almost, what I call a post-antibiotic era, much like the pre-antibiotic era.

I think part of it is the lack of creative imagination. People with the book that I wrote in 2017 would tell you I was a scare-mongerer, that I basically just did that as a horror movie. Now, hopefully, this event will be a wake-up call for modern public health, modern medicine, and modern world affairs to say, No, this is important, in many ways, as defense itself as we think about it from a military standpoint. The investments have to increase and we have to be able to have the tools that we need to respond quickly. Imagine if we were fighting a war today and we had Civil War muskets. Unfortunately, far too often, that's what we have in public health today.

Ralph Nader: Let's take what you just recommended to a level of international treaties. We have arms control treaties in the nuclear area; we have economic treaties, like the World Trade Organization. We even have some environmental treaties. Don't you think that we need to develop an international cooperative treaty system where we can provide adequate funds for what you're saying, the various nations? We can have interchange of epidemiologists. For example, more FDA inspectors in China. What would you favor here? Because, I think if we have different policy recommendations, the mechanism has to be some sort of international regime, international treaty in order to put all these parts in place, and so it isn't just a desperate catch-up when the outbreak occurs. Have you given any proposal to that, anybody in the public health area taken it to that level? Because, that's what usually gets more budgets, you see.

Dr. Michael Osterholm: You raise a very important point, and we do have the public health laws, in a sense, as through the World Health Organization, and how we are, as a world, supposed to act. A challenge we have is whether it's a treaty, or it's laws, or whatever, people can violate them if there are disincentives for them to comply. I think the challenge we have today is that we don't want to see a country penalized for discovering, uncovering, and disclosing a challenge that says, this could be everywhere around the world tomorrow. And that has been a major incentive for countries not to quickly identify something. The fact that the kitchen's on fire; I don't want the neighbors to know I have smoke in my house, so I'll just wait until the whole house is now on fire. I think that that is the issue. I'm not sure, as much, and I surely wouldn't minimize the treaty issue or that, but I think it's how do we, basically, protect countries who disclose, quickly, these problems, and allow for world resources to come in and help? I think it's a combination of all that.

Ralph Nader: Let's look at the World Health Organization [WHO]. I don't think many people realize how small its budget is compared to its responsibilities all over the world. It has a budget of about 4 to 5 billion dollars, which is basically what two large hospitals get in revenue in this country. And they have a focus, for example, on terrible epidemics in Africa. The Ebola epidemic was one; there was more than one. Then, there was a variant on a cholera epidemic that was even more lethal, and they actually worked with local efforts to head those off. But now they don't seem to be given the kind of resources, much less the authority that's needed. What's your view [on] Donald Trump has attacking the WHO, after he pushed for a cut in the U.S. contribution to the WHO? It does seem that you have The CDC has a budget, until recently, of $7 billion, and the WHO has this budget, 4 to 6 billion, and the Pentagon budget is $2 billion a day throughout the year. What kind of resources, and we want to focus on Congress getting back to work here because the money has to come from congressional appropriations. Before we get into the details of the present pandemic, what kind of overview would you have on this to head it off? Isn't it true that if China owned up to it publicly and, immediately, international cooperation kicked in, we probably would only have a fraction of this pandemic. Is that accurate?

Dr. Michael Osterholm: I'm not sure. I think that once a virus like this emerges, it's like a bullet being fired from the gun. Once the trigger has been pulled and executed, it's hard to stop it. At the same time, what we could have done is picked it up much quicker, and we could have had a much more comprehensive response. Even if we couldn't control it out of China, meaning it was eventually going to leak out, somehow, somewhere, our international opportunity to get vaccines out quickly and to protect people would have been substantially different if we'd had the tools you talked about. I think in your opening to this question, you made the case, as well as any person could, about the resource issue and how little we invest in this area and what we could do. Let me also say I have my challenges with the WHO. Our group came out and said on January 20th that this was going to be a coronavirus pandemic, and WHO didn't come out for weeks later to say that. While I have those challenges, I actually believe WHO is essential; it's critical. We need to have a strong international presence where when these events like this happen; we need to go back and reconstruct what happened, what could have been done better, and how does WHO need to change to be a modern international public health agency in the world. We need their air traffic control. If you look, the United States supplies a great deal of expertise to the WHO, as do other countries from around the world. You need to have that place where it's like an INTERPOL, almost, for infectious diseases where all this expertise can come together. I think it's a very short-sighted mistake to pull out of the WHO financially. I think it would be a real public health disaster if WHO was not strengthened as opposed to being weakened, and I think that there's just a lot more that we could do with the tool. I don't want to make this sound like it's a boondoggle, because everybody, at a time of a crisis, want to step up and get resources. I think, in this case, this is illustrating all the holes that we do have in the current system and what we could do to fix them, and this needs to be an international priority as we deal with this pandemic.

Ralph Nader: When we don't have this priority, trillions of dollars of economic activity crash in the United States, so it's easy to do a cost benefit analysis here. People who observe the WHO know that it is wary of offending foreign governments because it has to have entry. That's where it's wary, for example, of criticizing early China's belated publicity on what happened in Wuhan province. Do you believe that they have controlled it the way they have? If they had, it's quite an epidemiological success. The latest report is there is only one hospitalization for the Coronavirus in Wuhan city of 11 million. Do you believe that they have controlled it to that extent?

Dr. Michael Osterholm: I think they've done a remarkable job of driving this virus down, but they've not eliminated it. I would have to say that one of the things I'm concerned about right now is that we have full transparency with China. I will tell you right now, I think it's a problem. They have done through what, for lack of better term, we call the most draconian population limitation efforts any modern government has ever done for public health reasons. People were literally in their homes in the Wuhan area for weeks and weeks and weeks without being able to leave. They have facial recognition everywhere so they can track you, and if you turn up positive, they know every step you took in many locations in China. At the same time, we also, as you pointed, have very little activity recognizing the Wuhan area, but we see it in the other provinces right now, and we cannot understand how they can report 100 "asymptomatic infections" every day and then only one or two clinical cases. That makes no sense whatsoever. I think there is more going on there, but more importantly, when this virus decides to do what it's going to do, humans can only have some impact on that. Remember in 1918, and this is just an example, we had spring waves that adversely affected Chicago and New York in a big way, lots of illnesses and doubts. Hardly impacted Boston, Philadelphia, Baltimore, Washington D.C., or even here in the Midwest, Detroit and Minneapolis, very little activity; then it disappeared. Where did it go? It didn't go away because of human activity. It went away because whatever it does, it does, and then it came back with a vengeance in the fall of 1918, and we don't know where it was, why it came back and did what it did, and then communities that had no activity in the spring suddenly, were in very dire trouble in the fall. Even now, in China, I don't know how much of this is due to what the Chinese did and how much of it is due to what Mother Nature herself is doing. It also means if it goes away, it surely can come back, and we talked about this before. Until we get 60 to 70 percent of U.S. population infected and develop some sense of immunity, or we get a vaccine that accomplishes that same kind of herd immunity protection, this is like gravity; it's going to keep happening. We're going to see virus transmission, whether it's in China. Look at Singapore, another example of a country that was touted as having the ideal kind of control measures; now they're in a national state of emergency because of transmission. I think it's too early to say that they have successfully handled it in China, but what they did do to reduce Wuhan clearly was a remarkable effort that I'm not sure could be done in many countries of the world.

Ralph Nader: Let's talk about vaccine. There's a report in the New York Times that Oxford University is ahead of the pack in trying to develop a vaccine, and they may be ready in early fall, which is about a year earlier than predictions. Tell us about the probability of a vaccine working and safe. And also are there intermediate remedies short of a vaccine that can diminish the severity of this virus that patients are afflicted?

Dr. Michael Osterholm: Obviously, vaccine is the Holy Grail. That's what we need and want. That would be ideal, but what do we want in that vaccine? We want it to be effective, and by effective we mean it surely keeps us from getting infected and also it protects us for a long period of time. And we want it to be safe. The challenge we have right now with these vaccines is that, with coronaviruses in general, we've not had good luck in finding vaccines that induce long-term immunity. And this is just from our work with MERS and SARS, and other coronavirus infections like that. So while we surely may be able to induce short-term immunity, which I think is obvious from clinical disease, you recover. Also, there's several studies using macaque monkeys where animals were challenged with the virus, then allowed to recover, and then challenged again, and they were protected, meaning the previous infection of the macaques protected them. There's one study, in fact, using a vaccine that was administered from Oxford here in the study in the United States in monkeys that suggested, again, it provided an immunity shortly after the vaccination took place. The problem is we don't know how long this lasts, and we don't know how good it is. There's this one like influenza where, while it's a different mechanism, you'd have to get vaccinated every year for this kind of situation. We just don't know; so that's the number one thing. I think we can find a vaccine that will give us short-term protection. The challenge will be long term. The second thing is safety, and I do think we have some challenges here yet in the work that was done with SARS. There was a condition called antibody- dependent enhancement. ADE is a situation where if you make a little bit of antibody from the vaccine, it's not enough to be protective. When you do get infected, the virus and the antibody interact in such ways, it causes the cascade in your immune system that goes out of control and actually is very damaging to the human to the point of actually killing them. This is what we had happen with the dengue vaccine several years ago in the Philippines where it was withdrawn from the market because people who had been vaccinated started developing this ADE position. We're going to have to study this. We need to know this, but we don't have an option here to study it for years and years and years. We're on virus time right now, and what we need to have has been what we have in the next 16 to 18 months. I think, from that standpoint, we'll probably not have all the data we want for safety. We will have data on short-term protection. We won't have data on long-term protection, and we'll put those vaccines into play, I think, if possible, and I think the Oxford one is surely one of the candidates. I still don't believe that it'll happen though, however, anytime soon, meaning that we're still 16 months earliest before we could get vaccine out there, 18 months maybe where you have it studied, you have it approved, you have it manufactured, you have it distributed, and you have it going into people. I think we're a ways from that yet.

Ralph Nader: What about intermediate treatments, short of vaccines? Anything there?

Dr. Michael Osterholm: Actually, there was news breaking today about one of the Gilead drugs, Remdesivir, which was one that has been touted. The NIH has some data today that they'll be releasing later suggesting that there were some benefits from it. On the other hand, another study from China today which was just released said there were none. So, we'll have to wait and see. This is one of the challenges of dealing with a disease like this is that everybody wants the answers right now, and while we're doing a great deal to get them, I must say, this has been an incredible experience in terms of the number of clinical trials that were set up very quickly in a comprehensive manner. And so I'm optimistic we're going to get answers soon. But, again, as I said a moment ago, we're in virus time, not human time, and that makes it really tough to get this work done to have a meaningful impact. If we have a big wave of disease coming in this fall, what we don't have available at that point is what our tools are going to be.

Ralph Nader: You've written quite a bit in the Washington Post, New York Times about testing, and you're quite skeptical in a very meticulous way about the accuracy of these tests, whether they’re serology tests or whether the other more prominent type tests. Could you summarize that for our listeners, because I must say, that provoked a lot of pessimism among people who read it, and they said, "Good heavens, you can't rely on this; there are so many ways that these tests can be inaccurate and misleading, false positives, false negatives." Could you clarify that for our listeners?

Dr. Michael Osterholm: Be happy to. There are actually three aspects to this, and I have an op ed in today's New York Times about this very issue. The first one is we just have a shortage of testing for what we call the PCR test [Polymerase chain reaction]. This is the one that detects the actual virus itself-- finding some of the genetic material in it. Everybody keeps promising all this testing. We hear this almost daily at the news briefings that occur. The challenge has been that we need reagents, chemicals that run the test. That's really important, and if we don't have those, you can't run the test. It's like a car without gasoline. The chemical that we take the swab and put it in, basically, to take the virus out of the swab to open it up, grab the RNA material for the virus if it's there, and then present that to the next level of the catalyst. If you don't have that chemical, you can't do anything. It's a car without gas. What happened was, in December, when Wuhan emerged, clearly, testing went up substantially in China, and the world's resources for these reagents, the manufacturing capacity and supply chains handled it with some difficulty, but they handled it. Once the whole world caught on fire with COVID, everybody wanted the test. Billions of people needed testing done, and we just overran our headlights with regards to reagent capability. What we've needed is, really, a national/international effort, almost a Marshall Plan to figure out how we're going to, with the private sector and public sectors coming together, actually make these reagents in a timely way. What can we do? That hasn't happened yet. What we kind of have happening right now is, again, everybody's out there trying to get the reagents for themselves and there are not nearly enough. So, that's a test that we need to have. We should be testing every person who is clinically ill that may have COVID infection every day on that day. That would help us tremendously. The second problem we have is the FDA in reacting to CDC's failure to get a test on the market that we needed and the outcry that occurred because of that decided, well, one of the ways to respond is we'll just open up the floodgates of anybody and everybody who can test, let's let them test. And there was no major oversight for these tests. It was more for the real-time PCR test, but not nearly enough, and on top of it, for the antibody test, all you had to was basically sign a sheet that says, "I can do this with this test," and with no evidence of how effective they were in terms of how they perform. And so these serology tests, in particular, the antibody tests, are now being used out there, and they're horrible. As described by a senior FDA official themselves last week, "They're crap." This has to change. FDA has to agree to assume its responsible position of, really, oversight, of making sure that any test that's on the market works and that people who are going to use it in the clinical labs, and the healthcare settings know how well it works. The last piece is just when you use a screening test, and this is true for any condition, not just COVID infection that is occurring in a low, low level, the test will give you a number of false positives, meaning that, right now, we estimate that, at best, 5 to 15 percent of the U.S. population has been previously infected with this virus, higher in the New York City Metropolitan Area. In many parts of the country, it's still 5%. If you run an antibody test today, which has a very high level of sensitivity and specificity, meaning that you can pick up true positives and you can pick up true negatives, and that's good; you still have as many people testing positive for this antibody that are not as you do actual people who test positive who are. If I tell you, you're positive, but you have one of two chance it's not real.

Ralph Nader: Given the exponential growth of this virus, people ask me, "Is it true that if what we did in March, lockdown, social distance, etcetera, we did in late January, it would have prevented 90% of the cases?" Is there any truth to that?

Dr. Michael Osterholm: No, I don't think so. We surely can slow it down. Our goal, as a public health community, should be to minimize severe disease and death, first and foremost. Second, just prevent infections, period. We know that there are certain people that are higher risks that are having adverse outcomes, generally speaking, older, underlying health conditions, etcetera. We should be trying to keep them protected. Once this virus is out, it's going to spread. It's a respiratory-transmitted virus that basically transmits through aerosols, these very fine particles that you and I put out just talking. If you were here right now in this room that I've been in talking to you for the last X minutes, you'd see my little aerosols floating all around. Best way to remember what an aerosol looks like, when you think about seeing sunlight come through the window in your house and you see this stuff floating in the light, you think, "Oh, my house is dusty," those are aerosols, and just talking produces them. One of the challenges is this is going to transmit, but we could do a lot more to hold it back by the kind of testing, contact tracing, follow-up that we could have done that we didn't do. And this is where I think some countries surely have done a good job, or a better job, at least. The challenge they have, even if we have a big wave of infection, like say in 1918, it's not clear how much we can really do, except be prepared for its impact. It's like an F5 hurricane. You can't miss it. It's going to be there, but you can do a lot to make your community more resilient when it happens and have prepared it beforehand so that the destruction is limited.

Ralph Nader: Some practical advice. Let's say a family in apartment, family of four or five were in the house and one person comes down with it. What exactly should they do? What equipment should they have? And talk about [pulse] oximeters and face masks. What should that family do to protect the rest of them? Because, in China, they took these people and sent them to like warehouses, and they immediately segregated them. They pulled them right out of their families, the reports say, but what do you recommend that people do and be prepared for?

Dr. Michael Osterholm: Well, first of all, what we have to do is get people tested early to know. If you have any signs and symptoms, be tested, and then isolate yourself from the rest of the family. The problem is, I have to be honest with you and say that may be far too late. We know that you're highly infectious two to three days before you get sick. If you've been with your family for that time period, you probably already exposed them. Then, what you have to do is shelter in place together, meaning that I shouldn't be out in public at all, for sure, and my family members shouldn't be because they, then, may become infected, and you wouldn't pick it up until they became clinically ill. But then they were infectious two days before they got clinically ill. The way to stop this is not just to identify cases and remove them. That's almost too late. That's what makes it such a challenge. It really is about once you have been infected and you've exposed others, they then have to wait out this time period to see if they're going to get clinically ill, and that's how we're going to limit transmission.

Ralph Nader: What about immunity after you get infected and recover?

Dr. Michael Osterholm: At this point, we believe there surely is short-term immunity that occurs. The question is will it be long term, and we don't know that. I think in the short term, I'd be confident that somebody's not going to be reinfected, but I can't say, six months from now, they'll still have that protection.

Ralph Nader: Thank you very much. I know you have a lot of other things on your mind.

Dr. Michael Osterholm: I just appreciate this. Unfortunately, I have. Okay, talk to you later. Thank you.

Ralph Nader: Thank you very much, Mike.

Dr. Michael Osterholm: Have a good one, Ralph. Good bye, guys.

Steve Skrovan: We've been speaking with Dr. Michael Osterholm, who has a weekly podcast, the Osterholm Update, COVID-19. We will link to that at RalphNaderRadioHour.com. Now, we're going to take a short break. When we return, we will talk about what this global pandemic has done to our educational system. First, let's check in with our corporate crime reporter, Russell Mokhiber.
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Re: U.S. government gave $3.7 million grant to Wuhan lab at

Postby admin » Fri May 15, 2020 4:40 am

Coronavirus may never go away, World Health Organization warns
by bbc.com
14 May 2020



There are more than 100 potential vaccines currently in development

The coronavirus "may never go away", the World Health Organization (WHO) has warned.

Speaking at a briefing on Wednesday, WHO emergencies director Dr Mike Ryan warned against trying to predict when the virus would disappear.

He added that even if a vaccine is found, controlling the virus will require a "massive effort".

Almost 300,000 people worldwide are reported to have died with coronavirus, and more than 4.3m cases recorded.

The UN meanwhile warned the pandemic was causing widespread distress and mental ill health - particularly in countries where there's a lack of investment in mental healthcare.

The UN urged governments to make mental health considerations part of their overall response.

What did WHO say?

"It is important to put this on the table: this virus may become just another endemic virus in our communities, and this virus may never go away," Dr Ryan told the virtual press conference from Geneva.

"HIV has not gone away - but we have come to terms with the virus."

Dr Ryan then said he doesn't believe "anyone can predict when this disease will disappear".

There are currently more than 100 potential vaccines in development - but Dr Ryan noted there are other illnesses, such as measles, that still haven't been eliminated despite there being vaccines for them.

WHO Director-General Tedros Adhanom Ghebreyesus stressed it was still possible to control the virus, with effort.

"The trajectory is in our hands, and it's everybody's business, and we should all contribute to stop this pandemic," he said.

WHO epidemiologist Maria van Kerkhove also told the briefing: "We need to get into the mindset that it is going to take some time to come out of this pandemic."

Their stark remarks come as several countries began to gradually ease lockdown measures, and leaders consider the issue of how and when to reopen their economies.

Dr Tedros warned that there was no guaranteed way of easing restrictions without triggering a second wave of infections.

"Many countries would like to get out of the different measures," the WHO boss said. "But our recommendation is still the alert at any country should be at the highest level possible."

Dr Ryan added: "There is some magical thinking going on that lockdowns work perfectly and that unlocking lockdowns will go great. Both are fraught with dangers."
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Re: U.S. government gave $3.7 million grant to Wuhan lab at

Postby admin » Mon May 18, 2020 2:39 am

Trump’s covid-19 inaction killed Americans. Here’s a counter that shows how many.
by Eugene Jarecki



Trump Death Clock
Accessed: 5/17/20: 7:45 p.m. Arizona time
Estimated U.S. COVID-19 Deaths Due To POTUS Inaction
In January 2020, the Trump administration was advised that immediate action was required to stop the spread of COVID-19. According to NIAID Director Dr. Anthony Fauci, “there was a lot of pushback” to this advice. President Trump declined to act until March 16th. Epidemiologists now estimate that, had mitigation measures been implemented one week earlier, 60% of American COVID-19 deaths would have been avoided.

(This editorial first appeared in The Washington Post.)

The National Debt Clock hangs above New York City’s Avenue of the Americas as a persistent reminder of a clear message: The United States is recklessly living beyond its means, and this will have grave future consequences. In the same symbolic spirit, it is time for the establishment of a national “death clock” to measure the cost in human lives of President Trump and his team’s reckless handling of the coronavirus pandemic.

Reports show that as early as January, the president was advised by both his own experts and the intelligence services of the need for urgent mitigation measures against the spread of the virus. Instead, he engaged in petty political feuds and pollyannish predictions minimizing its significance. Finally, on March 16, he reversed his previously dismissive stance and announced “new guidelines for every American to follow.”

But by then it was too late; The United States was already the world leader in its rate of covid-19 infection and has since become home to one-third of the world’s cases and five times as many as any other country.

Trump Death Clock, Times Square NYC

Anthony S. Fauci, the director of the National Institute of Allergy and Infectious Diseases, has stated that, had the guidelines been implemented earlier, a crucial period in the exponential spread of the virus would have been mitigated and American lives saved. Leading epidemiologists have put a finer point on this, estimating that 50 to 80 percent of covid-19 deaths in New York and approximately 90 percent of all American covid-19 deaths can now be attributed to the administration’s delay between March 2 and 16.
This suffering cannot be forgotten.
As of today, tens of thousands of Americans have lost their lives as a consequence of the administration’s failure to act sooner, so it’s no wonder the president excoriates reporters who ask him why he waited so long to implement the guidelines. Trump’s fallback when he is under scrutiny is to deflect, attack, and distract. But will this work when his decisions have led to a loss of American lives? How will the President be held responsible?

It’s all in the branding, that stuff Trump himself does so well when he applies derisive nicknames to his rivals or attaches the name of a foreign power to a global pandemic. Accountability needs a brand, and the National Debt Clock is a helpful precedent. It demonstrates how to plant a symbolic flag in the numbers — one that can’t be knocked over by bluster or misleading campaign videos. This pandemic is ongoing, and the lives already unnecessarily lost demand we seek more responsible crisis leadership. Just as the names of fallen soldiers are etched on memorials to remind us of the cost of war, quantifying the lives lost to the president’s delayed coronavirus response would serve a vital public function.

Trump Death Clock, Times Square NYC

Trump’s career is built on finding shortcuts. Against the virus, there are none.

Designing a death clock must be based on mathematical models. Trump and his defenders may wish to assign blame to other countries, individuals, and institutions. His detractors, on the other hand, may wish to assess the consequences of his statements, decisions, and actions earlier than March. But a death clock must not reflect conjecture and needs to exist outside the news cycle, identifying only that portion of deaths which, according to experts, have resulted directly from the president and his team’s delayed response.

Conservatively, according to epidemiologists, had the Trump administration simply implemented mitigation guidelines by March 9, approximately 60 percent of American covid-19 deaths could have been avoided.

To let the numbers speak for themselves, my team and I have constructed an online counter at TrumpDeathClock.com, estimating the toll of the White House’s delayed response. The site displays both the number of people who have died in the country from covid-19 and an estimate of that portion whose lives would have been saved had the president and his administration acted just one week earlier.

What a powerful statement it would be if this clock could be displayed on billboards and projected on buildings in cities and small towns across America. This would begin to honor those who lost their lives and, in their memory, demand more responsive and responsible leadership.
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Re: U.S. government gave $3.7 million grant to Wuhan lab at

Postby admin » Mon May 18, 2020 2:55 am

Fauci admits earlier Covid-19 mitigation efforts would have saved more American lives
by Devan Cole
Updated 2:55 PM ET, Sun April 12, 2020



Washington (CNN)Dr. Anthony Fauci said Sunday that calls to implement life-saving social distancing measures faced "a lot of pushback" early in the US coronavirus outbreak and that the country is now looking for ways to more effectively respond to the virus should it rebound in the fall.

"I mean, obviously, you could logically say that if you had a process that was ongoing and you started mitigation earlier, you could have saved lives," Fauci, the nation's top infectious disease expert, told CNN's Jake Tapper on "State of the Union" when asked if social distancing and stay-at-home measures could have prevented deaths had they been put in place in February, instead of mid-March.

"Obviously, no one is going to deny that. But what goes into those decisions is complicated," added Fauci, who is a key member of the Trump administration's coronavirus task force. "But you're right, I mean, obviously, if we had right from the very beginning shut everything down, it may have been a little bit different. But there was a lot of pushback about shutting things down back then."

Asked why the President didn't recommend social distancing guidelines until mid-March -- about three weeks after the nation's top health experts recommended they be put in place -- Fauci said, "You know, Jake, as I have said many times, we look at it from a pure health standpoint. We make a recommendation. Often, the recommendation is taken. Sometimes it's not. But we -- it is what it is. We are where we are right now."

The comments from Fauci come a day after a report from The New York Times detailed the Trump administration's missteps in the early days of the pandemic and how President Donald Trump ignored his advisers' warnings of the potentially deadly disease.

An administration official separately confirmed to CNN that the government's top public health experts agreed in the third week of February on the need to begin moving away from a containment strategy and toward a mitigation strategy that would involve strong social distancing measures. The agreement among the health officials came after they held a tabletop exercise to game out the potential for a full-blown pandemic.

According to the Times report, Dr. Robert Kadlec, the top disaster response official at the Department of Health and Human Services, convened the White House coronavirus task force on February 21. During his meeting, the group conducted a mock-up exercise of the pandemic that predicted 110 million infections, 7.7 million hospitalizations and 586,000 deaths.

The group "concluded they would soon need to move toward aggressive social distancing, even at the risk of severe disruption to the nation's economy and the daily lives of millions of Americans," but it took more than three weeks for Trump to enact such guidelines on March 16.

Fauci told Tapper that "there is always a possibility, as we get into next fall and the beginning of early winter that we could see a rebound," in the virus, but the lessons learned from the first iteration of it should help the US better respond to a potential new wave.

"Hopefully, hopefully, what we have gone through now and the capability that we have for much, much better testing capability, much, much better surveillance capability, and the ability to respond with countermeasures, with drugs that work, that it will be an entirely different ball game," he said.

'Not going to be a light switch'

With health experts and some elected officials saying the US is starting to see the effectiveness of social distancing measures put in place last month, Americans are wondering when the country can begin to ease up on the guidance.

Fauci said Sunday that the process of returning to normal "is not going to be a light switch that we say, 'OK, it is now June, July' ... click -- the light switch goes back on."

He added: "It's going to be depending where you are in the country, the nature of the outbreak that you have already experienced and the threat of an outbreak that you may not have experienced. So it's going to have to look at the situation in different parts of the country."

Asked by Tapper when he thought that process could start, Fauci said he thinks "it could probably start at least in some ways maybe next month," but noted that it's "difficult" to make those types of predictions and officials are trying to open the country "appropriately."

Trump said Saturday night that he hopes to make a decision "fairly soon" on when to reopen the country amid the coronavirus pandemic, telling Fox News' Jeanine Pirro, "We have to bring our country back. So, I'll be making a decision reasonably soon, we're setting up a council now of some of the most distinguished leaders in virtually every field -- including politics, and business and medical -- and we'll be making that decision fairly soon."

But as Trump leans in to his desire to reopen the nation's economy by May 1, America's governors and mayors, who hold the power to enforce closures and who have often taken a far more aggressive posture on protecting public health, stand in his way.

An ominous warning

The director of the Institute for Health Metrics and Evaluation said Sunday that if the social distancing measures and closures were relaxed on May 1, the country would see a rebound of coronavirus cases.

"We don't think the capability in the states exists yet to deal with that volume of cases and so by July or August we could be back in the same situation we are in now" if there was premature opening of the country, Dr. Christopher Murray said on CBS, adding that West Coast states that are further along in the pandemic will still need "weeks of closures" beyond the peak for the opportunity to conduct proper testing and contact tracing.

Relaxing closures and social distancing measures on a rolling basis, he said, poses a new set of questions that have not been addressed.

"Of course there's a big issue of states are on different timings of their epidemics, which we know is the case. How are they going to control importation from other states into their state?" Murray said.

The inconsistent state mitigation policies have also been a problem for the modeling of the pandemic, according to Murray, who said that "incomplete implementation of social distancing closures in many states (is) adding a degree of uncertainty."

The World Health Organization special envoy, Dr. David Nabarro, went a step further in an interview with NBC on Sunday, issuing an ominous warning about coronavirus, which has already infected more than 1,827,000 people worldwide.

"We're not so sure that it will come in waves in the way that influenza does," he said. "We think it's going to be a virus that stalks the human race for quite a long time to come until we can all have a vaccine that will protect us and that there will be small outbreaks that will emerge sporadically and they will break through our defenses."

Nabarro said it will be "key" for countries to "pick up cases as soon as they appear, isolate them and stop outbreaks from developing."

There are more than 530,000 confirmed cases of coronavirus in the US, and more than 20,600 Americans have died, according to a tally from Johns Hopkins University.

This story has been updated with additional developments Sunday.

CNN's Kevin Bohn, Maeve Reston, Maegan Vazquez, Jason Hoffman, Kristen Holmes, Jeremy Diamond and Wes Bruer contributed to this report.
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Re: U.S. government gave $3.7 million grant to Wuhan lab at

Postby admin » Mon May 18, 2020 3:15 am

He Could Have Seen What Was Coming: Behind Trump’s Failure on the Virus: An examination reveals the president was warned about the potential for a pandemic but that internal divisions, lack of planning and his faith in his own instincts led to a halting response.
by Eric Lipton, David E. Sanger, Maggie Haberman, Michael D. Shear, Mark Mazzetti and Julian E. Barnes
New York Times
Published April 11, 2020
Updated May 4, 2020



WASHINGTON — “Any way you cut it, this is going to be bad,” a senior medical adviser at the Department of Veterans Affairs, Dr. Carter Mecher, wrote on the night of Jan. 28, in an email to a group of public health experts scattered around the government and universities. “The projected size of the outbreak already seems hard to believe.”

A week after the first coronavirus case had been identified in the United States, and six long weeks before President Trump finally took aggressive action to confront the danger the nation was facing — a pandemic that is now forecast to take tens of thousands of American lives — Dr. Mecher was urging the upper ranks of the nation’s public health bureaucracy to wake up and prepare for the possibility of far more drastic action.

“You guys made fun of me screaming to close the schools,” he wrote to the group, which called itself “Red Dawn,” an inside joke based on the 1984 movie about a band of Americans trying to save the country after a foreign invasion. “Now I’m screaming, close the colleges and universities.”

His was hardly a lone voice. Throughout January, as Mr. Trump repeatedly played down the seriousness of the virus and focused on other issues, an array of figures inside his government — from top White House advisers to experts deep in the cabinet departments and intelligence agencies — identified the threat, sounded alarms and made clear the need for aggressive action.

The president, though, was slow to absorb the scale of the risk and to act accordingly, focusing instead on controlling the message, protecting gains in the economy and batting away warnings from senior officials.
It was a problem, he said, that had come out of nowhere and could not have been foreseen.

Even after Mr. Trump took his first concrete action at the end of January — limiting travel from China — public health often had to compete with economic and political considerations in internal debates, slowing the path toward belated decisions to seek more money from Congress, obtain necessary supplies, address shortfalls in testing and ultimately move to keep much of the nation at home.

Unfolding as it did in the wake of his impeachment by the House and in the midst of his Senate trial, Mr. Trump’s response was colored by his suspicion of and disdain for what he viewed as the “Deep State” — the very people in his government whose expertise and long experience might have guided him more quickly toward steps that would slow the virus, and likely save lives.

In sum, Democrats and their supporters had the exact prosecutor they all agreed was the embodiment of competence and integrity in Robert Mueller. He assembled a team of prosecutors and investigators that countless media accounts heralded as the most aggressive and adept in the nation. They had subpoena power, the vast surveillance apparatus of the U.S. government at their disposal, a demonstrated willingness to imprison anyone who lied to them, and unlimited time and resources to dig up everything they could.

The result of all of that was that not a single American – whether with the Trump campaign or otherwise – was charged or indicted on the core question of whether there was any conspiracy or coordination with Russia over the election. No Americans were charged or even accused of being controlled by or working at the behest of the Russian government. None of the key White House aides at the center of the controversy who testified for hours and hours – including Donald Trump, Jr. or Jared Kushner – were charged with any crimes of any kind, not even perjury, obstruction of justice or lying to Congress.

These facts are fatal to the conspiracy theorists who have drowned U.S. discourse for almost three years with a dangerous and distracting fixation on a fictitious espionage thriller involved unhinged claims of sexual and financial blackmail, nefarious infiltration of the U.S. Government by familiar foreign villains, and election cheating that empowered an illegitimate President. They got the exact prosecutor and investigation that they wanted, yet he could not establish that any of this happened and, in many cases, established that it did not.

THE ANTI-CLIMACTIC ENDING of the Mueller investigation is particularly stunning given how broad Mueller’s investigative scope ended up being, extending far beyond the 2016 election into years worth of Trump’s alleged financial dealings with Russia (and, obviously, Manafort’s with Ukraine and Russia). There can simply be no credible claim that Mueller was, in any meaningful way, impeded by scope, resources or topic limitation from finding anything for which he searched.

Despite efforts today by long-time conspiracist theorists to drastically move goalposts so as to claim vindication, the historical record could not be clearer that Mueller’s central mandate was to determine whether crimes were committed by Trump officials in connection with alleged Russian interference in the election. The first paragraph of the New York Times article from May, 2017, announcing Mueller’s appointment, leaves no doubt about that:

The Justice Department appointed Robert S. Mueller III, a former F.B.I. director, as special counsel on Wednesday to oversee the investigation into ties between President Trump’s campaign and Russian officials, dramatically raising the legal and political stakes in an affair that has threatened to engulf Mr. Trump’s four-month-old presidency.

As recently as one month ago, former CIA Director and current NBC News analyst John Brennan was confidently predicting that Mueller could not possibly close his investigation without first indicting a slew of Americans for criminally conspiring with Russia over the election, and specifically predicted that Trump’s family members would be included among those so charged:

Terry Moran

John Brennan has a lot to answer for—going before the American public for months, cloaked with CIA authority and openly suggesting he’s got secret info, and repeatedly turning in performances like this.

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Obviously, none of that happened. Nor were any of the original accusations that launched this three-year-long mania — from an accusatory August, 2016 online commercial from the Clinton campaign — corroborated by the Mueller Report:

Indeed, so many of the most touted media “bombshells” claiming to establish Trump/Russia crimes have been proven false by this report. Despite an extensive discussion of Paul Manafort’s activities, nothing in the Report even hints, let alone states, that he ever visited Julian Assange in the Ecuadorian Embassy, let alone visited him three times, including during the 2016 election. How the Guardian could justify still not retracting that false story is mystifying.

Faring even worse is the Buzzfeed bombshell from January claiming that “President Donald Trump directed his longtime attorney Michael Cohen to lie to Congress about negotiations to build a Trump Tower in Moscow” and that “Cohen also told the special counsel that after the election, the president personally instructed him to lie — by claiming that negotiations ended months earlier than they actually did — in order to obscure Trump’s involvement.” Mueller himself responded to the story by insisting it was false, and his Report directly contradicts it, as it makes clear that Cohen told Mueller the exact opposite:

But Cohen said that he and the President did not explicitly discuss whether Cohen's testimony about the Trump Tower Moscow project would be or was false, and the President did not direct him to provide false testimony. Cohen also said he did not tell the President about the specifics of his planned testimony. During the time when his statement to Congress was being drafted and circulated to members of the JDA, Cohen did not speak directly to the President about the statement, but rather communicated with the President's personal counsel -- as corroborated by phone records showing extensive communications between Cohen and the President's personal counsel before Cohen submitted his statement and when he testified before Congress.

Equally debunked is CNN’s major blockbuster by Jim Sciutto, Carl Bernstein, and Marshall Cohen from last July that “Michael Cohen, President Donald Trump’s former personal attorney, claims that then-candidate Trump knew in advance about the June 2016 meeting in Trump Tower.” The Mueller Report says the exact opposite: that Cohen had no knowledge of Trump’s advanced knowledge.

And the less said about the Steele Dossier, pee-pee tapes, secret meetings in Prague, and indescribably unhinged claims like this one, the better:

But beyond the gutting of these core conspiracy claims is that Mueller’s investigation probed areas far beyond the initial scope of Trump/Russia election-conspiring, and came up empty. Among other things, Mueller specifically examined Trump’s financial dealings with Russia to determine whether that constituted incriminating evidence of corrupt links:

Because Trump’s status as a public figure at the time was attributable in large part to his prior business and entertainment dealings, this Office investigated whether a business contact with Russia-linked individuals and entities during the campaign period—the Trump Tower Moscow project, see Volume I, Section IV.A.1, infra—led to or involved coordination.

Indeed, Mueller’s examination of Trump’s financial dealings with Russia long pre-dates the start of the Trump campaign, going back several years before the election:

Between at least 2013 and 2016, the Trump Organization explored a similar licensing deal in Russia involving the construction of a Trump-branded property in Moscow. The project, commonly referred to as a "Trump Tower Moscow" or "Trump Moscow" project, anticipated a combination of commercial, hotel, and residential properties all within the same building. Between 2013 and June 2016, several employees of the Trump Organization, including then-president of the organization Donald J. Trump, pursued a Moscow deal with several Russian counterparties. From the fall of 2015 until the middle of 2016, Michael Cohen spearheaded the Trump Organization's pursuit of a Trump Tower Moscow project, including by reporting on the project's status to candidate Trump and other executives in the Trump Organization.290

Mueller additionally made clear that he received authorization to investigate numerous Americans for ties to Russia despite their not being formally associated with the Trump campaign, including Michael Cohen and Roger Stone. And regarding Cohen, Mueller specifically was authorized to investigate any attempts by Cohen to “receive funds from Russia-backed entities.” None of this deep diving to other individuals or years of alleged financial dealings with Russian resulted in any finding that Trump or any of his associates were controlled by, or corruptly involved with, the Russian government.

Then there is the issue of Manafort’s relationship with the Ukrainians, and specifically his providing of polling data to Konstantin Kilimnik, an episode which Trump/Putin conspiracist Marcy Wheeler, along with many others, particularly hyped over and over. To begin with, Mueller said his office “did not identify evidence of a connection” between that act and “Russian interference in the election,” nor did he “establish that Manafort otherwise coordinated with the Russian government on its election-inteference efforts”:

Because of questions about Manafort's credibility and our limited ability to gather evidence on what happened to the polling data after it was sent to Kilimnik, the Office could not assess what Kilimnik (or others he may have given it to) did with it. The Office did not identify evidence of a connection between Manafort's sharing polling data and Russia's interference in the election, which had already been reported by U.S. media outlets at the time of the August 2 meeting. The investigation did not establish that Manafort otherwise coordinated with the Russian government on its election-interference efforts.

Also endlessly hyped by Wheeler and other conspiracists were the post-election contacts between Trump and Russia: as though it’s unusual that a major power would seek to build new, constructive relationships with a newly elected administration. Indeed, Wheeler went so far as to cite these post-election contacts to turn her own source into the FBI on the ground that it constituted smoking gun evidence, an act for which she was praised by the Washington Post (nothing Wheeler claimed about the evidence “related to the Mueller investigation” that she claimed to possess appears to be in the Mueller Report). Here again, the Mueller Report could not substantiate any of these claims:

B. Post-Election and Transition-Period Contacts

Trump was elected President on November 8, 2016. Beginning immediately after the election, individuals connected to the Russian government started contacting officials on the Trump Campaign and Transition Team through multiple channels -- sometimes through Russian Ambassador Kislyak and at other times through individuals who sought reliable contacts through U.S. persons not formally tied to the Campaign or Transition Team. The most senior levels of the Russian government encouraged these efforts. The investigation did not establish that these efforts reflected or constituted coordination between the Trump Campaign and Russia in its election-interference activities.

The centerpiece of the Trump/Russia conspiracy – the Trump Tower meeting – was such a dud that Jared Kushner, halfway through the meeting, texted Manafort to declare the meeting “a waste of time,” and then instructed his assistant to call him so that he could concoct a reason to leave. Not only could Mueller not find any criminality in this meeting relating to election conspiring, but he could not even use election law to claim it was an illegal gift of something of value from a foreigner, because, among other things, the information offered was of so little value that it could not even pass the $2,000 threshold required to charge someone for a misdemeanor, let alone the $25,000 required to make it a felony.

Neither the Trump Tower meeting itself nor its participants – for so long held up as proof of the Trump/Russia conspiracy – could serve as the basis for any finding of criminality. Indeed, the key Trumpworld participants who testified about what happened at that meeting and its aftermath (Trump Jr. and Kushner) were not even accused by Mueller of lying about any of it.

NONE OF THIS IS TO SAY that the Mueller Report exonerates Trump of wrongdoing. Mueller makes clear, for instance, that the Trump campaign not only knew that Russia was interested in helping it win the election but was happy to have that help. There’s clearly nothing criminal about that. One can debate whether it’s unethical for a presidential campaign to have dirt about its opponent released by a foreign government, though anyone who wants to argue that has to reconcile that with the fact that the DNC had a contractor working with the Ukrainian government to help Hillary Clinton win by feeding them dirt on Trump and Manafort, as well as a paid operative named Christopher Steele (remember him?) working with Russian officials to get dirt on Trump.

Ukrainian efforts to sabotage Trump backfire
Kiev officials are scrambling to make amends with the president-elect after quietly working to boost Clinton.
By Kenneth P. Vogel and David Stern
01/11/2017 05:05 AM EST

As is true of all investigations, Mueller’s team could not access all relevant information. Some was rendered inaccessible through encryption. Other information was deleted, perhaps with corrupt motives. And some witnesses lied or otherwise tried to obstruct the investigation. As a result, it’s of course possible that incriminating evidence existed that Mueller – armed with subpoena power, unlimited resources, 22 months of investigative work, and a huge team of top-flight prosecutors, FBI agents, intelligence analysts and forensic accountants – did not find.

But anything is possible. It’s inherently possible that anyone is guilty of any crime but that the evidence just cannot be found to prove it. One cannot prove a negative. But the only way to rationally assess what happened is by looking at the evidence that is available, and that’s what Mueller did. And there’s simply no persuasive way – after heralding Mueller and his team as the top-notch investigators that they are and building up expectations about what this would produce – for any honest person to deny that the end of the Mueller investigation was a huge failure from the perspective of those who pushed these conspiracies.

Mueller certainly provides substantial evidence that Russians attempted to meddle in various ways in the U.S. election, including by hacking the DNC and Podesta and through Facebook posts and tweets. There is, however, no real evidence that Putin himself ordered this, as was claimed since mid-2016. But that Russia had done such things has been unsurprising from the start, given how common it is for the U.S. and Russia to meddle in everyone’s affairs, including one another’s, but the scope and size of it continues to be minute in the context of overall election spending:

To reach larger U.S. audiences, the IRA purchased advertisements from Facebook that promoted the IRA groups on the newsfeeds of U.S. audience members. According to Facebook, the IRA purchased over 3,500 advertisements, and the expenditures totaled approximately $100,000.

The section of Mueller’s report on whether Trump criminally attempted to obstruct the investigation is full of evidence and episodes that show Trump being dishonest, misleading, and willing to invoke potentially corrupt tactics to put an end to it. But ultimately, the most extreme of those tactics were not invoked (at times because Trump’s aides refused), and the actions in which Trump engaged were simply not enough for Mueller to conclude that he was guilty of criminal obstruction.

As Mueller himself concluded, a reasonable debate can be conducted on whether Trump tried to obstruct his investigation with corrupt intent. But even on the case of obstruction, the central point looms large over all of it: there was no underlying crime established for Trump to cover-up.

All criminal investigations require a determination of a person’s intent, what they are thinking and what their goal is. When the question is whether a President sought to kill an Executive Branch investigation – as Trump clearly wanted to do here – the determinative issue is whether he did so because he genuinely believed the investigation to be an unfair persecution and scam, or whether he did it to corruptly conceal evidence of criminality.

That Mueller could not and did not establish any underlying crimes strongly suggests that Trump acted with the former rather than the latter motive, making it virtually impossible to find that he criminally obstructed the investigation.

THE NATURE OF OUR POLITICAL DISCOURSE is that nobody ever needs to admit error because it is easy to confine oneself to strictly partisan precincts where people are far more interested in hearing what advances their agenda or affirms their beliefs than they are hearing the truth. For that reason, I doubt that anyone who spent the last three years pushing utterly concocted conspiracy theories will own up to it, let alone confront any accountability or consequences for it.

But certain facts will never go away no matter how much denial they embrace. The sweeping Mueller investigation ended with zero indictments of zero Americans for conspiring with Russia over the 2016 election. Both Donald Trump, Jr. and Jared Kushner – the key participants in the Trump Tower meeting – testified for hours and hours yet were never charged for perjury, lying or obstruction, even though Mueller proved how easily he would indict anyone who lied as part of the investigation. And this massive investigation simply did not establish any of the conspiracy theories that huge parts of the Democratic Party, the intelligence community and the U.S. media spent years encouraging the public to believe.

Those responsible for this can refuse to acknowledge wrongdoing. They can even claim vindication if they want and will likely be cheered for doing so.

But the contempt in which the media and political class is held by so much of the U.S. population – undoubtedly a leading factor that led to Trump’s election in the first place – will only continue to grow as a result, and deservedly so. People know they were scammed, that their politics was drowned for years by a hoax. And none of that will go away no matter how insulated media and political elites in Washington, northern Virginia, Brooklyn, and large West Coast cities keep themselves, and thus hear only in-group affirmation while blocking out all of that well-earned scorn.

-- Robert Mueller Did Not Merely Reject the Trump-Russia Conspiracy Theories. He Obliterated Them, by Glenn Greenwald

Decision-making was also complicated by a long-running dispute inside the administration over how to deal with China. The virus at first took a back seat to a desire not to upset Beijing during trade talks, but later the impulse to score points against Beijing left the world’s two leading powers further divided as they confronted one of the first truly global threats of the 21st century.

The shortcomings of Mr. Trump’s performance have played out with remarkable transparency as part of his daily effort to dominate television screens and the national conversation.

But dozens of interviews with current and former officials and a review of emails and other records revealed many previously unreported details and a fuller picture of the roots and extent of his halting response as the deadly virus spread:

The National Security Council office responsible for tracking pandemics received intelligence reports in early January predicting the spread of the virus to the United States, and within weeks was raising options like keeping Americans home from work and shutting down cities the size of Chicago. Mr. Trump would avoid such steps until March.

Despite Mr. Trump’s denial weeks later, he was told at the time about a Jan. 29 memo produced by his trade adviser, Peter Navarro, laying out in striking detail the potential risks of a coronavirus pandemic: as many as half a million deaths and trillions of dollars in economic losses.

The health and human services secretary, Alex M. Azar II, directly warned Mr. Trump of the possibility of a pandemic during a call on Jan. 30, the second warning he delivered to the president about the virus in two weeks. The president, who was on Air Force One while traveling for appearances in the Midwest, responded that Mr. Azar was being alarmist.

Mr. Azar publicly announced in February that the government was establishing a “surveillance” system in five American cities to measure the spread of the virus and enable experts to project the next hot spots. It was delayed for weeks. The slow start of that plan, on top of the well-documented failures to develop the nation’s testing capacity, left administration officials with almost no insight into how rapidly the virus was spreading. “We were flying the plane with no instruments,” one official said.

By the third week in February, the administration’s top public health experts concluded they should recommend to Mr. Trump a new approach that would include warning the American people of the risks and urging steps like social distancing and staying home from work. But the White House focused instead on messaging and crucial additional weeks went by before their views were reluctantly accepted by the president — time when the virus spread largely unimpeded.

When Mr. Trump finally agreed in mid-March to recommend social distancing across the country, effectively bringing much of the economy to a halt, he seemed shellshocked and deflated to some of his closest associates. One described him as “subdued” and “baffled” by how the crisis had played out. An economy that he had wagered his re-election on was suddenly in shambles.

He only regained his swagger, the associate said, from conducting his daily White House briefings, at which he often seeks to rewrite the history of the past several months. He declared at one point that he “felt it was a pandemic long before it was called a pandemic,” and insisted at another that he had to be a “cheerleader for the country,” as if that explained why he failed to prepare the public for what was coming.

Mr. Trump’s allies and some administration officials say the criticism has been unfair. The Chinese government misled other governments, they say. And they insist that the president was either not getting proper information, or the people around him weren’t conveying the urgency of the threat. In some cases, they argue, the specific officials he was hearing from had been discredited in his eyes, but once the right information got to him through other channels, he made the right calls.

“While the media and Democrats refused to seriously acknowledge this virus in January and February, President Trump took bold action to protect Americans and unleash the full power of the federal government to curb the spread of the virus, expand testing capacities and expedite vaccine development even when we had no true idea the level of transmission or asymptomatic spread,” said Judd Deere, a White House spokesman.

There were key turning points along the way, opportunities for Mr. Trump to get ahead of the virus rather than just chase it. There were internal debates that presented him with stark choices, and moments when he could have chosen to ask deeper questions and learn more. How he handled them may shape his re-election campaign. They will certainly shape his legacy.

The Containment Illusion

By the last week of February, it was clear to the administration’s public health team that schools and businesses in hot spots would have to close. But in the turbulence of the Trump White House, it took three more weeks to persuade the president that failure to act quickly to control the spread of the virus would have dire consequences.
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Re: U.S. government gave $3.7 million grant to Wuhan lab at

Postby admin » Wed Jun 03, 2020 8:15 am

COVID-19: Scientists Have High Hopes For Potential Breakthrough Virus Blocker
by Joe Lombardi
05/25/2020 7:03 p.m.

Strains of cannabis Photo Credit: MOCA via Wikimedia Commons

A team of scientists has high hopes for a potential breakthrough blocker for the novel strain of coronavirus (COVID-19).

It has discovered that strains of medical cannabis may help prevent contracting COVID infections.

At least a dozen cannabis plants of the hundreds tested were high in CBD that appeared to affect the ACE2 pathways that the virus uses to access the body, the researchers from the University of Lethbridge in Alberta, Canada discovered.

The findings won't lead to a vaccine, but rather other delivery methods that could make people more resistant to COVID-19, says the Calgary Herald in this report.

Early indications are that the cannabis extracts could be used in mouthwash and throat gargle products as well as inhalers for both at-home treatment and clinical practice, according to CTV News.

The scientists say COVID's entry points could potentially be reduced by as much as 70 to 80 percent by cannabis.

“Our work could have a huge influence — there aren’t many drugs that have the potential of reducing infection by 70 to 80 percent,” one of the scientists told the Calgary Herald.

The next steps are for the study to be peer-reviewed and for clinical trials to be scheduled.

The scientists' results were published in Preprints, an online journal.
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Re: U.S. government gave $3.7 million grant to Wuhan lab at

Postby admin » Sat Jul 18, 2020 12:38 am

A Sinking Ship’: Arizona Docs Say Ducey Steered State Into COVID-19 Surge
SWITCH FLIPPED: The state has 130,000 coronavirus cases, and hospital workers say it didn’t have to happen.
by Emily Shugerman
Updated Jul. 17, 2020 12:16PM ET Published Jul. 17, 2020 3:59AM ET


Matt Heinz, a hospital physician in Tucson, Arizona, remembers the day he knew a coronavirus surge was coming. Or really, it was two days: a night shift that stretched from the evening of June 3 into the early hours of June 4, when Heinz admitted four patients suspected of having COVID-19, instead of the usual one or zero. It was a little over two weeks after Gov. Doug Ducey allowed the state’s lockdown order to expire, Heinz said, and “it was like someone flipped a switch.”

“And someone did flip a switch,” said Heinz, a former Democratic state representative who also served in the Department of Health and Human Services. “It was the governor.”

As cases in Arizona skyrocket, physicians told The Daily Beast they feel increasingly abandoned by Ducey, who was one of the first leaders in the country to lift lockdown restrictions this spring. Despite the state’s record-setting spike in cases—and the urging of hundreds of health-care workers and multiple mayors—Ducey so far has refused to re-institute a lockdown order or issue a mask mandate, leaving doctors and nurses feeling helpless.

“You can’t bluff this virus,” said Quinn Snyder, an emergency physician in Mesa. “People keep trying to find shortcuts around the issues at hand, but the virus just doesn’t care about those kinds of shortcuts. It will win.”

“I have been trying to talk to people and speak up as much as possible,” he added. “And it feels like we are on a sinking ship.”

A spokesperson for the governor said Ducey had taken a number of steps to slow the spread of the virus, including prohibiting large gatherings and pausing the operations of gyms, bars, nightclubs, waterparks, and tubing establishments. He also noted that Ducey had allowed cities to pass their own mask ordinances and that nearly 90 percent of the state was now under a local mask mandate.

“We want everyone to wear a mask in public,” the spokesperson said. “Our approach has been focused on bringing about the maximum mask compliance possible.”

“It doesn’t seem like there’s any end in sight. But not necessarily because of the rhythm of the disease, but because of our government’s response to it.”

— Larry DeLuca

Arizona reported more than 3,200 new cases in a single day Thursday, putting it behind only Florida in the number of new cases per capita. The figures were actually a slight decrease from previous highs, but the situation in the hospitals still looked dire—the number of ICU beds and ventilators in use by suspected or confirmed coronavirus patients hit new records Sunday. On Thursday, 90 percent of the state’s ICU beds were taken and 53 percent of its ventilators were in use, according to state Health Department data.

Inside the hospitals, doctors told The Daily Beast they were working more than 100 hours a week, and “countless” nurses were out sick. At one Tucson-area hospital, a secondary ICU that closed when things leveled off over the spring recently reopened, and the post-anesthesia care unit was “cannibalized” to house coronavirus patients, according to emergency physician Larry DeLuca. Snyder said one of the hospitals where he works had started housing adult patients in its pediatric towers, and the emergency department was also shuffling beds to make room for COVID-positive patients.

Several of the half-dozen doctors who spoke to The Daily Beast characterized these next few weeks as a “tipping point” for Arizona, where things could go from under control to completely out of their hands.

“It doesn’t seem like there’s any end in sight,” DeLuca said. “But not necessarily because of the rhythm of the disease, but because of our government’s response to it.”

One ICU physician in Tucson, who asked not to be named for fear of employer retaliation, said the official numbers actually underplayed the severity of the crisis. When hospitals reported that 90 percent of their ICU beds and half of their ventilators were in use, the physician said, those numbers included the extra beds and machines they’d brought in for the pandemic. If those percentages ever reached 100, there would be no feasible way for the hospital to scale up.

“If you were going by our pre-COVID capacity, we would be actually operating at 120 percent of capacity,” the physician said, adding that the hospital where they work had run out of its own ventilator supply and was now using those supplied by FEMA.

Several hospitals have already launched part or all of their emergency plans, including calling in refrigerated trucks to use as morgues. The Maricopa County Medical Examiner’s Office also recently announced it is preparing for an increase in corpses, saying the office is “currently near capacity for body storage.” (It added that while this situation is common for this time of year, it is “further complicated by the current pandemic.”)

For many, the announcement called to mind the images of bodies being loaded into trucks by forklift during the height of the East Coast outbreak in March, or the weeks-long wait for funerals. But there is one key difference: While New York shut down all non-essential businesses and issued a mask mandate during the height of its surge, Arizona is still allowing haircuts, spa days, and indoor dining.

At a press conference earlier this month, on the same day the number of cases passed 112,000, Ducey acknowledged that his earlier shutdown order—one that mirrored many of New York’s restrictions—had worked. The number of new cases in the state stayed relatively stable from the time the order went out in March to the day it expired in mid-May. Cases began to skyrocket in June, shortly after the reopening.

But Ducey has refused to issue another lockdown order. Instead, at the press conference, he claimed that his June 29 order shuttering all gyms and bars—but allowing restaurants, barbershops, hair and nail salons to stay open—had achieved “some results.” And he decreased indoor dining allowances by only 50 percent, which public health officials said was totally inadequate. (A spokesperson for Ducey's office said the 50 percent reduction in restaurant capacity was part of recommendations made by the White House Coronavirus Task Force.)


Heinz described watching the governor's press conference in shock. “We all think, ‘Finally, thank God, the deaths are all starting to go up … He’s going to take this seriously,’” he recalled. “And he announces some ridiculous non-measure.”

“We should have a stay-at-home order for at least 30 days, and that should have been re-initiated for all of June,” Heinz added. “We’re halfway through July.”

Ducey has also refused to issue a statewide mask mandate, despite the urging of more than 900 medical providers and five mayors, and only recently allowed cities to issue their own such ordinances. Earlier this month, photos of the governor going maskless to a June 6 graduation party sparked an uproar in the medical community. “That’s the guy in charge, so you know we’re in trouble,” Heinz said.

The Ducey spokesperson noted that the photo was originally claimed to have been taken a month later than it actually was, and called it a “smear-tactic meant to deceive and mislead.”

Meanwhile, hospitals in the state appear to be gearing up for a long fight. The Arizona Department of Health Services recently announced a partnership with Vizient, Inc. to bring in nearly 600 critical care nurses, in addition to those the National Disaster Medical System sent last month. Banner Health, the largest health-care system in the state, also posted an ad this month looking for out-of-state doctors, saying Arizona was “running low on ICU and hospitalist trained physicians.”

In a statement to The Daily Beast, a spokesperson said Banner Health had brought in nearly 750 travel nurses and other specialists over the course of the pandemic and were expecting 200 to 400 more to come soon. The spokesperson said they had also “upskilled” more than 700 team members, meaning they had trained providers from another area of the hospital to work in respiratory units.

Andrew Carroll, a family medicine doctor in Chandler, is one of those “upskilled” providers. Banner asked him months ago to get his emergency medicine privileges in case of a surge, he said, and officially called him in a few weeks ago. His first stint in the emergency room will consist of three straight shifts next weekend.

Andrew Carroll, a family medicine doctor in Chandler, AZ
The American Academy of Family Physicians

Carroll said he was happy to help out, especially after hearing from so many emergency medicine colleagues who were already burned out. But he was also frustrated that it had come to this point.

“I'm angry that people still refuse to wear masks,” he said. “I'm angry that our government hasn’t made more mandatory public health policies.”

If the government had enacted those policies, he added, “I would not have to be dragged into the hospital to work three straight 12-hour shifts through the weekend, and come home and jump in the swimming pool before I see my family so they don’t get sick.”

“I'm willing, I’m ready, but I’m angry,” he said.
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Re: U.S. government gave $3.7 million grant to Wuhan lab at

Postby admin » Sat Jul 25, 2020 10:06 am

Prof. Francis Boyle Update: Covid-19 Bioweapon Is A Crime Against Humanity Interview
by Jason Liosatos, Outside The Box
Apr 29, 2020

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Re: U.S. government gave $3.7 million grant to Wuhan lab at

Postby admin » Sun Jul 26, 2020 8:43 pm

Part 1 of 3

A Proposed Origin for SARS-CoV-2 and the COVID-19 Pandemic [W/Comments]
by Jonathan Latham, PhD and Allison Wilson, PhD
Independent Science News for Food and Agriculture
July 15, 2020

Our supposition as to why there was a time lag between sample collection (in 2012/2013) and the COVID-19 outbreak is that the researchers were awaiting BSL-4 lab construction and certification, which was underway in 2013 but delayed until 2018.

We propose that, when frozen samples derived from the miners were eventually opened in the Wuhan lab they were already highly adapted to humans to an extent possibly not anticipated by the researchers. One small mistake or mechanical breakdown could have led directly to the first human infection in late 2019.

Thus, one of the miners, most likely patient 3, or patient 4 (whose thymus was removed), was effectively patient zero of the COVID-19 epidemic. In this scenario, COVID-19 is not an engineered virus; but, equally, if it had not been taken to Wuhan and no further molecular research had been performed or planned for it then the virus would have died out from natural causes, rather than escaped to initiate the COVID-19 pandemic.

-- A Proposed Origin for SARS-CoV-2 and the COVID-19 Pandemic, by Jonathan Latham, PhD and Allison Wilson, PhD

In all the discussions of the origin of the COVID-19 pandemic, enormous scientific attention has been paid to the molecular character of the SARS-CoV-2 virus, including its novel genome sequence in comparison with its near relatives. In stark contrast, virtually no attention has been paid to the physical provenance of those nearest genetic relatives, its presumptive ancestors, which are two viral sequences named BtCoV/4991 and RaTG13.

This neglect is surprising because their provenance is more than interesting. BtCoV/4991 and RaTG13 were collected from a mineshaft in Yunnan province, China, in 2012/2013 by researchers from the lab of Zheng-li Shi at the Wuhan Institute of Virology (WIV). Very shortly before, in the spring of 2012, six miners working in the mine had contracted a mysterious illness and three of them had died (Wu et al., 2014). The specifics of this mystery disease have been virtually forgotten; however, they are described in a Chinese Master’s thesis written in 2013 by a doctor who supervised their treatment.

We arranged to have this Master’s thesis translated into English. The evidence it contains has led us to reconsider everything we thought we knew about the origins of the COVID-19 pandemic. It has also led us to theorise a plausible route by which an apparently isolated disease outbreak in a mine in 2012 led to a global pandemic in 2019.

The origin of SARS-CoV-2 that we propose below is based on the case histories of these miners and their hospital treatment. This simple theory accounts for all the key features of the novel SARS-CoV-2 virus, including ones that have puzzled virologists since the outbreak began.

The theory can account for the origin of the polybasic furin cleavage site, which is a region of the viral spike protein that makes it susceptible to cleavage by the host enzyme furin and which greatly enhances viral spread in the body. This furin site is novel to SARS-CoV-2 compared to its near relatives (Coutard, et al., 2020). The theory also explains the exceptional affinity of the virus spike protein for human receptors, which has also surprised virologists (Letko et al., 2020; Piplani et al, 2020; Wrapp et al., 2020; Walls et al., 2020). The theory further explains why the virus has barely evolved since the pandemic began, which is also a deeply puzzling aspect of a virus supposedly new to humans (Zhan et al., 2020; van Dorp et al., 2020; Chaw et al., 2020). Lastly, the theory neatly explains why SARS-CoV-2 targets the lungs, which is unusual for a coronavirus (Huang et al., 2020).

We do not propose a specifically genetically engineered or biowarfare origin for the virus but the theory does propose an essential causative role in the pandemic for scientific research carried out by the laboratory of Zheng-li Shi at the WIV; thus also explaining Wuhan as the location of the epicentre.

Why has the provenance of RaTG13 and BtCoV/4991 been ignored?

The apparent origin of the COVID-19 pandemic is the city of Wuhan in Hubei province, China. Wuhan is also home to the world’s leading research centre for bat coronaviruses. There are two virology labs in the city, both have either collected bat coronaviruses or researched them in the recent past. The Shi lab, which collected BtCoV/4991 and RaTG13, recently received grants to evaluate by experiment the potential for pandemic pathogenicity of the novel bat coronaviruses they collected from the wild.

To add to these suggestive data points, there is a long history of accidents, disease outbreaks, and even pandemics resulting from lab accidents with viruses (Furmanski, 2014; Weiss et al., 2015).

This paper presents an historical review of outbreaks of PPPs [Potentially Pandemic Pathogens] or similarly transmissible pathogens that occurred from presumably well-funded and supervised nationally supported laboratories. It should be emphasized that these examples are only the “tip of the iceberg” because they represent laboratory accidents that have actually caused illness outside of the laboratory in the general public environment. The list of laboratory workers who have contracted potentially contagious infections in microbiology labs but did not start community outbreaks is much, much longer. The examples here are not “near misses;” these escapes caused real-world outbreaks.

-- Laboratory Escapes and “Self-fulfilling prophecy” Epidemics, by Martin Furmanski MD, Scientist’s Working Group on Chemical and Biologic Weapons, Center for Arms Control and Nonproliferation, February 17, 2014

For these and other reasons, summarised in our article The Case is Building that COVID-19 Had a Lab Origin, we (a virologist and a geneticist) and others have concluded that a lab outbreak is a credible thesis. Certainly, a lab origin has at least as much circumstantial evidence to support it as does any natural zoonotic origin theory (Piplani et al., 2020; Segreto and Deigin, 2020; Zhan et al., 2020).

Executive Summary

Biological threats—natural, intentional, or accidental—in any country can pose risks to global health, international security, and the worldwide economy. Because infectious diseases know no borders, all countries must prioritize and exercise the capabilities required to prevent, detect, and rapidly respond to public health emergencies. Every country also must be transparent about its capabilities to assure neighbors it can stop an outbreak from becoming an international catastrophe. In turn, global leaders and international organizations bear a collective responsibility for developing and maintaining robust global capability to counter infectious disease threats. This capability includes ensuring that financing is available to fill gaps in epidemic and pandemic preparedness. These steps will save lives and achieve a safer and more secure world.

The Global Health Security (GHS) Index is the first comprehensive assessment and benchmarking of health security and related capabilities across the 195 countries that make up the States Parties1 to the International Health Regulations (IHR [2005]).2 The GHS Index is a project of the Nuclear Threat Initiative (NTI) and the Johns Hopkins Center for Health Security (JHU) and was developed with The Economist Intelligence Unit (EIU). These organizations believe that, over time, the GHS Index will spur measurable changes in national health security and improve international capability to address one of the world’s most omnipresent risks: infectious disease outbreaks that can lead to international epidemics and pandemics.

The GHS Index is intended to be a key resource in the face of increasing risks of high-consequence3 and globally catastrophic4 biological events and in light of major gaps in international financing for preparedness. These risks are magnified by a rapidly changing and interconnected world; increasing political instability; urbanization; climate change; and rapid technology advances that make it easier, cheaper, and faster to create and engineer pathogens.

Developed with the guidance of an international expert advisory panel, the GHS Index data are drawn from publicly available data sources from individual countries and international organizations, as well as an array of additional sources including published governmental information, data from the World Health Organization (WHO), the World Organisation for Animal Health (OIE), the Food and Agriculture Organization of the United Nations (FAO), the World Bank, country legislation and regulations, and academic resources and publications. Unique in the field, the GHS Index provides a comprehensive assessment of countries’ health security and considers the broader context for biological risks within each country, including a country’s geopolitical considerations and health system and whether it has tested its capacities to contain outbreaks.

Knowing the risks, however, is not enough. Political will is needed to protect people from the consequences of epidemics, to take action to save lives, and to build a safer and more secure world.


It is likely that the world will continue to face outbreaks that most countries are ill positioned to combat. In addition to climate change and urbanization, international mass displacement and migration—now happening in nearly every corner of the world—create ideal conditions for the emergence and spread of pathogens. Countries also face an increased potential threat of accidental or deliberate release of a deadly engineered pathogen, which could cause even greater harm than a naturally occurring pandemic. The same scientific advances that help fight epidemic disease also have allowed pathogens to be engineered or recreated in laboratories. Meanwhile, disparities in capacity and inattention to biological threats among some leaders have exacerbated preparedness gaps. The GHS Index seeks to illuminate those gaps to increase both political will and financing to fill them at the national and international levels. Unfortunately, political will for accelerating health security is caught in a perpetual cycle of panic and neglect. Over the past two decades, decision makers have only sporadically focused on health security, despite concerns stemming from the 2001 anthrax attacks, the emergence of the Severe Acute Respiratory Syndrome and Middle East Respiratory Syndrome coronaviruses, and the looming threat of a pandemic caused by a novel strain of influenza.

In September 2014, the United Nations (UN) Security Council met in crisis over the growing Ebola epidemic in West Africa. Massive global assistance was needed to stop the outbreak because of insufficient national capacities in Guinea, Liberia, and Sierra Leone to quickly detect and respond to the epidemic.

As a result, the West Africa Ebola epidemic killed at least 10,000 people and infected more than 28,000.5 The three affected countries lost $2.8 billion in combined GDP, and a massive global response totaled billions of dollars before the outbreak was contained. The crisis awakened the world to the reality that pathogens can emerge unexpectedly, and when outbreaks occur in countries that are unprepared, they can spill beyond borders, threatening the peace, health, and prosperity of all countries.
However, despite newly available vaccines and therapies, response to the Ebola outbreak that began in 2018 in eastern Democratic Republic of Congo has been hampered by violence and instability, community resistance to outbreak mitigation measures, hospital transmission, delays in detection and isolation, and lack of funding and resources.

Delays in the global response to Ebola in 2014 led to a restructuring of the WHO and prompted calls for measurement and transparent reporting of countries’ public health capacities, including the launch of the voluntary WHO IHR Joint External Evaluations (JEEs). Since then, health, policy, and security leaders have developed numerous high-level reviews and recommended ways to identify, finance, and fill major preparedness gaps. These recommendations are relevant for epidemic threats, such as Ebola, and high-consequence pandemic threats, such as a fast-spreading respiratory disease agent that could have a geographic scope, severity, or societal impact and could overwhelm national or international capacity to manage it.6 Some of those recommendations have been implemented, but many have been shelved owing in part to lack of financing. Nearly all recommendations pointed to a need to better understand and measure—on a transparent, global, and recurring basis—the state of international capability for preventing, detecting, and rapidly responding to epidemic and pandemic threats.

The GHS Index is designed to meet this need.


The NTI, JHU, and EIU project team—with generous grants from the Open Philanthropy Project, the Bill & Melinda Gates Foundation, and the Robertson Foundation—worked with an international advisory panel of 21 experts from 13 countries to create a detailed and comprehensive framework of 140 questions, organized across 6 categories, 34 indicators, and 85 subindicators to assess a country’s capability to prevent and mitigate epidemics and pandemics.

The GHS Index relies entirely on open-source information: data that a country has published on its own or has reported to or been reported by an international entity. The GHS Index was created in this way with a firm belief that all countries are safer and more secure when their populations are able to access information about their country’s existing capacities and plans and when countries understand each other’s gaps in epidemic and pandemic preparedness so they can take concrete steps to finance and fill them. The indicators and questions that compose the GHS Index framework also prioritize analysis of health security capacity in the context of a country’s broader national health system and other national risk factors.

The 140 GHS Index questions are organized across six categories:

1. PREVENTION: Prevention of the emergence or release of pathogens

2. DETECTION AND REPORTING: Early detection and reporting for epidemics of potential international concern

3. RAPID RESPONSE: Rapid response to and mitigation of the spread of an epidemic

4. HEALTH SYSTEM: Sufficient and robust health system to treat the sick and protect health workers

5. COMPLIANCE WITH INTERNATIONAL NORMS: Commitments to improving national capacity, financing plans to address gaps, and adhering to global norms

6. RISK ENVIRONMENT: Overall risk environment and country vulnerability to biological threats

Among its 140 questions, the GHS Index prioritizes not only countries’ capacities, but also the existence of functional, tested, proven capabilities for stopping outbreaks at the source. Several questions in the GHS Index are designed to determine not only whether a capacity exists, but also whether that capacity is regularly—for example, annually—tested and shown to be functional in exercises or real-world events.

The GHS Index also includes indicators of nations’ capacities and capabilities to reduce Global Catastrophic Biological Risks (GCBRs), which are biological risks of unprecedented scale that could cause severe damage to human civilization at a global level, potentially undermining civilization’s long-term potential.7 These are events that could wipe out gains in sustainable development and global health because of their potential to cause national and regional instability, global economic consequences, and widespread morbidity and mortality.


This report summarizes the results of the first GHS Index, including overall findings about the state of national health security capacity across each of the six GHS Index categories, as well as additional findings specific to functional areas of epidemic and pandemic preparedness. The full report also offers 33 recommendations to address gaps identified by the GHS Index. All the findings and recommendations are summarized on pages 12–15 and described in detail throughout the full report, which begins on page 31.

Whereas every country has a responsibility to understand, track, improve, and sustain national health security, new and increased global biological risks may require approaches that are beyond the control of individual governments and will necessitate international action. Therefore, the recommendations contained in this report are made with the understanding that health security is a collective responsibility, and a robust international health security architecture is required to support countries at increased risk. As a result, in addition to the many recommendations intended for national leaders, the GHS Index also includes recommendations aimed at decision makers within the UN system, international organizations, donor governments, philanthropies, and the private sector. These are especially important in the case of fast-spreading, deliberately caused, or otherwise unusual outbreaks that could rapidly overwhelm the capability of national governments and international responders.

OVERALL FINDING: National health security is fundamentally weak around the world. No country is fully prepared for epidemics or pandemics, and every country has important gaps to address.

The GHS Index analysis finds no country is fully prepared for epidemics or pandemics. Collectively, international preparedness is weak. Many countries do not show evidence of the health security capacities and capabilities that are needed to prevent, detect, and respond to significant infectious disease outbreaks. The average overall GHS Index score among all 195 countries assessed is 40.2 of a possible score of 100. Among the 60 high-income countries, the average GHS Index score is 51.9. In addition, 116 high- and middle-income countries do not score above 50. Overall, the GHS Index finds severe weaknesses in country abilities to prevent, detect, and respond to health emergencies; severe gaps in health systems; vulnerabilities to political, socioeconomic, and environmental risks that can confound outbreak preparedness and response; and a lack of adherence to international norms.

Specific scores for the GHS Index categories are as follows:

PREVENTION: Fewer than 7% of countries score in the highest tier8 for the ability to prevent the emergence or release of pathogens.

DETECTION AND REPORTING: Only 19% of countries receive top marks for detection and reporting.

RAPID RESPONSE: Fewer than 5% of countries scored in the highest tier for their ability to rapidly respond to and mitigate the spread of an epidemic.

HEALTH SYSTEM: The average score for health system indicators is 26.4 of 100, making it the lowest-scoring category.

COMPLIANCE WITH INTERNATIONAL NORMS: Less than half of countries have submitted Confidence-Building Measures under the Biological Weapons Convention (BWC) in the past three years, an indication of their ability to adhere to important international norms and commitments related to biological threats.

RISK ENVIRONMENT: Only 23% of countries score in the top tier for indicators related to their political system and government effectiveness.



1. As of April 16, 2013, there are 196 States Parties to the World Health Organization (WHO) 2005 International Health Regulations (IHR), including the Holy See. The Holy See is a sovereign juridical entity under international law, but it was not included in the country-specific research for this Index in light of the Holy See’s lack of an independent health system. This report will refer to the assessed “States Parties” as “195 countries.”

2. The WHO IHR (2005) is the foundational international standards for health. The IHR (2005) is a binding legal instrument to address cross-border public health risks. The goal of the IHR (2005) is to prevent, protect, control, and respond without disrupting international trade and traffic. The IHR (2005) provided the guiding regulations behind many of the indicators included in the GHS Index.

3. High-consequence biological events are defined here as infectious disease outbreaks that could overwhelm national or international capacity to manage them. For example, although international health security has improved following the 2014–2016 Ebola epidemic in West Africa, countries and international responders are not prepared to quell outbreaks that occur in violent or insecure settings; deliberate biological events that require close coordination and investigative links between security, health, and humanitarian actors; and fast-moving respiratory diseases with high mortality that could spread rapidly to become global pandemics.

4. Global Catastrophic Biological Risks are biological risks of unprecedented scale that could cause severe damage to human civilization at a global level, potentially undermining its long-term potential. See Nick Alexopoulos, “Center for Health Security Publishes First Working Definition of Global Catastrophic Biological Risks,” Johns Hopkins Center for Health Security, July 27, 2017, http://www.centerforhealthsecurity.org/ ... ition.html.

5. Centers for Disease Control and Prevention, “2014–2016 Ebola Outbreak in West Africa,” http://www.cdc.gov/vhf/ebola/history/20 ... index.html.

6 United Nations General Assembly, “Protecting humanity from future health crises: Report of the High-level Panel on the Global Response to Health Crises,” https://www.un.org/ga/search/view_doc.a ... l=A/70/723.

7. Monica Schoch-Spana et al.,“Global Catastrophic Biological Risks: Toward a Working Definition,” Health Security 15, no. 4 (2017): 323–28, http://www.liebertpub.com/doi/full/10.1089/hs.2017.0038.

8 The GHS Index scoring system includes three tiers. Countries that score between 0 and 33.3 are in the bottom tier (also called “low scores”), countries that score between 33.4 and 66.6 are in the middle tier (also called “moderate scores”), and countries that score between 66.7 and 100 are in the upper or “top” tier (also called “high scores”)

-- 2019 Global Health Security Index: Building Collective Action and Accountability, by Nuclear Threat Initiative, Center for Health Security, Johns Hopkins Bloomberg School of Public Health, and The Economist Intelligence Unit

The media, normally so enamoured of controversy, has largely declined even to debate the possibility of a laboratory escape. Many news sites have simply labelled it a conspiracy theory.

For decades, Dr. Daniel R. Lucey, an infectious disease specialist at Georgetown University, has crisscrossed the globe to study epidemics and their origins. His attention now is on the Covid-19 pandemic, which first came to public notice late last year in Wuhan, China. Its exact beginnings are sufficiently clouded that the World Health Organization has begun a wide inquiry into its roots. The advance team is to leave for China this weekend, and Dr. Lucey has publicly encouraged the health agency to address what he considers eight top questions....

The sixth and seventh questions go to whether the deadly pathogen leapt to humans from a laboratory. Although some intelligence analysts and scientists have entertained that scenario, no direct evidence has come to light suggesting that the coronavirus escaped from one of Wuhan’s labs.

Even so, given the wet market’s downgrading in the investigation, “It is important to address questions about any potential laboratory source of the virus, whether in Wuhan or elsewhere,” Dr. Lucey wrote in his blog post.

To that end, he urges the W.H.O. investigators to look for any signs of “gain of function” research — the deliberate enhancement of pathogens to make them more dangerous. The technique is highly contentious. Critics question its merits and warn that it could lead to catastrophic lab leaks. Proponents see it as a legitimate way to learn how viruses and other infectious organisms might evolve to infect and kill people, and thus help in devising new protections and precautions.

Debate over its wisdom erupted in 2011 after researchers announced success in making the highly lethal H5N1 strain of avian flu easily transmissible through the air between ferrets, at least in the laboratory.

Prompted by controversy over dangerous research and recent laboratory accidents, the White House announced Friday that it would temporarily halt all new funding for experiments that seek to study certain infectious agents by making them more dangerous.

It also encouraged scientists involved in such research on the influenza, SARS and MERS viruses to voluntarily pause their work while its risks were reassessed.

Opponents of this type of research, called gain of function — for example, attempts to create a more contagious version of the lethal H5N1 avian influenza to learn which mutations made it that way — were elated.

“Brilliant!” said Peter Hale, the executive director of the Foundation for Vaccine Research, which opposes such experiments. “The government has finally seen the light. This is what we have all been waiting for and campaigning for. I shall sleep better tonight.”

The announcement, which was made by the White House Office of Science and Technology Policy and the Department of Health and Human Services, did not say how long the moratorium would last. It said a “deliberative process to assess the potential risks and benefits” would begin this month and stretch at least into next year.

The move appeared to be a sudden change of heart by the Obama administration, which last month issued regulations calling for more stringent federal oversight of such research and requiring scientists and universities to disclose that their work might be risky, rather than expecting federal agencies to notice.

Critics at the time dismissed those rules as too weak.

The moratorium is only on research on influenza virus and the coronaviruses that cause SARS and MERS. It made no mention of Ebola or any related filovirus. Ebola is already extremely lethal, but it is not easily transmissible.

No scientist has publicly announced an attempt to make Ebola as easy to transmit with a sneeze as flu is. Given the current panic around Ebola, and congressional anger at federal health agencies, it is unlikely that federal funding for such a project would be given out.

The debate over the wisdom of “gain of function” research erupted in 2011 when the labs of Ron Fouchier of Erasmus University in the Netherlands, and Yoshihiro Kawaoka of the University of Wisconsin-Madison, separately announced that they had succeeded in making the lethal H5N1 avian flu easily transmissible between ferrets, which are a model for human susceptibility to flu.

The debate heated up further this year when the Centers for Disease Control and Prevention admitted it had suffered laboratory accidents that exposed dozens of workers to anthrax and shipped deadly avian flu virus to another federal lab that had asked for a more benign flu strain. Also this year, vials of smallpox that had been forgotten for 50 years were found in a lab at the National Institutes of Health.

The White House said the moratorium decision had been made “following recent biosafety incidents at federal research facilities.”

Dr. Kawaoka said he would not start any new gain-of-function experiments and would consult with the N.I.H. about which ones he had underway that met their criteria for the moratorium.

Many scientists were furious that such work had been permitted and even supported with American tax dollars. But others argued that it was necessary to learn which genetic mutations make viruses more dangerous. If those mutations began appearing naturally as the viruses circulated in animals and people, warnings could be issued and vaccines designed, they said.

Some scientists argued that the two scientists should not be permitted to publish all the details of their experiments, for fear that terrorists or unscrupulous scientists would duplicate them and start a fatal pandemic.

Others, like Richard H. Ebright, a molecular biologist and bioweapons expert at Rutgers University, argued that the long history of accidental releases of infectious agents from research labs made such work extremely risky and unwise to perform in the first place.

Dr. Ebright called Friday’s announcement “an important, albeit overdue, step.”

Michael T. Osterholm, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, called the moratorium “a wise move — I congratulate the U.S. government on taking this step.”

The new policy had to be announced now, he explained, because the National Science Advisory Board for Biosecurity is to meet later this month. It will have 11 new members, and gain of function research is a principal agenda item.

Dr. Osterholm was one of 11 previous members who were removed from the board in the middle of the controversy.

All, like him, had been on it many years past their original five-year appointments and were due to be replaced, but had routinely been asked to stay, he said.

In April, he was the author of a letter to the National Institutes of Health complaining about government pressure on the advisory board. The institutes gave grants to support gain of function work.

The explanation given was that they had outlasted their tenures, but Dr. Osterholm said that “in the same week as the anthrax accident at the C.D.C., we all got an email on a Sunday night from a junior staffer telling us we were out.”

He called that a public relations failure: “P.R. zero point zero.”

-- White House to Cut Funding for Risky Biological Study, by Donald G. McNeil Jr., NYT, Oct. 17, 2014

In his blog, Dr. Lucey asks “what, if any,” gain-of-function studies were done on coronaviruses in Wuhan, elsewhere in China, or in collaboration with foreign laboratories.

“If done well scientifically, then this investigation should allay persistent concerns about the origin of this virus,” he wrote. “It could also help set an improved standard for investigating and stopping the awful viruses, and other pathogens, in the decades ahead.”

Finally, Dr. Lucey asks the W.H.O. team to learn more about China’s main influenza research lab, a high-security facility in Harbin, the capital of China’s northernmost province. In May, he notes, a Chinese paper in the journal Science reported that two virus samples from Wuhan were studied there in great detail early this year, including in a variety of animals. It reported that cats and ferrets were highly susceptible to the pathogen; dogs were only mildly susceptible; and pigs, chickens and ducks were not susceptible at all.

-- 8 Questions From a Disease Detective on the Pandemic’s Origins: Dr. Daniel R. Lucey wants answers to pointed questions that bear on how the coronavirus leapt from bats to humans, by William J. Broad, NYT, July 8, 2020

The principal reason for media dismissals of the lab origin possibility is a review paper in Nature Medicine (Andersen et al., 2020). Although by Jun 29, 2020 this review had almost 700 citations it also has major scientific shortcomings. These flaws are worth understanding in their own right but they are also useful background for understanding the implications of the Master’s thesis.

An influential paper was published in Nature Medicine on 17 March 2020. Andersen et al observed that several mutations have occurred in the receptor binding domain of SARS-CoV-2. These, they suggested, therefore sustain an hypothesis of natural evolution (Andersen et al., 2020). We do not agree. We do agree that it is indeed correct that several such mutations are to be seen and in a forthcoming companion article to this one, about three other viruses of interest, we will discuss further Andersen et al's evidence and argumentation in that context. But here we observe only that the contention that it is improbable that Covid-19 emerged through laboratory manipulation of a related SARS-CoV-like coronavirus because the ACE2 binding is not ideal is weakened because Andersen et al cite two authorities which actually say the reverse of what they say that they say.

Wan et al are cited by Andersen et al but offer them no support (Wan et al., 2020). Wan et al say, correctly in our view, that computational structural modelling of complex virus-receptor interactions can be used for structural predictions and that such models can potentially be used for Gain-Of-Function modelling. It is well known that models have been developed from data generated in animal model systems such as the palm civet. Wan et al say that the SARS-CoV-2 binding to the ACE2 receptor confirms the accuracy of the structural predictions. Therefore the data and conclusion in Wan et al contradicts Andersen et al's opinion that it is improbable that the virus could have emerged through laboratory manipulation.

There is a similar problem with (Sheahan et al., 2008). This deals with research on a civet strain SZ16 and the infective strain SARS-CoV Urbani. These strains were used to create a chimeric virus icSZ16-S. Sheahan et al go on to explain that by in vitro evolution of the chimeric virus icSZ16-S on human airway epithelial (HAE) cells in the lab, they have been able to produce two new viruses binding to such HAE cells. Therefore this reference supports the very opposite of the Andersen et al hypothesis. We are immediately wary of any paper containing such egregious errors.

-- The Evidence which Suggests that This Is No Naturally Evolved Virus: A Reconstructed Historical Aetiology of the SARS-CoV-2 Spike, by Birger Sørensen, Angus Dalgleish & Andres Susrud

The Nature Paper vs. the Lab-Made Hypothesis

But didn’t that Nature article refute the lab-made hypothesis? No, not really. There is no irrefutable evidence against it in the paper, just a loud “we don’t believe so” based on a shaky foundation. Judge for yourself — here are the authors’ key arguments in support of their conclusions:

While the analyses above suggest that SARS-CoV-2 may bind human ACE2 with high affinity, computational analyses predict that the interaction is not ideal and that the RBD sequence is different from those shown in SARS-CoV to be optimal for receptor binding. Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.

In the original paper, the quoted sentences are just below the diagram showing identical RBMs between CoV2 and pangolin-2019. So I am puzzled as to what “computational analysis” has to do with anything. Obviously, the most likely scenario for the lab-made hypothesis is the transfer of RBM from one strain to another — which virologists have done many times before. Therefore, the author’s chain of arguments does not make sense: “computer says binding is not ideal, thus CoV2 must be the result of natural selection. Ergo, this is strong evidence that CoV2 is not lab-made.” Wait, just because CoV2 differs from some “optimal” virus, doesn’t mean it could not have been created in a lab. Not the lab trying to create “optimal” bioweapons, but a lab creating chimeras of naturally found strains, say, in bats and pangolins.

The authors continue to surprise:

Furthermore, if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used. However, the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone.

Again, the same questionable logic dressed in categorical adjectives: “genetic analysis irrefutably proves that CoV2 was not created on the basis of previously known strains!” Well thanks, Captain Obvious. But why couldn’t potential creators of CoV2 make a cDNA backbone from unpublished strains related to or even derived from RaTG13? Then they could easily insert the pangolin RBM into it, as well as add a furin site (or maybe the cDNA backbone already had one). Virologists have been doing things like this for 20 years, and modern genetic engineering tools make such manipulations accessible even to a grad student.

As for the chances of the furin site arising in cell culture, the authors also express strange ideas:

The acquisition of both the polybasic cleavage site and predicted O-linked glycans also argues against culture-based scenarios. New polybasic cleavage sites have been observed only after prolonged passage of low-pathogenicity avian influenza virus in vitro or in vivo. Furthermore, a hypothetical generation of SARS-CoV-2 by cell culture or animal passage would have required prior isolation of a progenitor virus with very high genetic similarity, which has not been described. Subsequent generation of a polybasic cleavage site would have then required repeated passage in cell culture or animals with ACE2 receptors similar to those of humans, but such work has also not previously been described.

First off, the authors themselves cite previous works where the furin site arose in vitro as viruses were cultured in cells. And second, what do they mean, a strain with high genetic similarity has not been described — what about RaTG13? If it had its RBM replaced by one from the pangolin strain, and then the chimeric strain was cultured in vitro, then the furin site could well have arisen in this matter. Additionally, the new strain could thus acquire other mutations that distinguish CoV2 from RaTG13 and pangolin-2019.

But in terms of the potential lab-based origin of the furin site, I am more inclined to hypothesize a specific insertion — as in the Beijing paper from October 2019 with chicken coronavirus. After that, the synthetic strain could have acquired new mutations by subsequent culturing in vitro or in vivo — like the MA15 murine strain in 2007, for example. Or maybe even using the same mouse model with humanized lung tissues and immune system that was created at UNC by Baric’s and other groups in 2018, in which they reported testing several viruses including MERS:

The human innate and adaptive immune system of BLT-L mice

We generated an in vivo model with human lung implants and an autologous human immune system by constructing BLT mice with autologous human lung implants (BLT-L humanized mice).

Finally, even if CoV2 is the product of selection rather than intelligent design, that does not rule out a lab leak either — selection can happen in the lab just as well, both natural and artificial kinds. Different strains can recombine in research animals or in vitro by design or by chance.

-- Lab-Made? SARS-CoV-2 Genealogy Through the Lens of Gain-of-Function Research, by Yuri Deigin

Andersen et al., a critique

The question of the origin of the COVID-19 pandemic is, in outline, simple. There are two incontrovertible facts. One, the disease is caused by a human viral pathogen, SARS-CoV-2, first identified in Wuhan in December 2019 and whose RNA genome sequence is known. Second, all of its nearest known relatives come from bats. Beyond any reasonable doubt SARS-CoV-2 evolved from an ancestral bat virus. The task the Nature Medicine authors set for themselves was to establish the relative merits of each of the various possible routes (lab vs natural) by which a bat coronavirus might have jumped to humans and in the same process have acquired an unusual furin site and a spike protein having very high affinity for the human ACE2 receptor.

When Andersen et al. outline a natural zoonotic pathway they speculate extensively about how the leap might have occurred. In particular they elaborate on a proposed residence in intermediate animals, likely pangolins. For example, “The presence in pangolins of an RBD [Receptor Binding Domain] very similar to that of SARS-CoV-2 means that we can infer that this was probably in the virus that jumped to humans. This leaves the insertion of [a] polybasic cleavage site to occur during human-to-human transmission.” This viral evolution occurred in “Malayan pangolins illegally imported into Guangdong province”. Even with these speculations there are major gaps in this theory. For example, why is the virus so well adapted to humans? Why Wuhan, which is 1,000 Km from Guangdong? (See map).

china province guide

The authors provide no such speculations in favour of the lab accident thesis, only speculation against it:

“Finally, the generation of the predicted O-linked glycans is also unlikely to have occurred due to cell-culture passage, as such features suggest the involvement of an immune system.” (italics added).

[Passaging is the deliberate placing of live viruses into cells or organisms to which they are NOT adapted for the purpose of making them adapted, i.e. speeding up their evolution.]

It is also noteworthy that the Andersen authors set a higher hurdle for the lab thesis than the zoonotic thesis. In their account, the lab thesis is required to explain all of the evolution of SARS-CoV-2 from its presumed bat viral ancestor, whereas under their telling of the zoonotic thesis the key step of the addition of the furin site is allowed to happen in humans and is thus effectively unexplained.

A further imbalance is that key information needed to judge the merits of a lab origin theory is missing from their account. As we detailed in our previous article, in their search for SARS-like viruses with zoonotic spillover potential, researchers at the WIV have passaged live bat viruses in monkey and human cells (Wang et al., 2019). They have also performed many recombinant experiments with diverse bat coronaviruses (Ge et al., 2013; Menachery et al., 2015; Hu et al., 2017). Such experiments have generated international concern over the possible creation of potential pandemic viruses (Lipsitch, 2018). As we showed too, the Shi lab had also won a grant to extend that work to whole live animals. They planned “virus infection experiments across a range of cell cultures from different species and humanized mice” with recombinant bat coronaviruses. Yet Andersen et al did not discuss this research at all, except to say:

“Basic research involving passage of bat SARS-CoV-like coronaviruses in cell culture and/or animal models has been ongoing for many years in biosafety level 2 laboratories across the world”

This statement is fundamentally misleading about the kind of research performed at the Shi lab.

A further important oversight by the Andersen authors concerns the history of lab outbreaks of viral pathogens. They write: “there are documented instances of laboratory escapes of SARS-CoV”. This is a rather matter-of-fact allusion to the fact that since 2003 there have been six documented outbreaks of SARS from labs, not all in China, with some leading to fatalities (Furmanski, 2014).

Andersen et al might have also have noted that two major human pandemics are widely accepted to have been caused by lab outbreaks of viral pathogens, H1N1 in 1977 and Venezuelan Equine Encephalitis (summarised in Furmanski, 2014). Andersen could even have noted that literally hundreds of lab accidents with viruses have resulted in near-misses or very localised outbreaks (summarised by Lynn Klotz and Sam Husseini and also Weiss et al., 2015).

Also unmentioned were instances where a lab outbreak of an experimental or engineered virus has been plausibly theorised but remains uninvestigated. For example, the most coherent explanation for the H1N1 variant ‘swine flu’ pandemic of 2009/10 that resulted in a death toll estimated by some as high as 200,000 (Duggal et al., 2016; Simonsen et al. 2013), is that a vaccine was improperly inactivated by its maker (Gibbs et al., 2009). If so, H1N1 emerged from a lab not once but twice.

Given that human and livestock viral outbreaks have frequently come from laboratories and that many scientists have warned of probable lab escapes (Lipsitch and Galvani, 2014), and that the WIV [Wuhan Institute of Virology] itself has a questionable biosafety record, the Andersen paper is not an even-handed treatment of the possible origins of the COVID-19 virus.

This chapter makes the case against performing exceptionally dangerous gain-of-function experiments that are designed to create potentially pandemic and novel strains of influenza, for example, by enhancing the airborne transmissibility in mammals of highly virulent avian influenza strains. This is a question of intense debate over the last 5 years, though the history of such experiments goes back at least to the synthesis of viable influenza A H1N1 (1918) based on material preserved from the 1918 pandemic. This chapter makes the case that experiments to create potential pandemic pathogens (PPPs) are nearly unique in that they present biosafety risks that extend well beyond the experimenter or laboratory performing them; an accidental release could, as the name suggests, lead to global spread of a virulent virus, a biosafety incident on a scale never before seen. In such cases, biosafety considerations should be uppermost in the consideration of alternative approaches to experimental objectives and design, rather than being settled after the fact, as is appropriately done for most research involving pathogens. The extensive recent discussion of the magnitude of risks from such experiments is briefly reviewed. The chapter argues that, while there are indisputably certain questions that can be answered only by gain-of-function experiments in highly pathogenic strains, these questions are narrow and unlikely to meaningfully advance public health goals such as vaccine production and pandemic prediction. Alternative approaches to experimental influenza virology and characterization of existing strains are in general completely safe, higher throughput, more generalizable, and less costly than creation of PPP in the laboratory and can thereby better inform public health. Indeed, virtually every finding of recent PPP experiments that has been cited for its public health value was predated by similar findings using safe methodologies. The chapter concludes that the unique scientific and public health value of PPP experiments is inadequate to justify the unique risks they entail and that researchers would be well-advised to turn their talents to other methodologies that will be safe and more rewarding scientifically.

-- Why Do Exceptionally Dangerous Gain-of-Function Experiments in Influenza?, by Marc Lipsitch

Yet its text expresses some strong opinions: “Our analyses clearly show that SARS-CoV-2 is not a laboratory construct or a purposefully manipulated virus….It is improbable that SARS-CoV-2 emerged through laboratory manipulation of a related SARS-CoV-like coronavirus…..the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used backbone….the evidence shows that SARS-CoV2 is not a purposefully manipulated virus….we do not believe that any type of laboratory-based scenario is possible.” (Andersen et al., 2020).

It is hard not to conclude that what their paper mostly shows is that Drs. Andersen, Rambaut, Lipkin, Holmes and Garry much prefer the natural zoonotic transfer thesis. Their rhetoric is forthright but the evidence does not support that confidence.

Indeed, since the publication of Andersen et al., important new evidence has emerged that undermines their zoonotic origin theory. On May 26th the Chinese CDC ruled out the Huanan “wet” market in Wuhan as the source of the outbreak. Additionally, new research on pangolins, the favoured intermediate mammal host, suggests they are not a natural reservoir of coronaviruses (Lee et al., 2020; Chan and Zhan, 2020). Furthermore, SARS-CoV-2 was found not to replicate in bat kidney or lung cells (Rhinolophus sinicus), implying that SARS-CoV-2 is not a recently-adapted spill over Chu et al., 2020).

The Mojiang mine and the Master’s thesis

In our own search to resolve the COVID-19 origin question we chose to focus on the provenance of the coronavirus genome sequences BtCoV/4991 and RaTG13, since these are the most closely related sequences to SARS-CoV-2 (98.7% and 96.2% identical respectively). See FIG 1. (reproduced from P. Zhou et al., 2020).

Similarity of SARS-CoV-2 to RaTG13 (blue line) and other coronaviruses (red, green, pink) (Image from Zhou et al., 2020). The higher the line the more similar the virus.

For comparison, the next closest virus to SARS-CoV-2 is RmYN02 (not shown in Fig 1.) (H. Zhou et al., 2020). RmYN02 has an overall similarity to SARS-CoV-2 of 93.2%, making its evolutionary distance from SARS-CoV-2 almost twice as great.

BtCoV/4991 was first described in 2016. It is a 370 nucleotide virus fragment collected from the Mojiang mine in 2013 by the lab of Zeng-li Shi at the WIV [Wuhan Institute of Virology] (Ge et al., 2016). BtCoV/4991 is 100% identical in sequence to one segment of RaTG13. RaTG13 is a complete viral genome sequence (almost 30,000 nucleotides) that was only published in 2020, after the pandemic began (P. Zhou et al., 2020).

Despite the confusion created by their different names, in a letter obtained by us Zheng-li Shi confirmed to a virology database that BtCoV/4991 and RaTG13 are both from the same bat faecal sample and the same mine. They are thus sequences from the same virus.
In the discussion below we will refer primarily to RaTG13 and specify BtCoV/4991 only as necessary.

These specifics are important because it is these samples and their provenance that we believe are ultimately key to unravelling the mystery of the origins of COVID-19.

The story begins in April 2012 when six workers in that same Mojiang mine fell ill from a mystery illness while removing bat faeces. Three of the six subsequently died.

In a March 2020 interview with Scientific American Zeng-li Shi dismissed the significance of these deaths, claiming the miners died of fungal infections. Indeed, no miners or deaths are mentioned in the paper published by the Shi lab documenting the collection of RaTG13 (Ge et al., 2016).

But Shi’s assessment does not tally with any other contemporaneous accounts of the miners and their illness (Rahalkar and Bahulikar, 2020). As these authors have pointed out, Science magazine wrote up part of the incident in 2014 as A New Killer Virus in China?. Science was citing a different team of virologists who found a paramyxovirus in rats from the mine. These virologists told Science they found “no direct relationship between human infection” and their virus. This expedition was later published as the discovery of a new virus called MojV after Mojiang, the locality of the mine (Wu et al., 2014).

What this episode suggests though is that these researchers were looking for a potentially lethal virus and not a lethal fungus. Also searching the Mojiang mine for a [potentially lethal] virus at around the same time was Canping Huang, the author of a PhD thesis carried out under the supervision of George Gao, the head of the Chinese CDC.

All of this begs the question of why the Shi lab, which has no interest in fungi but a great interest in SARS-like bat coronaviruses, also searched the Mojiang mine for bat viruses on four separate occasions between August 2012 and July 2013, even though the mine is a 1,000 Km from Wuhan (Ge et al., 2016). These collecting trips began while some of the miners were still hospitalised.

Fortunately, a detailed account of the miner’s diagnoses and treatments exists. It is found in a Master’s thesis written in Chinese in May 2013. Its suggestive English title is “The Analysis of 6 Patients with Severe Pneumonia Caused by Unknown viruses“.

The original English version of the abstract implicates a SARS-like coronavirus as the probable causative agent and that the mine “had a lot of bats and bats’ feces”.

The findings of the Master’s thesis

To learn more, especially about the reasonableness of this diagnosis, we arranged to have the whole Master’s thesis translated into English and are here making the translation available. To read it in full see the embedded document below (or download it here).

Master's Thesis: "The Analysis of Six Patients With Severe Pneumonia Caused By Unknown Viruses"

The six ill miners were admitted to the No. 1. School of Clinical Medicine, Kunming Medical University, in short succession in late April and early May 2012. Kunming is the capital of Yunnan province and 250 Km from Mojiang.

The Syndromes of the six Mojiang Mine patients

Of the descriptions of the miners and their treatments, which include radiographs and numerous CAT scans, several features stand out:

1) From their admission to the hospital their doctors informed the “medical office” of a potential “outburst of disease” i.e. a potential epidemic outbreak. Thus, the miners were treated for infections and not as if they had inhaled noxious gases or other toxins.

2) The symptoms (on admission) of the six miners were: a) dry cough, b) sputum, c) high fevers, especially shortly before death d) difficulty breathing, e) myalgia (sore limbs). Some patients had hiccoughs and headaches. (See Table 1).

3) Clinical work established that patients 1-4 had low blood oxygen “for sure it was ARDS” (Acute Respiratory Distress Syndrome) and immune damage considered indicative of viral infection.
Additionally, a tendency for thrombosis was noted in patients 2 and 4. Symptom severity and mortality were age-related (though from a sample of 6 this must be considered anecdotal).

4) Potential common and rare causes of their symptoms were tested for and mostly eliminated. For patients 3 and 4 these included tests for HIV, Cytomegalovirus, Epstein-Barr Virus (EBV), Japanese encephalitis, haemorrhagic fever, Dengue, Hepatitis B, SARS, and influenza. Of these, only patient 2 tested positive for Hepatitis and EBV.

5) Treatment of the six patients included ventilation (patients 2-4), steroids (all patients), antivirals (all except patient 5), and blood thinners (patients 2 and 4). Antibiotics and antifungal medications were administered to counter what were considered secondary (but significant) co-infections.

6) A small number of remote meetings were held with researchers at other universities. One was with Zhong Nanshan at Sun Yat-Sen University, Guangdong. Zhong is the Chinese hero of the SARS epidemic, a virologist, and arguably the most famous scientist in China.

7) Samples from the miners were later sent to the WIV in Wuhan and to Zhong Nanshan, further confirming that viral disease was strongly suspected. Some miners did test positive for coronavirus (the thesis is unclear on how many).

8) The source of infection was concluded to be Rhinolophus sinicus, a horseshoe bat and the ultimate conclusion of the thesis reads “the unknown virus lead to severe pneumonia could be: The SARS-like-CoV from the Chinese rufous horseshoe bat.” Thus the miners had a coronavirus but it apparently was not SARS itself.
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Part 2 of 3

The significance of the Master’s thesis

These findings of the thesis are significant in several ways.

First, in the light of the current coronavirus pandemic it is evident the miners’ symptoms very closely resemble those of COVID-19 (Huang et al, 2020; Tay et al., 2020; M. Zhou et al., 2020). Anyone presenting with them today would immediately be assumed to have COVID-19. Likewise, many of the treatments given to the miners have become standard for COVID-19 (Tay et al., 2020).

Second, the remote meeting with Zhong Nanshan is significant. It implies that the illnesses of the six miners were of high concern and, second, that a SARS-like coronavirus was considered a likely cause.

Third, the abstract, the conclusions, and the general inferences to be made from the Master’s thesis contradict Zheng-li Shi’s assertion that the miners died from a fungal infection. Fungal infection as a potential primary cause was raised but largely discarded.

Fourth, if a SARS-like coronavirus was the source of their illness the implication is that it could directly infect human cells. This would be unusual for a bat coronavirus (Ge et al., 2013). People do sometimes get ill from bat faeces but the standard explanation is histoplasmosis, a fungal infection and not a virus (McKinsey and McKinsey, 2011; Pan et al., 2013).

Fifth, the sampling by the Shi lab found that bat coronaviruses were unusually abundant in the mine (Ge at al., 2016). Among their findings were two betacoronaviruses, one of which was RaTG13 (then known as BtCoV/4991). In the coronavirus world betacoronaviruses are special in that both SARS and MERS, the most deadly of all coronaviruses, are both betacoronaviruses. Thus they are considered to have special pandemic potential, as the concluding sentence of the Shi lab publication which found RaTG13 implied: “special attention should particularly be paid to these lineages of coronaviruses” (Ge at al., 2016). In fact, the Shi and other labs have for years been predicting that bat betacoronaviruses like RaTG13 would go pandemic; so to find RaTG13 where the miners fell ill was a scenario in perfect alignment with their expectations.

The Mojiang miners passaging proposal

How does the Master’s thesis inform the search for a plausible origin of the pandemic?

In our previous article we briefly discussed how the pandemic might have been caused either by a virus collection accident, or through viral passaging, or through genetic engineering and a subsequent lab escape. The genetic engineering possibility deserves attention and is extensively assessed in an important preprint (Segreto and Deigin, 2020).

The origin of SARS-CoV-2 is still controversial. Comparative genomic analyses have shown that SARSCoV-2 is likely to be chimeric, most of its sequence being very close to the CoV detected from a bat, whereas its receptor binding domain is almost identical to that of CoV obtained from pangolins. The furin cleavage site in the spike protein of SARS-CoV-2 was previously not identified in other SARS-like CoVs and might have conferred the ability to cross species and tissue barriers. Chimeric viruses can be the product of natural recombination or genetic manipulation. The latter could have aimed to identify pangolins as possible intermediate hosts for bat-CoV potentially pathogenic for humans. Theories that consider a possible artificial origin for SARS-CoV-2 are censored as they seem to support conspiracy theories. Researchers have the responsibility to carry out a thorough analysis, beyond any personal research interests, of all possible causes for SARS-CoV-2 emergence for preventing this from happening in the future.

Several months have passed since the outbreak of SARS-CoV-2 in Wuhan, China, and its origin is still controversial. The theory that the Wuhan’s Huanan Seafood Wholesale Market was the first source for animal–human virus transmission has lost credibility. During the first phase of the epidemic in Wuhan, several hospitalized patients with confirmed SARS-CoV-2 infections had no link with the market.1 Unfortunately, the market was quickly closed and sanitized before enough animal samples could have been collected; the few market samples that did get collected exhibit only human-adapted SARS-CoV-2 and no traces of zoonotic predecessor strains.2

-- Is Considering a Genetic-Manipulation Origin for SARS-CoV-2 a Conspiracy Theory That Must Be Censored?, by Rossana Segreto, University of Innsbruck, and Yuri Deigrin, Youthereum Genetics Inc.

We do not definitively rule out these possibilities. Indeed it now seems that the Shi lab at the WIV did not forget about RaTG13 but were sequencing its genome in 2017 and 2018. However, we believe that the Master’s thesis indicates a much simpler explanation.

We suggest, first, that inside the miners RaTG13 (or a very similar virus) evolved into SARS-CoV-2, an unusually pathogenic coronavirus highly adapted to humans. Second, that the Shi lab used medical samples taken from the miners and sent to them by Kunming University Hospital for their research. It was this human-adapted virus, now known as SARS-CoV-2­, that escaped from the WIV in 2019.

We refer to this COVID-19 origin hypothesis as the Mojiang Miners Passage (MMP) hypothesis.

Passaging is a standard virological technique for adapting viruses to new species, tissues, or cell types. It is normally done by deliberately infecting a new host species or a new host cell type with a high dose of virus. This initial viral infection would ordinarily die out because the host’s immune system vanquishes the ill-adapted virus. But, in passaging, before it does die out a sample is extracted and transferred to a new identical tissue, where viral infection restarts. Done iteratively, this technique (called “serial passaging” or just “passaging”) intensively selects for viruses adapted to the new host or cell type (Herfst et al., 2012).

At first glance RaTG13 is unlikely to have evolved into SARS-CoV-2 since RaTG13 is approximately 1,200 nucleotides (3.8%) different from SARS-CoV-2. Although RaTG13 is the most closely related virus to SARS-CoV-2, this sequence difference still represents a considerable gap. In a media statement evolutionary virologist Edward Holmes has suggested this gap represents 20-50 years of evolution and others have suggested similar figures.

We agree that ordinary rates of evolution would not allow RaTG13 to evolve into SARS-CoV-2 but we also believe that conditions inside the lungs of the miners were far from ordinary. Five major factors specific to the hospitalised miners favoured a very high rate of evolution inside them.

i) When viruses infect new species they typically undergo a period of very rapid evolution because the selection pressure on the invading pathogen is high. The phenomenon of rapid evolution in new hosts is well attested among corona- and other viruses
(Makino et al., 1986; Baric et al., 1997; Dudas and Rambaut 2016; Forni et al., 2017).

ii) Judging by their clinical symptoms such as the CT scans, all the miner’s infections were primarily of the lungs. This localisation likely occurred initially because the miners were exerting themselves and therefore inhaling the disturbed bat guano deeply. As miners, they may already have had damaged lung tissues (patient 3 had suspected pneumoconiosis) and/or particulate matter was present that irritated the tissues and may have facilitated initial viral entry.

In contrast, standard coronavirus infections are confined to the throat and upper respiratory tract. They do not normally reach the lungs (Perlman and Netland, 2009). Lungs are far larger tissues by weight (kilos vs grammes) than the upper respiratory tract. There was therefore likely a much larger quantity of virus inside the miners than would be the case in an ordinary coronavirus infection.

Comparing a typical coronavirus respiratory tract infection with the extent of infected lungs in the miners from a purely mathematical point of view indicates the potential scale of this quantitative difference. The human aerodigestive tract is approximately 20cm in length and 5cm in circumference, i.e. approximately 100 cm2 in surface area. The surface area of a human lung ranges from 260,000-680,000 cm2(Hasleton, 1972). The amount of potentially infected tissue in an average lung is therefore approximately 4500-fold greater than that available to a normal coronavirus infection. The amount of virus present in the infected miners, sufficient to hospitalise all of them and kill half of them, was thus proportionately very large.

Evolutionary change is in large part a function of the population size. The lungs of the miners, we suggest, supported a very high viral load leading to proportionately rapid viral evolution.

Furthermore, according to the Master’s thesis, the immune systems of the miners were compromised and remained so even for those discharged. This weakness on the part of the miners may also have encouraged evolution of the virus.

iii) The length of infection experienced by the miners (especially patients 2, 3 and 4) far exceeded that of an ordinary coronavirus infection. From first becoming too sick to work in the mine, patient 2 survived 57 days until he died. Patient 3 survived 120 days after stopping work. Patient 4 survived 117 days and then was discharged as cured. Each had been exposed in the mine for 14 days prior to the onset of severe symptoms; thus each presumably had nascent infections for some time before calling in sick (See Table 2 of the thesis).

In contrast, in ordinary coronavirus infections the viral infection is cleared within about ten to fourteen days after being acquired (Tay et al., 2020). Thus, unlike most sufferers from coronavirus infection, the hospitalised miners had very long-term bouts of disease characterised by a continuous high load of virus. In the cases of patients 3 and 4 their illnesses lasted over 4 months.

iv) Coronaviruses are well known to recombine at very high rates: 10% of all progeny in a cell can be recombinants (Makino et al., 1986; Banner and Lai, 1991; Dudas and Rambaut, 2016). In normal virus evolution the mutation rate and the selection pressure are the main foci of attention. But in the case of a coronavirus adapting to a new host where many mutations distributed all over the genome are required to fully adapt to the new host, the recombination rate is likely to be highly influential in determining the overall speed of adaptation by the virus population (Baric et al., 1997).

Inside the miners a large tissue was simultaneously infected by a population of poorly-adapted viruses, with each therefore under pressure to adapt. Even if the starting population of virus lacked any diversity, many individual viruses would have acquired mutations independently but only recombination would have allowed these mutations to unite in the same genome. To recombine, viruses must be present in the same cell. In such a situation the particularities of lung tissues become potentially important because the existence of airways (bronchial tubes, etc.) allows partially-adapted viruses from independent viral populations to travel to distal parts of the lung (or even the other lung) and encounter other such partially-adapted viruses and populations. This movement around the lungs would likely have resulted in what amounted to a passaging effect without the need for a researcher to infect new tissues. Indeed, in the Master’s thesis the observation is several times made that areas of the lungs of a specific patient would appear to heal even while other parts of the lungs would become infected.

v) There were also a number of unusual things about the bat coronaviruses in the mine. They were abnormally abundant but also there were many different kinds, often causing co-infections of the bats (Ge et al., 2016). Viral co-infections are often more infectious or more pathogenic (Latham and Wilson, 2007).

As the WIV researchers remarked about the bats in the mine:

“we observed a high rate of co-infection with two coronavirus species and interspecies infection with the same coronavirus species within or across bat families. These phenomena may be owing to the diversity and high density of bat populations in the same cave, facilitating coronavirus intra- and interspecies transmissions, which may result in recombination and acceleration of coronavirus evolution.” (Ge et al., 2016).

The diversity of coronaviruses in the mine suggests that the miners were similarly exposed and that their illness may potentially have begun as co-infections.

Combining these observations, we propose that the miners’ lungs offered an unprecedented opportunity for accelerated evolution of a highly bat-adapted coronavirus into a highly human-adapted coronavirus and that decades of ordinary coronavirus evolution could easily have been condensed into months. However, we acknowledge that these conditions were unique.
They and their scale have no exact scientific precedent we can refer to and they would be hard to replicate in a lab; thus it is important to emphasize that our proposal is fully consistent with the underlying principles of viral evolution as understood today.

In support of the MMP theory we also know something about the samples taken from the miners. According to the Master’s thesis, samples were taken from patients for “scientific research” and blood samples (at least) were sent to the WIV.

“In the later stage we worked with Dr. Zhong Nan Shan and did some sampling. The patient* tested positive for serum IgM by the WuHan Institute of Virology. It suggested the existence of virus infection” (p62 in the section “Comprehensive Analysis”.)

(*The original does not specify the number of patients tested.)

The Master’s thesis also states its regret that no samples for research were taken from patients 1 and 2, implying that samples were taken from all the others.

We further know that, on June 27th, 2012, the doctors performed an unexplained thymectomy on patient 4. The thymus is an immune organ that can potentially be removed without greatly harming the patient and it could have contained large quantities of virus. Beyond this the Master’s thesis is unfortunately unclear on the specifics of what sampling was done, for what purpose, and where each particular sample went.

Given the interests of the Shi lab in zoonotic origins of human disease, once such a sample was sent to them, it would have been obvious and straightforward for them to investigate how a virus from bats had managed to infect these miners. Any viruses recoverable from the miners would likely have been viewed by them as a unique natural experiment in human passaging offering unprecedented and otherwise-impossible-to-obtain insights into how bat coronaviruses can adapt to humans.

The logical course of such research would be to sequence viral RNA extracted directly from unfrozen tissue or blood samples and/or to generate live infectious clones for which it would be useful (if not imperative) to amplify the virus by placing it in human cell culture. Either technique could have led to accidental infection of a lab researcher.

Our supposition as to why there was a time lag between sample collection (in 2012/2013) and the COVID-19 outbreak is that the researchers were awaiting BSL-4 lab construction and certification, which was underway in 2013 but delayed until 2018.

We propose that, when frozen samples derived from the miners were eventually opened in the Wuhan lab they were already highly adapted to humans to an extent possibly not anticipated by the researchers. One small mistake or mechanical breakdown could have led directly to the first human infection in late 2019.

Thus, one of the miners, most likely patient 3, or patient 4 (whose thymus was removed), was effectively patient zero of the COVID-19 epidemic.
In this scenario, COVID-19 is not an engineered virus; but, equally, if it had not been taken to Wuhan and no further molecular research had been performed or planned for it then the virus would have died out from natural causes, rather than escaped to initiate the COVID-19 pandemic.

Evidence in favour of the MMP proposal

Our proposal is consistent with all the principal undisputed facts concerning SARS-CoV-2 and its origin. The MMP proposal has the additional benefit of reconciling many observations concerning SARS-CoV-2 that have proven difficult to reconcile with any natural zoonotic hypothesis.

For instance, using different approaches, numerous researchers have concluded that the SARS-CoV-2 spike protein has a very high affinity for the human ACE2 receptor (Walls et al., 2020; Piplani et al., 2020; Shang and Ye et al., 2020; Wrapp et al., 2020). Such exceptional affinities, ten to twenty times as great as that of the original SARS virus, do not arise at random, making it very hard to explain in any other way than for the virus to have been strongly selected in the presence of a human ACE2 receptor (Piplani et al., 2020).

In addition to this, a recent report found that the spike of RaTG13 binds the human ACE2 receptor (Shang and Ye et al., 2020). We proposed above that the virus in the mine directly infected humans lung cells. The main determinant of cell infection and species specificity of coronaviruses is initial receptor binding (Perlman and Netland, 2009). Thus RaTG13, unlike most bat coronaviruses, probably can enter and infect human cells, providing biological plausibility to the idea that the miners became infected with a coronavirus resembling RaTG13.

Moreover, the receptor binding domain (RBD) of SARS-CoV-2, which is the region of the spike that physically contacts the human ACE2 receptor, has recently been crystallised to reveal its spatial structure (Shang and Ye et al., 2020). These authors found close structural similarities between the spikes of SARS-CoV-2 and RaTG13 in how they bound the human ACE2 receptor:

“Second, as with SARS-CoV-2, bat RaTG13 RBM [a region of the RBD] contains a similar four-residue motif in the ACE2 binding ridge, supporting the notion that SARS-CoV-2 may have evolved from RaTG13 or a RaTG13-related bat coronavirus (Extended Data Table 3 and Extended Data Fig. 7). Third, the L486F, Y493Q and D501N residue changes from RaTG13 to SARS CoV-2 enhance ACE2 recognition and may have facilitated the bat-to-human transmission of SARS-CoV-2 (Extended Data Table 3 and Extended Data Fig. 7). A lysine-to-asparagine mutation at the 479 position in the SARS-CoV-2 RBD (corresponding to the 493 position in the SARS-CoV-2 RBD) enabled SARS-CoV to infect humans. Fourth, Leu455 contributes favourably to ACE2 recognition, and it is conserved between RaTG13 and SARS CoV-2; its presence in the SARS CoV-2 RBM may be important for the bat-to-human transmission of SARS-CoV-2″ (Shang and Ye et al., 2020). (italics added)

The significance of this molecular similarity is very great. Coronaviruses have evolved a diverse set of molecular solutions to solve the problem of binding ACE2 (Perlman and Netland, 2009; Forni et al., 2017). The fact that RaTG13 and SARS CoV-2 share the same solution makes RaTG13 a highly likely direct ancestor of Sars-CoV-2.

A further widely noted feature of SARS-CoV-2 is its furin site (Coutard et al., 2020). This site is absent from RaTG13 and other closely related coronaviruses. The most closely related virus with such a site is the highly lethal MERS (which broke out in 2012). Possession of a furin site enables SARS-CoV-2 (like MERS) to infect lungs and many other body tissues (such as the gastrointestinal tract and neurons), explaining much of its lethality (Hoffman et al., 2020; Lamers et al., 2020). However, no convincing explanation for how SARS-CoV-2 acquired this site has yet been offered. Our suggestion is that it arose due to the high selection pressure which existed in the miner’s lungs and which in general worked to ensure that the virus became highly adapted to the lungs. This explanation, which encompasses how SARS-CoV-2 came to target lung tissues in general, is an important aspect of our proposal.

The implication is therefore that the furin site was not acquired by recombination with another coronavirus and simply represents convergent evolution (as suggested by Andersen et al., 2020).

An intriguing alternative possibility is that SARS-CoV-2 acquired its furin site directly from the miner’s lungs. Humans possess an epithelial sodium channel protein called ENaC-a whose furin cleavage site is identical over eight amino acids to SARS-CoV-2 (Anand et al., 2020). ENaC-a protein is present in the same airway epithelial and lung tissues infected by SARS-CoV-2.
It is known from plants that positive-stranded RNA viruses recombine readily with host mRNAs (Greene and Allison, 1994; Greene and Allison, 1996; Lommel and Xiong, 1991; Borja et al., 2007). The same evidence base is not available for positive-stranded animal RNA viruses, (though see Gorbalenya, 1992) but if plant viruses are a guide then acquisition of its furin site via recombination with the mRNA which encodes ENaC-a by SARS-CoV-2 is a strong possibility.

A further feature of SARS-CoV-2 has been the very limited adaptive evolution of its genome since the pandemic began (Zhan et al., 2020; van Dorp et al., 2020; Starr et al., 2020). It is a well-established principle that viruses that jump species undergo accelerated evolutionary change in their new host (e.g. Baric et al., 1997). Thus, SARS and MERS (both coronaviruses) underwent rapid and readily detectable adaptation to their new human hosts (Forni et al., 2017; Dudas and Rambaut, 2016). Such an adaptation period has not been observed for SARS-CoV-2 even though it has now infected many more individuals than SARS or MERS did. This has even led to suggestions that the SARS-CoV-2 virus had a period of cryptic circulation in humans infections that predated the pandemic (Chaw et al., 2020). The sole mutation consistently observed to accumulate across multiple studies is a D614G substitution in the spike protein (e.g. Korber et al., 2020). The numerically largest analysis of SARS-CoV-2 genomes, however, found no evidence at all for adaptive evolution, even for D614G (van Dorp et al., 2020).

The general observation is therefore that Sars-CoV-2 has remained functionally unchanged or virtually so (except for inconsequential genetic changes) since the pandemic began. This is a very important observation. It implies that SARS-CoV-2 is highly adapted across its whole set of component proteins and not just at the spike (Zhan et al., 2020). That is to say, its evolutionary leap to humans was completed before the 2019 pandemic began.

It is hard to imagine an explanation for this high adaptiveness other than some kind of passaging in a human body (Zhan et al., 2020). Not even passaging in human cells could have achieved such an outcome.

Two examples illustrate this point. In a follow up to Shang and Ye et al., (2020), a similar group of Minnesota researchers identified a distinct strategy by which the spike (S) protein (which contains the receptor bind domain; RBD) of SARS-CoV-2 evades the human immune system (Shang and Wan et al., 2020). This strategy involves more effective hiding of its RBD, but it implies again that the spike and the RBD evolved in tandem and in the presence of the human immune system (i.e. in a human body and not in tissue culture).

The Andersen authors, in their critique of a possible engineered origin for SARS-CoV-2, also stress the need for passaging in whole humans:

“Finally, the generation of the predicted O-linked glycans is also unlikely to have occurred during cell-culture passage, as such features suggest the involvement of an immune system” (Andersen et al., 2020).

The final point that we would like to make is that the principal zoonotic origin thesis is the one proposed by Andersen et al. Apart from being poorly supported this thesis is very complex. It requires two species jumps, at least two recombination events between quite distantly related coronaviruses and the physical transfer of a pangolin (having a coronavirus infection) from outside China (Andersen et al., 2020). Even then it provides no logical explanation of the adaptedness of SARS-CoV-2 across its whole genome or why the virus emerged in Wuhan.

By contrast, our MMP proposal requires only the one species jump, which is documented in the Master’s thesis.
Although we do not rule out a possible role for mixed infections in the lungs of the miners, nor the possibility of recombination between closely related variants in those lungs, nor the potential acquisition of the furin site from a host mRNA, only mutation was needed to derive SARS-CoV-2 from RaTG13. Hence our attention earlier to the figure from P. Zhou et al., 2020 showing that RaTG13 is the most closely related virus to SARS-CoV-2 over its entire length. This extended similarity is perfectly consistent with a mutational origin of SARS-CoV-2 from RaTG13.

In short, the MMP theory is a plausible and parsimonious explanation of all the key features of the COVID-19 pandemic and its origin. It accounts for the propensity of SARS-CoV-2 infections to target the lungs; the apparent preadapted nature of the virus; and its transmission from bats in Yunnan to humans in Wuhan.

Further questions

The hypothesis that SARS-CoV-2 evolved in the Mojiang miner’s lungs potentially resolves many scientific questions about the origin of the pandemic. But it raises others having to do with why this information has not come to light hitherto. The most obvious of these concern the actions of the Shi lab at the WIV.

Why did the Shi lab not acknowledge the miners’ deaths in any paper describing samples taken from the mine (Ge et al., 2016 and P. Zhou et al., 2020)? Why in the title of the Ge at al. 2016 paper did the Shi lab call it an “abandoned” mine? When they published the sequence of RaTG13 in Feb. 2020, why did the Shi lab provide a new name (RaTG13) for BtCoV/4991 when they had by then cited BtCoV/4991 twice in publications and once in a genome sequence database and when their sequences were from the same sample and 100% identical (P. Zhou et al., 2020)? If it was just a name change, why no acknowledgement of this in their 2020 paper describing RaTG13 (Bengston, 2020)? These strange and unscientific actions have obscured the origins of the closest viral relatives of SARS-CoV-2, viruses that are suspected to have caused a COVID-like illness in 2012 and which may be key to understanding not just the origin of the COVID-19 pandemic but the future behaviour of SARS-CoV-2.

These are not the only questionable actions associated with the provenance of samples from the mine. There were five scientific publications that very early in the pandemic reported whole genome sequences for SARS-CoV-2 (Chan et al., 2020; Chen et al., 2020; Wu et al., 2020; P. Zhou et al., 2020; Zhu et al., 2020). Despite three of them having experienced viral evolutionary biologists as authors (George Gao, Zheng-li Shi and Edward Holmes) only one of these (Chen et al., 2020) succeeded in identifying the most closely related viral sequence by far: BtCoV/4991 a viral sequence in the possession of the Shi lab at the WIV that differed from SARS-CoV-2 by just 5 nucleotides.

As we noted in our earlier article, the most important of the questions surrounding the origins of SARS-CoV-2 could potentially be resolved by a simple examination of the complete lab notebooks and biosafety records of relevant researchers at the WIV. Now that a credible and testable lab escape hypothesis exists this task becomes potentially much easier. This moment thus represents an opportune one to renew that call for an independent and transparent investigation of the WIV.

In requesting an investigation we are aware that no scientific institution anywhere has made a comparable request. We believe that this failure undermines public trust in a “scientific response” to the pandemic. Instead, the scientific establishment has labeled the lab escape theory a “rumor“, an “unverified theory” and a “conspiracy” when its proper name is a hypothesis. By taking this stance the scientific establishment has given the unambiguous message that scientists who take the possibility of a lab origin seriously are jeopardising their careers. Thus, while countless scientific publications on the pandemic assert in their introductions that a zoonotic origin for SARS-CoV-2 is a matter of fact or near-certainty (and Andersen et al has 860 citations as of July 14th), there is still not one published scientific paper asserting that a lab escape is even a credible hypothesis that deserves investigation.

Anyone who doubts this pressure should read the interview with Birger Sørensen in Norway’s Minerva magazine in which Sørensen discusses the “reluctance” of journals to publish his assessment that the existence of a virus that is “exceptionally well adjusted to infect humans” is “suspicious” and “cannot have evolved naturally”. The source of this reluctance, says Sørensen, is not rationality or scientific evidence. It results from conflicts of interest. This mirrors our experience. To find genuinely critical analysis of COVID-19 origin theories one has to go to Twitter, blog posts, and preprint servers. The malaise runs deep when even scientists start to complain that they don’t trust science.

Therefore we hypothesise the reconstructed historical aetiology of the Spike as follows:

In 2008, Dr Zheng-Li Si and WIV colleagues successfully demonstrated technical capabilities to interchange RBD’s between bat SARS-like and human SARS viruses. Building upon this, the 2010 work (Hou et al, 2010) perfected the ability to express receptors on human cells. On these foundations, the central Gain of Function work that underpins the functionalities of SARS-CoV-2 took place, carrying the WIV spike and plasmid materials to bond successfully to a UNC Chapel Hill human epithelial cell-line. This work (Menachery et al) produced a highly infectious chimeric virus optimised to the human upper respiratory tract.
In convergent support of this hypothesis, both Lu (Lu et al, 2020) and Jia (Jia et al, 2020) have now, in January and April 2020, shown that SARS-CoV-2 has a bat SARS-like backbone but is carrying an RBD from a human SARS and Zhan et al have, like us, noted unusual adaption to humans from the first isolate. In the 2015 Chapel Hill work it was only ACE2 receptors that were discussed. However, in 2018 Zhou P. et al demonstrated capabilities to clone other receptors like APN and DPP4 and to test and compare these against the (intestine) tissue specific SADS-CoV identified. Then, in the 2019-20 Covid-19 pandemic, profuse symptoms indicating compromise of the bitter/sweet receptors are reported. Taken all together, this implies that by employing insights gained after 2015, as just deduced, a further optimization of the 2015 chimeric virus for additional binding to receptors/co-receptors such as bitter/sweet specific upper airway epithelia receptors occurred. That would help to explain the otherwise puzzling high infectivity and pathology associated with SARS-CoV-2 and hence also help to explain the social epidemiology of its spread.

-- The Evidence which Suggests that This Is No Naturally Evolved Virus: A Reconstructed Historical Aetiology of the SARS-CoV-2 Spike, by Birger Sørensen, Angus Dalgleish & Andres Susrud

We nevertheless hope that journalists will investigate some of the conflicts of interest that are keeping scientists and institutions from properly investigating the lab escape hypothesis.


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