He would love to be wrong and coincide with the WHO Wuhan Commission on CoV-2 origin. But too many hard evidence point to the lab theory. It’s Wednesday, February 16 2021, 5:30 pm in Taipei, Taiwan’s capital, from where he grants me this interview. Physician, inventor and entrepreneur, Dr. Steven Carl Quay recieved his MD & PhD from the University of Michigan. He was postdoctorate fellow at the MIT Chemistry Department with Nobel Laureate Gobind Khorana, resident at the Harvard-Massachusetts General Hospital, and spent a decade on the faculty of Stanford University School of Medicine. Chairman and CEO of Atossa Therapeutics, a clinical-stage biopharmaceutical company based in Seattle, Dr. Quay holds 87 U.S. patents, 7 FDA-approved pharmaceutical inventions and he is also a very prolific and cited author. Coronavirus prevention and treatment is one of his fields of research and his last book,the best selling ‘Stay Safe’, is precisely a kind of coronavirus survival manual.
But our conversation will focus on his amazing outcome about Covid-19 origin. A pandemic that has a 99,8% chance of coming from a laboratory, and only a 0,2% probability of being a natural virus. At least according to the result of his report titled: “A Bayesian analysis concludes beyond a reasonable doubt that SARS-CoV-2 is not a natural zoonosis but instead is laboratory derived”. A full of facts & figures 193 pages statistical study, pre-published last January 29 at Zenodo CERN open repository. A paper on the way of his peer-review that since it’s first upload has an average of 6.000 views and downloads per day and a total view of over ninety-eight thousand. No wonder why. If proven to be true, this conclusion would change the whole narrative of the pandemic, the role of advanced bioresearch on it, and above all its political regulation to prevent a next catastrophe.
DrQ: The starting probability of my report was setted at 98,5% likelihood in favor of the natural-zoonotic origin. A very conservative approach that leaved the laboratory hypothesis just a 1,2% chance. But due to the available evidence, after the math adjusments the results shifted to a 99,8% that SARS-CoV-2 is a laboratory derived virus. This exceeds the parameters for a “beyond a reasonable doubt” conclusion.
A direct application of the Bayes Theorem, so a little tribute to the English mathematician Thomas Bayes (1702-1761), a Presbyterian minister who wrote this method of doing analysis. His notes where found when he died so it was published posthumously.
It’s a very standard model of statistical inference. We all actually do Bayesian analysis in real life. Its basically the way we bet in the World Cup or whatever sport. You have certain ideas of who is going to win at the begining of the season, before the first football is kicked. And then as games get played you adjust that, and that adjusment is your own Bayesian analysis. You are trying to predict who is going to win the Cup and then you go into the final games. That’s the process.
Yes, you have to think of it in three ways. You start with what is your prior estimate of the likelihood: if nature or laboratory origin. Then you drop evidence in, you turn a little mathematical crank and see if the probabilities change. So by the end of my analysis, after going through 26 different pieces of evidence, the outcome was that Covid-19 has a one in five hundred chance of coming from nature.
No, and the beauty of a Bayesian analysis is this: If you bring me a 27th piece of evidence we can drop it in, turn the crank and see what it does. Its like having an extra game in the World Cup. But everything I’ve learned since I wrote my report continues to point in the direction of the laboratory.
Remarkably, in the three hour interview the WHO group gave they did provide new facts. It’s quite interesting. In China, over 62,000 different potential animals have been tested over the last year for the virus. Individually. Every animal had either blood or tissue taken and the PCR test was done. And at this point of time they have found zero out of 62,000 of any of the intermediate host animal that they predicted.
Now, why is 0 out of over 62,000 important? Let’s go back to 2003, with SARS-CoV-1. Once they knew within four months that it came from civet cats in a market, 90% of every cat that they tested from that point forward had SARS-CoV-1. And in 2015, when a similar coronavirus broke out in the Middle East, ten months after the first human patient they knew it was from camels and, again, 92% of every camel had the virus. So now we’ve done a random study in all of China for a year in over 62,000 animals and we found zero virus. The probability of that being similar to prior zoonosis its just abnormally low.
Yes, I did get some confidential feedback from the individuals on the Commissions, that I’m going to incorporate when I update. But it’s not going to change the statistics very much. One of the criticisms, for example, was that if there is an infinite number of species of coronaviruses and I don’t find a “furin site” in six hundred, is that really meaningful? So it turns out that one member of both Commissions, Dr. Peter Daszak, has actually estimated how many different species of coronaviruses there are in the world: 3.204. So instead of having an infinite number, I can drop 3.204 into my analysis. Which modifies the number by only about 0.5.
But it was a useful observation and it made me rethink things. I mean, there are very clear evidence of coming from a zoonosis that could possibly flip my analysis. But every time someone has provided evidence in those directions it points away from it, from coming from nature.
It’s very timely, your comment, because I did ask them: Could you please share with me those criticisms so I can incorporate them into a new version? And about thirty minutes ago I received an email from them. They’ve changed the disclaimer. Now it simply informs that it hasn’t been peer-review.
I really appreciate they changed it. I am willing to debate any of the people, in a public forum, with my data and their data. And let’s just have it out, because again, I would love to be wrong. Life would be a lot easier if I am wrong. It would require a change in the way we do, perhaps, urbanization… There are always outcomes from the understanding of the origin of something. But I believe the outcome here is that we need to relook at Gain-of-Function (GoF) research and decide whether the benefit-cost ratio shows its justified. That’s my long term goal.
Look, I want to get to the truth, but I also want to do it in the most aggressive way I can. So wherever I could, I either used data from Dr. Daszak, who’s widely published, Dr. Shi at the Wuhan Institute of Virology (WIV) or Dr. Baric from North Carolina and leading coronavirus US expert.
Yes Jorge, that’s right. They were the ones that studied 540 people for what’s called seroconversion. In SARS-CoV-1 and MERS there were blood samples in a refrigerator from people who had an early infection that wasn’t strong enough to become an epidemic. But they showed evidence of having antibodies. That’s called seroconversión. And it was about 1 to 3% in SARS-CoV-1 and MERS that you could find it in stored, refrigerated samples. But with CoV-2, in March 2020 the WHO examined 540 samples from Wuhan and found zero seroconversions. The probability of this is less than one on twenty that it was running around in Wuhan before the epidemic broke out.
Posterior diversity is the virus version of what I describe for seroconversion. In a zoonosis you have three living forms: an animal host, a human and a virus. And in a natural process it jumps into the human but it doesn’t have all the tools it needs to cause an epidemic. For example, in SARS-CoV-1, the first human case had only 17% of the mutations it needed to become an epidemic, the first time around. But with SARS-CoV-2 it has 99.5% of the best mutations from the very first patient. So the posterior diversity is that process where as it intermediate host jumps to humans, gets mutations but it also jumps back and forth inside the intermediate host.
Yes, in the first six months of the epidemic about every other patient got it from an animal. The intermediate host, either civet cats or the camels, developed those really good mutations to get into humans as well among themselves. So when you look at the virus in humans where the epidemic happens, you can trace the virus back through the mutations. If it traces back a year earlier or two years earlier that’s called posterior diversity. That means that the virus was really jumping into humans from cousins of the virus as opposed to a single primary parent virus.
In CoV-2 we have over a hundred million cases and they all trace through one patient: a patient the end of December at the People’s Liberation Army (PLA) hospital in Wuhan, about three kilometers from the Wuhan Institute of Virology (WIV). That patient had what was called Lineage A. Every CoV-2 in the entire world is a descendant of that one. Even the one President Trump got. They all can trace back to that single individual patient. In SARS-CoV-1 you had multiple jumps from animals into humans. In MERS you had multiple jumps from camels into humans. CoV-2 is a one to one. You have one jump into one human from one animal. An animal in a laboratory I believe.
Let me explain that. We all have a key that gets us into our house. It goes into the lock, we turn it, and the door opens. Thats how it works. Coronavirus is the same process. It has a Spike protein which is the key, so that attaches to the cell. But then another event like the turn of the key has to happen before it opens your cells. The virus get’s your own cells to clip the Spike protein, in a particular spot, to sort of release the spring and spring load the RNA into your cells. The enzyme or scissors that we have, that we help the virus with, its called “furin”.
Yes, and there are at least eleven different laboratories around the world, including the WIV, that have purposely put a furin cleavage site in a Spike protein. They put a particular set of amino acids and the furin enzyme clipper says: Oh, I like that spot. Then they clip it and the virus goes into the cell. And every time that’s been done since 1992 it always increases the infectivity, the transmissibility and the lethality of the virus. So when you see a furin cleavage site in a coronavirus you know it has a great significance. Now, SARS-CoV-2 comes from a subgroup of coronaviruses called the sarvecovirus. But it’s the only one of this subgroup, this subgenera that has a furin site.
If we look at between six and nine hundred other Sarbecoviruses, it depends on the numbers you use: zero have a furin cleavage site. All the furin cleavage sites are in distant relatives of this subgenera and the virologists tell me, and they agree, that recombination can’t occur that far apart. Different species we know can have an offspring. In viruses they recombine but only within a certain groups. Covid-2 comes from a group that has no other furin sites. So where did it get it? That’s the first point about the aminoacids, the part the scissors that furin attaches to. I worked at MIT for Gobind Khorana, who discovered the genetic code, which means that all the amino acids that make our enzymes have a code behind them, where each aminoacid has a three letter word. So the furin cleavage site has to have two R genes: RR. There are six different three-letter words for arginine.
Exactly. So the two codons in SARS-CoV-2, the two three letter words for arginine, are the least frequently used codons in all coronaviruses in the entire world: the CGG codon. Coronaviruses hate the CGG codon. And in Covid-2 there is two of them together. I looked at 580.000 codons in other coronaviruses and I didn’t find a single CGG-CGG pair. Not one. So nature doesn’t use those codons. But what happens in the laboratory? Now, when a scientist wants to put an arginine into a genetic code they buy the DNA, the RNA, and they drop it in. And what is their favorite arginine codon? CGG. So the codon that nature never uses, and the codon the laboratory always uses, is the one found in SARS-CoV-2.
The RaTG13 has the unique sequences necessary to be the precursor of SARS-CoV-2, with two rare restriction sites that fit with a synthetic bio lab technique called “No See’Em”. The chance of these two sites, present and placed at their exact location, as an act of nature, is of one in a billion. On the other hand, the additional steps needed to créate SARS-CoV-2 from RaTG13 are not clearly identified in the genome and so there are likely additional laboratory viruses involved in the process.
I really want to stick with evidence. And I want to act almost like I am in a court of law. You can’t go in a court and say: My neighbour did this. You have to bring the neighbour, he has to swear and then make his statment. So one of the statments that I put in the analysis at the end was that Dr. Shi was very carefully when she said that none of the viruses that she collected in the wild matched SARS-CoV-2. Which I believe its a true statement. But one that is a little bit tricky. Because what you just said its not what she actually said. You said that none of the viruses in the lab matched SARS-CoV-2. But Dr. Shi did not say that. What she said is: None of the viruses collected in the wild matched SARS-CoV-2. But if she collected a virus in the wold and then manipulated it in the laboratory, her careful statement would be true.
Yes, that is true. Gain-of-Function is a kind of research where you genetically manipulate an infectious agent to make it more infectious, more transmissible and more lethal. The academic goal of that is to say: Ok, let me make nature’s worst case virus, and then let me figure out how do I stop it? How do I find a vaccine or a therapeutic against it? Arguably its noble research in some ways.
I can talk about that in great detail. Anyway, the dangerous experiments in 2014 scared everybody and the virology community said: Maybe we shouldn’t publish some of it. There were discussions, hearings and the government placed a moratorium. United States refused to fund GoF research and asked the world community to participate as well. But in May of 2017, after a large report was produced by the end of 2016 by the the National Institute of Health (NIH), the moratorium was lifted.
I think in both cases it was the NIH and not specifically the President.. If you have an organizational chart you’ll see President at the top and the NIH down beneath. In 2014 the NIH, probably with concurse of the White House of course, put the moratorium in place. And I think the reversal was done in May of 2017. It was the NIH who announced the release and allowing the funds going back into that space.
Making something more infectious for you can get ahead of it and prevent a pandemic is a risky option. And the history of laboratory leaks is really troubling, in the context of making something that is so deadly as a GoF experiment.
I was a little surprised by one of the WHO individuals who said that lab accidents are rare and so I sent him an email. In my Bayesian análisis there is a reference that showed that in Asia there was 0.8 laboratory leaks every year over a 30 year period.
Yes Jorge! Maybe that’s rare for some people, but if every leak is a lethal virus that can lead to an epidemic that’s much to high. These experiments are very sophisticated, and if you are techy they are really cool. But I think there are other sophisticated ways of doing GoF with vectors and things that cannot reproduce. The key thing of GoF is you take something that can reproduce and spread around the world and you add new tools to it, new weapons to it. But there are psudoviruses. HIV if you can believe that. There is a model system that you can use in a high school laboratory because it has only a couple of the elements of HIV, and you can packed it with whaever you want and it cannot possibly infect anybody. So you could use that. But you could also do a little GoF on something that you know it couldn’t replicate. Not as much fun as the Full Monty, but much safer.
I have assisted some major organizations. I can’t get into their names for confidentiality reasons. But my analysis is being used by some very large organizations. There is a process I want to go through. The problem is no journal that I am aware will publish a 193 pages manuscript. I have published hundreds of peer-reviewed papers so I know how this works. But its important to have this peer-reviewed and I’m in the process of getting that done. So I’m writing a distilled version and hope to get it up in the next three to four weeks.
I’m a bit of a nerd. I’m always looking at scientific papers on the weekends and that sort of thing. So obviously last January, when the coronavirus hit, I started to study it. And it turns out that the “furin cleavage site” it contains is something that I was researching when I was a young, thirty-year-old in the Faculty of Stanford University.
Yes, the active component of the bee venom, the melitin, that causes all the pain when you get stung by a bee, its basically a furin cleavage site in a small peptide. And for about five years I was sort of the world’s expert on bee venom. So as soon as I saw the furin site in January I said: I know what that’s going to do to cells and maybe I can get a therapeutic to prevent it. So I went to the board of the Company and got permission to develop two therapeutics, one of which is in the clinic now and moving their way to approval at some point of time. Treatments for either preventing the virus to get into the cells, or preventing it from getting into the lungs in a nebulized form. That’s how I’ve started. And now we have two drugs in development.
I guess when I saw the aforementioned Lancet statement. These twenty-seven authors were saying, with no science, that the lab hypothesis was just a conspiracy theory. And I said: But, what’s the evidence for that? Because when I looked for references there was no evidence. So I was bothered. Because if you are a scientist you want science to be respected, for the truth, and the last thing we need is to have one more thing politized, science.
It absolutely is. And I am really hopeful that truth will prevail and that we’ll end up with some discussion around what elements of Gain-of-Function we can do to help prevent further pandemics. But to stop the current process from continuing. I mean, Chemistry was used in World War I with chemical warfare, and then it was banned. Then Physics was used in World War II with nuclear bombs… Now it seems to be Biology’s turn to show its darks arts.
I do not. I belive it was an accidental release or a scientist with a laboratory-acquired infection. Of course, in my paper I urge the world to gather further data to support or refute the bioweapon probability. But the report only concludes that SARS-Cov-2 is a lab-made derived virus and that the Wuhan Institute of Virology is the laboratory where it was created.
First recognize that the horse has left its stall, has left the barn, and is running free. So it will be hard but not imposible to catch it and put it back in the barn. Part of the process is to control the supply chain of how you make these things. So if this was a biological GoF process some steps could be taken. The tools for doing GoF can be bought from certain companies that make them. You could perhaps do everything from scratch, but it gets really hard. Like when we say: Well, we let people dig uranium ore and then they can purify it. But with uranium you don’t worry about that. You worry about the pure uranium and following its custody.
If we really wanted this. And we should want it. One of the most striking papers I read in last February or March, was from a group of about thirty young scientists from Switzerland. What they basically had done was to take some sourdough bread yeast, bought a some chemicals from a laboratory, and in a week they were able to get yeast to make coronavirus out of these chemicals off the shelve. They were true scientists, so they were really excited and proud about what they did.
Exactly. So when I look at that paper and see its been downloaded 60.000 times I wonder: Are there sixty thousand laboratories in the world interested in this or maybe there are people learning how to do it who have dangerous intentions like, you know: Would you like some coronavirus in your sourdough bread? Not a good picture.
I wasn’t involve in that. Though I have written to Richard a coupled of times and we had a nice exchange regarding the science I’m doing. But I believe they lost the debate. It kind of went by the wayside.
Yes, a spray and ventilators are both in different ends of the spectrum. The nasal spray contains three inhibitors of the host of the furin… To simplify. We have three enzymes: Furin, ACE-2 and TMPRSS-2. These are the three diffferent scissors that can cut the Spike protein of the virus. Coronavirus doesn’t want to miss his chance to get into a cell, and has three different enzymes that can do the job. So I have put an inhibitor on all three of those enzymes in a nasal spray.
The coronavirus gets a new mutation once every two weeks. The virus goes into every patient and goes out of that patient with a new mutation. But the enzymes on the surface of our cells don’t change over a lifetime. So the purpose of these inhibitors is to slow down the infection if you can use it early on, like within a 24-48 hours in a PCR positive case. But also maybe more important, to give it to the other adults in your home. That product has finished a Phase One study. We are wrapping up the data, then going to the US Food & Drug Administration (FDA) for a study again in early patients, or reduce their symptoms, and to prevent in patients who where exposed in a household.
Go to the other spectrum of patients. You are in the hospital, having trouble breathing and they put you in a ventilator. We know that, even now, being on a ventilator with Covid is a very dangerous situation. So what we do is to nebulize inhibitors that block the Spike protein.
But here we are not working on the enzymes of the cell, we are actually trying to make what I call a chemical vaccine. Basically it wraps around the Spike protein and the furin site. Something I learned teaching at Stanford back in 80’s. Its a product I’m pretty excited about. Because if you are on a ventilator you have a large chance of never coming off and passing away. So I think they are both important products. With vaccines they will become less important, but still valuable. Influenza its been around for three decades and we still spend a billion dollars a year on pharmaceuticals for treating patients with influenza. So we are going to end up with a belt and suspenders approach on this. I’m quite sure.
Look, it’s really easy to criticize people in retrospect, so I want to be really careful. Having said that, we knew from a study of 80,000 people in China in February 2020, and I posted on my website, that this virus had a huge impact on mortality-morbidity based almost totally on age, on the elderly. And that fact hasn’t changed in a year. So I guess that if I’ve been an advisor in the Spring of 2020 and they asked me I would have said: Well, let’s use this data and see the world that we live in. We have children, we have schools, we have young teachers… Maybe forty or thirty and under is the teacher population. And schools don’t seem to be a place where the virus is either very deadly or passes very easily. Last year we’ve still lost more people under 18 years old from influenza than from SARS-CoV-2.
I think we should do things for people of 60 and older who don’t want to go to work and prefer to do it from home. We need laws in place so they don’t get fired or discriminated and get hurt economically. But people in between we should let them do their own thing.
There have been so many studies on masks. They probably have a small incremental benefit and they definitivey have no detrimental factor. I have a lot of friends that are anti-maskers. They made me go into all the literature, but there is no evidence that masks have any detrimental factor I can find. Maybe you get the mask infected and you get an infecton from it, but still not very solid. Its a non-risk some-benefit proposition. So just wear the mask.
In another study from China, where they tracked 200 cases, they found 2 from outdoors and all the rest, 198, from indoors. So this idea of getting the people out into nature taking walks in the woods or in the street is a really good idea. Actually the more you lock people into small spaces you probable enhance the infection. Because we know that 80% of the infection cases are passed within the household. And I think some of the cultures that have a common three generation household, perhaps in Italy and others, may have been one of the contributing factors to some of their consequences of the pandemic.
I don’t think lockdowns are a good idea.
Named like that, by the way, not because it was from Spain, but because the Spanish press was the only one that was free to report about it, while all of the other countries locked down their newspapers.
Just the truth.
I think you are absolutely right there. If you look at the average mortality rates during the pandemic they are not changing much with the ones before 2019 or 2018. People are dying at about the same age. They are just dying of Covid and not of something else. So it’s really skewed towards the elderly. We should have done a better job with them. And we should have done a better job with the youngsters. But I kind of letting this out and I am not about of a politician. I don’t understand how we ended up doing what we did, which is basically kind of destroying the world economy for a year, in a process never seen before. It was a global experiment that has never been done before in public health. And in retrospective it didn’t turn up very well.
Its been a pleasure. I absolutely will be updating all of this things that I found and that I want to be sure on before I release information. So Stay tuned as they say.
* The Spanish translation of this interview is published in El Imparcial, 24 Feb 2021, Madrid digital newspaper. I wish to pay my special regards to Dr. Steven C. Quay, MD, PhD, for his correction on my original english manuscript.