Dhru Purohit Show - #260: A Deep Dive into Covid-19 Origins, Lab Leak, and the Next Pandemic with Dr. Steven Quay

Episode Date: January 24, 2022

This episode is brought to you by Pendulum. We’re constantly learning more and more about COVID-19. How it interacts with our immune systems, risk factors, and hospitalization and death rates are all topics that are extensively covered in the news.  But the origin of COVID is something that is much less talked about. Why does this even matter? Understanding COVID’s origin story is key in helping us prevent a future pandemic. Today on The Dhru Purohit Podcast, Dhru talks to Dr. Steven Quay to hear about his investigation into how COVID infected humans in the first place.  Dr. Steven Quay has 360+ published contributions to medicine and has been cited over 10,000 times, placing him in the top 1% of scientists worldwide. He holds 87 US patents and has invented seven FDA-approved pharmaceuticals which have helped over 80 million people. He is the author of the bestselling book on surviving the pandemic, Stay Safe: A Physician's Guide to Survive Coronavirus. He is the CEO of Atossa Therapeutics Inc., a clinical-stage biopharmaceutical company developing novel therapeutics for oncology and infectious diseases. In this episode, we dive into:   -The two competing hypotheses of COVID-19 (7:13) -How SARS-CoV-1 began (12:23) -Gain of opportunity vs. gain of function research (13:46) -Dr. Quay’s research concluding that SARS-CoV-2 is laboratory-derived (17:19) -International inquiry into the origins of this particular coronavirus (44:08) -The implications if we don’t learn the lessons of the true origin of SARS-CoV-2 (55:03) -Natural immunity vs. vaccinated immunity (1:11:17) -Understanding the omicron variant (1:14:21) Also mentioned in this episode:   -"A Bayesian analysis concludes beyond a reasonable doubt that SARS-CoV-2 is not a natural zoonosis, but instead is laboratory-derived" - https://zenodo.org/record/4642956#.Yeo1SljMKBR   -Paris Group Letter - https://www.nytimes.com/interactive/2021/03/04/us/covid-origins-letter.html   -Did COVID-19 Leak From A Lab? A Reporter Investigates—And Finds Roadblocks - https://www.npr.org/2021/06/17/1007539626/did-covid-19-leak-from-a-lab-a-reporter-investigates-and-finds-roadblocks For more on Dr. Steven Quay, visit his website www.drquay.com. Email him at [e-mail], Check out his book, Stay Safe: A Physician’s Guide to Survive Coronavirus at https://drquay.com/survivalguide/. This episode is brought to you by Pendulum. Pendulum is the first company to figure out how to harness the amazing benefits of Akkermansia in a probiotic capsule. To receive 20% off your first purchase of Pendulum’s Akkermansia probiotic supplement, go to Pendulumlife.com and use code DHRU20. Hosted on Acast. See acast.com/privacy for more information. Learn more about your ad choices. Visit megaphone.fm/adchoices

If you don't know how this started, then you can't change any behaviors that could prevent one in the future. I want to talk to you about a groundbreaking flagship bacterial strain that's been linked in thousands of scientific publications from everything from weight loss and better blood sugar control to lowering overall levels of inflammation. So what's this strain called? It's called Accramancy and it's made by the company Pendulum. So why the heck do you want Accomancy and what does it do for our overall? overall gut health and microbiome. So acrimancia feeds on our intestinal mucosal layer and modulates its thickness. That's a good thing.

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Right now, if you're interested in acrimancia, this flagship bacterial strain, pendulum is offering my community 20% off your first purchase of their pendulum acrimancia probiotic supplement. All you have to do is go to their website, pendulumlife.com. That's pendulum, P-E-U-L-U-M-L-U-M-L-I-F-E dot com, and use the code Drew 20, spelled D-H-R-U-T-R-U-20 for 20% off your first purchase. Welcome to the Drew Proodd podcast. Each week we explore the inner workings of the brain and the body with one of the brightest minds in wellness, medicine, and mindset. Today, we're talking about the COVID-19 origins with Dr. Stephen Quay. Dr. Stephen Quay has been called upon Congress to testify, as well as he's been called upon

the state department to look into the origins of COVID-19, primarily because everybody's asking the question, where did this virus come from? And more importantly, if we understand where it came from, we can help protect ourselves further when it comes to the next pandemic. Now, early on in the pandemic, there was a concerted effort to squash out any alternative theories that COVID-19 came from anywhere except a wet market in China and went from a bat to a human being. Dr. Quay's work has been focused on how that likelihood, based on the raw data that is available to everyone, is more unlikely than a laboratory leak that came from a human being, most likely a scientist in China and the Wuhan area,

working on the virus, practicing what we call game of function research. Now, this is nothing new. This laboratory leak hypothesis has gotten more attention last year, and some notable podcast and media outlets have covered it. But Dr. Quay's work goes so much deeper on the topic, and I thought it would be useful to have him on the Drew Proet podcast to review his groundbreaking piece. paper that came out last year that made a lot of noise, and that scientific manuscript was entitled, a Bayesian analysis concludes beyond a reasonable doubt that SARS-CoV-2 is not, is not a natural

zoonosis, but instead laboratory-derived. This paper has been viewed over 190,000 times online. Now, a little bit about Dr. Quay, and then a couple more notes about why I think today's podcast matters. Dr. Quay has 360 published contributions to medicine and has been cited over 10,000 times, placing him in the top of one percent of scientists worldwide. He holds 87 U.S. patents and has invented seven FDA-approved pharmaceuticals, which have helped over 80 million people. When the pandemic first arrived and made it splash, the world and COVID-19 started infecting people. He wrote a book called Stay Safe, a physician's guide to surviving coronavirus. He is also the CEO of Atosa Therapeutics,

a clinical stage biopharmaceutical company developing novel therapeutics for oncology and infectious diseases. He received his MD and PhD from the University of Michigan, was a postdoctoral fellow in the chemistry department at MIT and worked along with Nobel laureates. He was a resident at Harvard MGH Hospital and spent almost a decade on the faculty of Stanford University's School of Medicine. In today's podcast, in addition to summarizing his work in that groundbreaking paper, we're also going to talk about why we need to think differently about gain of function research that's being conducted on viruses around the world and how there's a new virus that's being looked at that scientists are working on with game of function research,

a methodology of optimizing viruses to see if we can make them more transmutable to animals and human beings. There's a virus called the NEPA virus that's being worked on right now today. That is extremely deadly that Dr. Quay is sounding the alarm on. that we need to set up an institutional review board and make sure that the scientists, many of them, in fact, most of them, well-intentioned who are trying to protect humanity, but that the cat could easily get out of the bag and lead to the next pandemic if we don't set up processes to keep us safe. I think you'll enjoy this interview. If you are familiar with the lab leak theory,

there will be some things that we will cover that you've heard it before. And if you're not, it's a great summary about the origins of COVID-19, the likely origins, and again, why it matters. I hope you enjoy today's interview. You can follow Dr. Stephen Quay through his website. You can find the show notes below as well on Twitter. All right, let's jump in. Dr. Stephen Quay, welcome to the podcast. I'd love to jump right in talking a little bit about COVID origins. Why is it so important that we have and continue to have an honest discussion around the origins of the coronavirus and what implications that has for the future? Well, that last part is exactly the reason we need to have this discussion.

If you don't know how this started, then you can't change any behaviors that could prevent one in the future. So right now, the two competing hypotheses are what's called a natural spillover, where this virus goes from living in a bat, where it stays for decades literally without ever impacting it, intermediate host and then jumping to humans. So that's a spillover, typically in a wet market in Southeast Asia places. Or it escaped from a laboratory, and it was being studied in the laboratory, perhaps genetically manipulated in the laboratory. Those are two very different scenarios, and they require very different responses from the world in terms of how we prevent the next pandemic.

The first scenario that you mentioned of was taken as sort of basically fact or consensus approach when the pandemic first took place. At what point in time did an alternative idea around COVID origins hit your desk and have you start asking questions. Yeah, so let's address that. And I think it's proper to frame this. So for virologists, for scientists, we always start with what we know

and then we look at an observation in the world and then we try to see if what we know comports with that. So December 2019, all of us knew that approximately eight times a year, there's a new microbe that jumps from an animal to a human somewhere in the world. There's a spillover, about eight per year. We also knew that the published literature showed that about one lab acquired infection happened per year. So eight to one spillover, you know, once a year a lab leak.

So you see something new happen. Your first, you know, you go to what you know, which is that SARS-1 came from a wet market, MERS came from markets in which camels were being traded in the Middle East. So probably SARS-2 came from a market. So that's where you start. But then, you know, the real estate mantra of location, location, location, when you realize it's from Wuhan, and I think most people didn't know much about Wuhan, it's an 11 million-person city.

So it's, you know, bigger than any U.S. city. But nonetheless, I think Wuhan would not have passed many man on the street kind of quizzes, right? Where it was. But when you look at Wuhan, which is where it began, and we have lots and lots of evidence that it began there, and then you realize that a laboratory in Wuhan, which has published 60% of the entire world's literature on coronaviruses for the last 30 years, is six miles, seven miles from the wet market where we thought this begins. suddenly you say, whoa, that's either an incredible coincidence or maybe we need to look into this. So it was, we started in the wet market with the 8 to 1 ratio, but then the location just was,

just compelled a deep examination because SARS one escaped from laboratories, you know, MERS escaped from laboratories, and people all went to the hospital next to the laboratory. So, you know, showing up at a hospital in Wuhan could very well mean you came from the laboratory as well as a wet market. So I think at this point in time, most people are aware of the lab leak hypothesis of the origins. They may not know a lot of the details and that's some of the things that we want to get a chance to explore here. So just expand on that if you could. What do you mean when you say that SARS-CoV-1 escape from a lab or that a virus escape from a lab? How does that happen?

And how could that take place? Yeah, I mean, language is so important. And we've been miscommunicating about this from, you know, really from the beginning. You know, viruses don't really escape in the true sense of we think. And they're not lab leaks in the, to me, a lab leak conjures up, you know, sort of a plumbing issue, maybe, or something where you need a plumber to come in and, you know, there's pipes that are clogged or something. That's why I used, was careful in my first description, which it's a laboratory acquired infection. So it's someone who's working in a laboratory. They wear gloves.

They wear masks. They do all the right things. But then one day, they do one little thing wrong. And it's like gravity. You know, you can not fall off a cliff your whole life. And then you make one mistake and gravity kicks in. It's always waiting. And these viruses are always waiting to infect someone.

And then they walk out the front door. So laboratory acquired infection is probably a better term. And SARS-1 is a perfect example of the, of the, the two bookends of the theories. It began in wet markets in southern China near the Hong Kong border in an animal called a civet cat, which was sold for meat in that culture. And the cats got the virus and then the humans in the market got it. People that worked in restaurants got it. And then they went back to the restaurant and spread it inside the restaurant. There's all these examples of spillovers from an individual animal in a market to an individual person and then to other people.

That's how SARS-1 began. July 2004, the WHO came in and said, it's over. We've contained SARS-1. There's no more cases. And that was true for cases from the world, but there were six more cases. all of those were people in laboratories somewhere in the world experimenting with SARS-1, getting sick, going out into the world, going to a hospital. In one case, one woman's mother, who was a physician, died taking care of her. So the last six SARS-1 infections were laboratory-acquired infections. So it began as a spillover. It ended as a laboratory-acquired infection.

They both are relevant in the SARS-2 conversation. When you talk about a lab work. working on a virus, take us through the background of what are labs doing with viruses in the first place? What's the highest hope? And what's the history around lab slippage or lab acquired infections? How long has that been going on? Probably as long as we've been collecting microbes, which would be about 1880, 1890. You know, the last smallpox death was, a stenographer in a building in London who was two floors down from someone working in a, in a laboratory with the smallpox virus. It got into the air circulation system. She got it.

She died. The scientist was so distraught. He actually committed suicide over it. So it's, you know, it's part and parcel of working with these, with these dangerous viruses. So there is a field of, there's a field of horology where they want to try to prevent the next pandemic, and they do two activities. They do what I call gain of opportunity, which I think is a dangerous thing to do. It's why I kind of frame it that way. And then they do gain of function research, and each of those are distinct. What I mean by gain of opportunity is places like the Wu-on Institute of Virology will send their scientists out into the world to Africa, to India, to Indonesia, to Laos, to Vietnam, to collect bat feces or bat swabs, and then to grow the

viruses in the laboratory. So at one point in time, the one in the virology was sort of advertising, promoting that they had 3,000 different viruses in their facility. So what I mean by gain of opportunity is if you take a virus from a cave in, you know, southern China, we know that bats live within about a 34-kilometer range of their, of their cave. So they're born, they live, and they die within 34-kilometer circle. So if they end up in a laboratory, 1,400,000, away, that's a huge gain of opportunity for a virus. It also gets purified, so it's not fighting with other viruses in the laboratory. I mean, you put it in a test tube. It's pure, absolutely pure, so it gets to do everything it wants. And then you grow it in different ways. So that's gain of opportunity.

The other side is gain of function. And here, the virologists in this particular field, there are about 25, 30 of them in the world. Their goal is to say, well, what could nature do genetically with this virus, let me do it in anticipation of what nature could do, and then let me try to figure out how to get around, you know, how to prevent it. So I'll come up with a therapeutic, I'll come up with a vaccine in this sort of anticipatory fashion. But it's really dangerous because I can, in an afternoon in a gain of function experiment, I can do two or three thousand years of natural evolution, just, you know, between lunch and dinner. And so you create these crazy things that would probably literally never happen in nature.

You know, they say they will, but they never do. And so both of those, both of those need to be controlled if we think that this kind of research is dangerous, which I absolutely do. I have some good ways, I think, balancing win-win ways of controlling them. But, you know, that's what we mean by my laboratory work on virology, gain of opportunity where you collect from all over the world. world, gain a function by doing things inside the virus, manipulating them. So you wrote a paper. You've written a bunch. We'll link to your website where people can find all these that are there.

In fact, in my show notes that I have over here, we have you listed in the opening intro that we have for you as one of the top 1% of scientists worldwide in terms of how often you've been cited. So you had written an analysis called a Bayesian analysis concludes beyond a reasonable doubt that SARS-CoV-2 is not a natural zoonosis, but instead laboratory derived. What did you find out that led to the publication of that paper in terms of what was happening in the early days in Wuhan that could be linked to lab research? Sure, sure. So, and maybe a little backdrop, since this has now been published, you know, by other people, I can talk

about it, but I was contacted in the fall of 2020 to, because of some work I had just sort of, you know, published, was contacted to help assist in the analysis around the origin of SARS COVID-2. And the Bayesian analysis was the outcome, you know, of some of that work. I wasn't paid. I was just, you know, doing it on my spare time sort of thing. Got no financial benefit. There's someone who implied that I might have, but I didn't. But a basing analysis is a really fancy mathematical term that scientists like to throw around. It's really, it's really basically, you know, your sports, you know, your sports stats that you have in the office kind of thing. So before the season, you rank the teams, you know, who you think is going to be win the

World Series number two, number three. But, but, you know, and then so you fix that. And so that's your, that's what's called your prior in a Bayesian analysis. And then something happens. In baseball, it's a game in my Bayesian analysis. It was a piece of evidence. And then you rework the analysis and maybe, you know, maybe the, you know, the pitcher, you know, on your number one team, you know, throws his arm out and is gone for the season. So suddenly your probabilities of who's going to win the World Series change. Now, it's only, you know, the important thing in a basic analysis is you're approaching truth, but you don't know truth. You don't know who's going to win the World Series until the last game is over, right? And we all know, we all know the ninth inning, you know, surprises and that sort of thing.

It is a commonly used tool in science, in finance, for taking, for establishing probabilities, taking a new piece of evidence, turning a small mathematical crank called the Basin theorem, coming up with new probabilities. I did it 26 times in the paper, and so I began with a 98% probability it came from nature. So, right, we've already talked about. One of my priors was this 8-1 ratio of natural to lab-acquired infection, 8 to 1, that's, you know, that's 88%. So I used a, I used the number of those, and I got to 98% on my prior. But by the time I was done with the 26, it had flipped. And it's really one in 500 chance that it did not come from a laboratory.

You had mentioned that you had done the analysis over 20 times of the Bayesian analysis to different, call them, aspects that amount up to the closest, what is the more likely answer to come to. to the end conclusions that you came to. Out of those over 20 that you did, let's take a top couple of them and start to break them down in terms of what, how did you start leaning in a direction that this may not be of natural origins? Yeah, sure. So let me frame it first. So what is a zoonosis? So it has the word zoo in it, Z-O-O.

And so all zoonoses have three components. they have a microbe, in this case a virus, in this case a coronavirus. They have a microbe. They have an animal that's infected with that micro somewhere, a population of animals, not just one animal. And then they have a human, and it jumps to human. You know, we're very sort of anthropomorphic. So things only get exciting when they affect humans.

So a zoonosis means it's been in animals, we didn't care about it, and now it jumps to humans, and we're not happy about it. But anyway, so if you think of, so you should always look at a zoonosis in terms of a microbe, a virus, an animal, and a human. The origin is where the animal was when the jump occurred. So if the animal is in a market, as the animal is in nature, as the animal is in a cave, it's a spillover. It's a natural spillover. If the animal is in a laboratory, or if it sells from an animal in a test tube, then it's a laboratory-acquired infection. So they really have all three components, though, and it's a nice way to think.

about it. So having said that, you know, I think the number one still goes back to location. So the coronaviruses in the world have a different genetic background. So let's back up. So there's coronaviruses that were existing about 3,000, B.C. And then they split into alpha, beta, gamma, coronavirus, about 3,500 BC. The beta, coronaviruses were just one species until about 1,100 AD, when William was sailing across the channel to take over the United Kingdom. At that point in time, there were what's called subgenres. So now we have subiricaviruses, murkyvirus. So there's four different subgroups from 1,100 to the present. So when you look at coronaviruses, you can see where they came from because their genetics maps to a physical

location, you know, on a map. Again, they live inside of bats. That's their reservoir. And bats only go 34 kilometers. So they're kind of pocketed geographically around the world. So when you look at the virus that caused SARS-CoV-2, you can look at its genetics. You can run a program called a phylogenetic tree. And you can see that the closest viruses to it are 1,400 miles away in Wuhan. So now you've got this distance problem. And the distance for folks in America that I like to talk about in my book is it's like an animal in the Everglades, you know, showing up in a restaurant in Manhattan and causing a disease, right? It's that same distance, which is pretty remarkable. So the fact that it shows up in Wuhan in the middle of winter, fall, the bats are all hibernating starting about mid-October in Wuhan in Hubei province, which is where Wuhan is.

because it's quite north compared to this, you know, southern China. So from about mid-October to about, you know, mid-March, April 1st, the bats are hibernating. So they're not out and about. They're not caught. Even if people ate them, which they don't do all that often, you know, they're not available. So the location became my number one issue. And, you know, I ran some work there. There's some other folks inside of drastic that also did work.

but the probability that a virus with this genealogy could have happened in Wuhan, where there also is a laboratory that's done 60% of the coronavirus research, is itself about a one in a million probability. And so that drops in, you know, right away. The other three then are looking at each of the three compartments. So with respect to the animals, with SARS-1, and with MERS, when it jumped to humans in 2003, 2015, respectively, within three to ten months, we had found that intermediate host animal.

We had found the animal who was jumping from because in the markets, it was present in 90, 95% of all the animals in the market had it. And so you could, you know, you could test five animals and four out of five would have the virus. camels in the markets in the cities where the where mers first appeared, 90% of the animals had had MERS and 100% of them had antibodies as if they'd had an infection. So that's fact one. And then China looked at 80,000 animals, 409 species over a one-year period of time. And when the WHO came in, they cataloged that. So 80,000 animals, 409 different species of animals.

How many had SARS-CoV-2? Zero. Zero. That's not expected. And even in the wet market, there wasn't a single animal in the wet market that was positive. There were some samples in the sewers. There were some people that had it, but no animals. The second is the virus. The virus every two weeks, whether it's in a bad or a human or every two weeks, when it transmits from one animal to another, one human to another, it makes one mistake out of the 30,000 letters in its genetic alphabet. One mistake every two weeks. 26 mistakes a year. So that is a marker of time in the past. When you looked at SARS-1 or you looked at MERS and you looked at the variety,

when you took the virus from, you know, 100 different people and you looked at the variety of mutations, you could predict that SARS-1 had been in animals, couple years, MERS had been in Camels about five years. When you look at SARS-2, there's no what's called posterior diversity. When you look backwards, it's all the same. Basically, it was one virus, one pure virus around October 15th. That's the statistical date that we come up with. So what you'll see is a pattern here in my discussions. Spillovers have the word diversity in every element they go on. So a diverse number of animals, a diverse virus, and diverse humans. We saw, we see no diversity in animals. We don't, we see zero in animals. We see no genetic

diversity. And even the, the virologists who have been, you know, sort of publicly saying this couldn't possibly be in a lab leak, early on, we're remarking on the fact that unlike SARS 1 and SARS 2, this virus is different because the darn thing is absolutely pure when it started. And of course, one of the hallmarks of laboratory work is you work with pure viruses. You never work with a mixture of two viruses, two anythings. It's too confusing. It just multiplies your laboratory issues. So Pasteur was the one that taught us that we always work with pure cultures.

And now, you know, 140 years later, we're still doing it. So the virus was genetically pure when it came out. And finally, the people. So in prior Zuinoses, SARS-1 and MERS, the virus doesn't the virus is growing remember it grows really nicely for decades in bats and then it jumps to cats or it jumps to camels it's it's not it's not perfect but it takes and it takes a while to to get embedded in that population a couple years with the civet cats five years with the mers with the in the camels but then it's well adapted um and what you'll what you see is it doesn't

just jump once to one human it's jumping all the time Sometimes it doesn't cause an infection. Sometimes it causes an infection nobody knows and it goes away because it's not really well adapted to humans. So it does all these practice jumps over a period of six, 12, 18 months. Once you have a pandemic and epidemic and you have a blood test for someone who's had an infection, you can go back to the hospitals, back to the blood banks, and you could take samples out and you could say, how many people in this environment were getting this virus before we knew it was an epidemic? pandemic, right? And it turns out that in southern China with SARS-1 or in the Middle East with

MERS, 3, 4, 5, 15% of people, depending on the population, whether you went and, you know, workers in the market or just people on the street, that sort of thing, 3 to 15% had antibodies to SARS-1 or they had antibodies to MERS, meaning it was practicing jumping. So it jumped to a human, it jumped back to the camel, would go back and forth. And then finally it got the changes it needed to establish itself in humans and an epidemic begins. They did that in Wuhan. They took 10,000 specimens from hospitals from blood banks that in the year before the pandemic in 2019, late 2018,

hominy were positive for SARS-2. Remember, we're expecting 3 to 15%. So that's 300 to 1,500. Zero. Zero. There was no person who had any, evidence of having SARS-CoV-2 before December 1st. So, you know, so in each of those is like a one-and-a-million event. So the location is really bad for a natural spillover. No animals have it

in nature, and it's supposed to be 90%. The virus is absolutely pure like it came from a laboratory, as opposed to talking in numbers now. SARS-1 had on average about 30 mutations in the first 100 patients. MERS on average had about 150 mutations in the first 100 patients. SARS-CoV-2 had zero mutations in the first 100 patients. So, you know, those four pieces of evidence together kind of make it really hard. And then there's, there's, you know, smaller pieces and different versions of those. But I mean, the other side of it is, was the laboratory doing gain-of-function research? Well, yes, they've done a lot of it. Were they doing it? Were they doing the kind that could have ended up with SARS-CoV-2, absolutely. And then we've learned that

they even wanted to, you know, they told the U.S. government they wanted to in some release documents last fall. So that's how you flip a 98% from nature to a 99.0.2% from, or 99.8% from the lab. One of the things you referenced earlier was that often when there's a laboratory-based infection, a worker at the lab getting an infection, and then taking it, laboratory-acquired infection, is that they often will end up at the nearest, you know, hospital to the lab. And was that the case in the instance of what was going on in Wuhan and the Center for Virologology out there? Yeah. So just backing up, I actually did part of this analysis in, you know, in my Bayesian analysis. But if you look at the six cases of

SARS 1 and the hospital where they presented, they were all within 15 kilometers of the lab where they got infected. So the hospital to the lab was 15 kilometers. When I did the analysis of SARS-CoV-2, I actually broadened it, and this was actually the analysis that got the attention of the State Department. So Wuhan, very modern city, it has some 3,000-year-old historical centers. I mean, it was there 3,000 years ago at the very prehistory, but nonetheless, very modern, 11 million person city has a very, a very well built, new, brand new, shiny, new, subway system. Subway system there, and they have nine, they have nine lines. So what I did was I took the hospitals where all the patients from December 1st to January 15th, December 15th,

December 15th, January 15th, 2020, when it was really breaking out that six-week period of time. and I mapped the hospitals that they went to in Wuhan, and then I overlay that on the subway system. So there's 46 hospitals in all of Wuhan, but there are only 11 hospitals that saw those early patients. And they all, the closest subway to those hospitals, was line two of the Wuhan system. So there's nine lines.

Now, line two is really an amazing line. before the pandemic, it carried a million people a day. So again, in America, we don't think in terms of public transportation this way, but they, you know, they know how to do it. So a million people a day would come from the outskirts of Hubei province into Wuhan to work and then go back out at night, you know, back and forth. Half a million in the morning, half a million at night. Line two has four important stops. One is the wet market. the wet market where the early patients were tied to.

One is the Wuhan Institute of Virology. So that's kind of interesting. The line that's closest to the two hypothetical sites of spillover events are on line too. The other two is really dramatic is the main station in Wuhan that sends high-speed rail all over China. So the same stop where you go to the wet market, you can also go on a high-speed rail and within four or five hours be any place in China. And then the westernmost end of line two is guess what? The Wuhan airport where there were 15 non-stop flights around the world. So you can literally go from the Wuhan Institute of Aerology.

You can walk down the stairs to the subway and line two, go to the airport, go up inside, go inside the airport, get on a plane. come out in New York City, come out in Houston, come out in L.A., come out in London, come out in Dubai. And so I call it the line two COVID conduit because not only does it, it was it probably responsible for the early spread inside of Wuhan itself, but it really was a conduit into the world very early. And one of the other studies I did was to show that people were Googling, I can't smell, I can't taste in Northern California, the end of December, 2019, you know, before we had really heard about it, before it actually, the WHO had actually announced it.

There were excess Google searches for those key words. So, I mean, I think this line two issue is a really important one. I mean, I think it gets to what we should do in the future is we probably, if we're going to build these things, as much as people want to be, you know, in the exciting, you know, big city, you know, the young scientists, it might be better to put these out in the middle of nowhere, right? So, you know, a million people, a million people a day aren't, you know, in contact with someone coming out of the lab. We're recording this podcast. It's Monday, January 17th. And could you give us a little bit of a summary of what the, there are multiple sort of investigations that

are happening around the world, some that have been concluded, some that are kind of ongoing, some by the World Health Organization. You mentioned the State Department, reached out to you, and they've looked at it. Our own government's been, you know, looking at it. Biden came into office and said this was, you know, going to be a priority. China had had its own investigations.

I think there was a press release just that came out today on my alerts that the World Health Organization had an update to their investigation. But could you summarize what some of those findings are in terms of the origins of COVID-19 and how they compare a contrast to the findings that you put together in your paper. Yeah. So, I mean, again, let's build a timeline here. December 2019, it's really showing up in Wuhan, January 2020. The whole world knows about it now. And we don't think it's going to be a big deal. We think it's going to be combined to China. But nonetheless, that's kind of the starting frame. But of course, that doesn't happen. And it goes global. And by March and April,

you know, many countries are doing lockdowns. We have serious spikes of infections. Hospitals are overflowing. Icues are overflowing. Excess deaths are through the roof. September of 2020, the W.HO, well, in May of 2020, the W.O says we're going to do an investigation on the origin. September of 2020, they put together what's called a term of reference, which is kind of a, it's a contract is too strong a word, but it's a bit of a contract. It's an agreement between an organization like the WHO or the UN who's going to do an investigation. It lays out, here's what we're looking for, here's what we're going to look at, here's the way we're going to do it. And in the case of this origin, because it started in China, it required the agreement of the Chinese government.

And so I think all of us who were looking at this from a balanced point of view of spillover versus origin from a lab, looked at the terms of reference and said, hey, they're not even looking at the lab here. And this is all, you know, just biased towards spillover. So but it was what it was. And no one changed it. We, we, everyone made noise, but that was, that was extended. They physically went to China in, you know, in January or January through February of 2021. Their report came out on April 1st of 2021.

It's, it's kind of an amazing document. So the report itself is a couple hundred pages. They have an appendices of about 400 pages. And as I looked at it, that document has the best raw material for a proper investigation of anything in the world. Because they, you know, if you look through it. Now, the interesting thing is the conclusions of that were that it likely was a spillover, it likely came from the wet market, and that the lab origin was very unlikely. That was done.

We now know, again, in retrospect, we know, that was done by a show of hands in me, where the scientists had, you know, sort of Chinese minders. So I don't, you know, who knows were the military or, but nonetheless, everyone was kind of being observed and it was a, it was a show of hands. So you weren't allowed to kind of, you know, right on, you know, it wasn't a, a ballot where you could write your, you read to really thought and put it in a box and nobody could know what you were saying. Everyone was raising their hand in front of, in front of everyone else.

So that, but that's, that's done. That's, that's, it's, it's in the binders. it's done. Sometime, I don't remember, around May maybe in 2021, excuse me, President Biden said, I need to have an update on this. So he gave the Intelligence Committee 90 days to come up with a report of their own to go back and look through all the data they could and come up with their own report. In June, excuse me, get a drink here.

In June of 2021, I was asked to testify at Congress for one of the subcommittees on the origin. So there have been several House committees and a Senate committee kind of looking at this, but it's fact-gathering. I would say it's not really, it's not sworn testimony and it's not deep dives and it's not really investigative. It's more sort of fact-finding and collecting. August, September, the IC committee came out and said, we really think, we really don't know, but we think probably from nature and a couple of the intelligence groups, we don't know for sure, but the scuttlebutt is the FBI said, you know, maybe it really was. About three of the 20 or so said maybe it did come from a laboratory.

So that's where we are. Now, the WHO has reconvened their terms. of reference in their first investigation was called Part 1, and this is called Part 2. They now want to talk about expanding the origin to other countries, other countries in Southeast Asia, maybe Fort Dietrich in the U.S., you know, maybe Europe. I mean, there's been some, there's been, you know, some, I was almost going to use the word crazy, but I don't want to, I don't want to be a pejorative. There were some very unlikely hypotheses that were put forward that, that,

that were urged to run to ground. So one was, for example, that it was coming on frozen foods from overseas into China and that, you know, the really original virus came from, you know, somewhere in Europe on a frozen, you know, fish stick package or something like that. Or that it was actually planted during the Wuhan military games in October 2019. There's an Olympics of soldiers. There's a soldiers Olympics where they do events related to soldiers. Sometimes they're running and shooting, you know, when your heart's beating, trying to hit targets and things.

So the Wuhan Olympics occurred in, I misspoke, the military Olympics occurred in Wuhan, October 2019. And some folks are thinking that that, you know, that China has said, you know, maybe the U.S. shipped it in, you know, into those and infected. Lots of these hypotheses. So that's what part two is going to be about. But other than that, there really is no formal investigation going on. I mean, I think that's one of the frustrations for some folks like me, although I'm not getting as frustrated. I think I've just about completed my analysis. Got a couple more months of some deep dives on some things that I want to complete scientifically.

And then I think I'm going to wrap it up in some sort of format like a book and put it out there and with recommendations about what we should do. Because, again, the most important thing is that we take the right steps to prevent. the next virus because part of my investigation showed that in addition to probably coming from one institute of virology, which is a hypothesis with a lot of evidence for it, but I have actual evidence that they were doing genetic manipulation on the NEPA virus, which is 50 to 90% lethal, as opposed to coronaviruses, which are, you know, under 1% to 2% maybe something in that neighborhood. So this lab is teed up to be, you know, a second spillover. of a virus that could kill half the planet.

So we really need to address this, I think, in a thoughtful fashion. Thank you for that summary on the reports and their status and what's been done and what's not been done. You know, in your paper and in the op-ed that you've written and some of the podcasts that you've been on, one of the things that you've noted is that not only does there not seem to be the open discussion around looking at some of the raw data that leans more heavily towards a laboratory involvement in terms of the initial infection, but that there were actually some players involved early on. And we may not know their motivations, but there were

some players that were involved early on who were really trying to dissuade any kind of conversation around the laboratory involvement in this. Who are some of those players? And what did you find out as you continued to put your reports together? Yeah. So, I mean, look, I'm, I'm a, I'm a pretty old school scientist. So my, my concept of science is you, you know, Lewis Thomas, 50 years ago, 60 years ago, wrote, you know, it's like, it's like you've got an elephant in the middle of a room and you've got a bunch of people around it and they're all trying to study it in different ways. And even if the janitor walks in and says, hey, you know, there's something interesting. you take their observation and you amalgamated, and you're free to have any legitimate discussion around data.

You're also free to have a discussion without having to bring your credentials, right? So you don't have to be a virologist to do statistics. And in fact, I use a UCLA statistician because my statistics are not as good as my ideas around statistics. But in any case, but so this idea that you had to be a credential virologist was part of the gatekeeping that was done. But it wasn't the only gatekeeping. I mean, I've participated in a group. They've been loosely called the Paris Group. I don't speak for them and no one is allowed to speak for them. But about 30 scientists, you know, I've gone off into business, but some of them are very highly, highly, you know, credentialed academics with decades and decades of work. We put together

a list of about 15 publications, which we sent for peer review around, aspects of the lab origin. The way peer-reviewed science works, the way science has worked my whole life, I have 360 publications that have been pure-reviewed is you write a paper, you put it in, they send it out to two readers. They're usually anonymous, but sometimes not, and they beat it up. They really make you feel like you don't know anything. You rework it, you make it a better paper. You send it back, and maybe they have just a couple edits. And then finally, there's an agreement between you and these people who've torn it apart, and it gets published. And that's the beauty and the power of peer-reviewed science. So all of us were expecting, hey, let's put our papers in,

and let's get this discussion going. For the first time in my experience, and for many of them, we got a pre-peer review rejection. So you send in a paper to a journal, and you don't get, they don't tear it to shreds, which is what you're hoping they'll do so you don't embarrass yourself in public, they simply say, this is not appropriate or this is not acceptable or this is not something, and they don't give you any feedback whatsoever. And then publicly, they talked to the public and they said, well, look, we're willing to have any discussion as long as it's a peer-reviewed science paper. And we're standing back there saying, hey, wait a second, you won't peer-review our papers. Why won't you peer-review these papers?

They're legitimate papers. So, you know, Steve Quay doesn't have an academic appointment anymore. I did teach at Stanford Medical School. So, you know, and I was in the Harvard faculty for a while. But, you know, but these people are today. They're, you know, at major universities around the world and they're putting papers in. And they're also getting rejected without being peer reviewed. So this gatekeeping function is, is quite dramatic. So part of, part of the thing that got me more suspicious, I guess, than, you know, than I should have was, was the behavior of some of the scientists in, you know, in February and March of 2020, where this paper in Lancet came out, you know, 15 of the who's who of virology and science and, you know, biology and medicine and

that sort of thing, basically saying, we know it's not a, we know it's not from the laboratory, and this is a conspiracy theory, we shouldn't talk about it. I'm sitting here thinking, this is February, you know, 2020. We don't know anything about this. How are you saying that it's a conspiracy. And then, you know, and then the nail in the coffin of that was a paper by, again, about eight of the premier virologists in the world, was called the Proximal Origin of SARS-CoV-2, basically saying this couldn't possibly have come from a lab. And in the paper, what's missing, when you talk to a scientist and you want the scientist to talk to you like a scientist. You should look for two things. You should look for them talking in two ways. They

should talk about data, particular observations, and then they talk about their conclusions. If they skip this part, you can politely ask them, well, what's the data behind that? And if they never go there, they're not a scientist. They're no longer a scientist. I finally decided that I'm going to not play polite with these folks. And there are statements in their papers saying that it couldn't come from the laboratory that are not supported by data. And so they're not scientific statements, their speculation, their opinion, their wishes. And people should realize that because we're now in a, our governments are depending on scientists for policy decisions. And if the scientists aren't using the scientific method, which is a very powerful way of thinking, it's all

it is. It's not a religion. Maybe it's becoming a religion for certain people, but it's not supposed to be a religion. It's just a way of thinking. And in fact, every child until they're four or five years old is effectively a scientist. If you watch them, they collect data and they make conclusions about the world. They drop a block. They drop it seven times. And then they say something's, you know, gravity. They learn about gravity. They don't know the word, but they know that every time they drop it, etc. They're scientists doing data conclusions, data conclusions. So I don't want to name names. I mean, I think there's a lot of, there's a lot of name calling out there. It's really disappointing where some of these major people who've spent their lifetime to get at the pinnacle,

and they should be in a position to advise us with their very best advice, have put a veneer of politics over it. You know, one of the ones actually said on Twitter, you know, I said, a lot of us were not saying it came from a lab because President Trump was saying that, and we didn't want to look like we were supporting President Trump. And I'm scratching my head. I'm saying, this doesn't even equate to me. We've got, you know, we now have probably 20 million people dead from this.

We have to know where this came from. I don't care who said what. Trump's comments mean nothing. They're not data. You know, the data is about the virus and things. So, sorry, that's a rant. Oh, it's an important rant. I mentioned to you before we started recording that when I first heard about your paper being published

and I was in touch with a team that was helping you out, helping you to get the word out, They had recommended another guest for my podcast. I had shared that at the time, this was around the time that, you know, there was tweets going out from, you know, places like the New York Times. Again, you know, some great papers and writing and journalism they've done. And just like any organization, some stuff that maybe isn't the best that's out there. But there was one particular thread in tweets by the correspondent who was covering COVID-19 saying that, you know, when are we going to understand the that any talk around the lab leak theory, the lab infection theory, as we're calling in this podcast here, has, you know, racist origins. And again, people might have their thoughts and

ideas about, you know, different things that are out there. And there may be people, bad actors that are trying to mischaracter things or using things as an opportunity to go after a particular group, country, religion, race. But we have to still be able to have an honest conversation about it. And that was one of the challenges is that we weren't really able to have an honest conversation. I also had one or two YouTube videos that we're just talking about the data around vitamin D and some of the other components that were out there and the importance of losing weight, some of the challenges of cloth masks compared to some of that more higher-end masks. And that video was flagged and removed from YouTube. So you have a

I'm sure there's some well-intentioned people that are there at YouTube. I know there are, right? There's well-intentioned people, and they're looking to the CDC, and they're looking to places like The Lancet and other major journals that are out there to say, hey, what is science and what isn't? And when a journal says, we're not even going to peer-review your paper, all of a sudden they've shut down the conversation before it can get started. So I think it's an important rant, and I think that, like all things,

the answer's in the middle, but we have to be willing to be able to be able to, able to have the discussion to get through that and step out of any tribalism to political party, to country, to have an honest discussion. Now, let me ask you, what are the implications if we simply, especially in the context of us recording and the spread of where COVID-19 is right now and the new variant and, you know, it looking like we are very clearly heading towards an endemic situation. What are the implications if we don't learn the lessons on the true origin? We hinted at this a little bit in the beginning, but let's talk a little bit more practically, especially in the context of some of these viruses that are still floating around that are

being studied and looked at from a gain of opportunity place. Yeah. So, so again, from here on, let's just assume for the purpose. of this discussion that we think it probably came from a lab. And I want to be very clear, though, it's kind of a – this was a lab that was built with French technology in China. It's a lab that was partially financed by the U.S. NIH. It's a lab that uses resources from the University of North Carolina humanized mice. It's a lab where the Chinese scientists were trained in Galvest in Texas and in the North Carolina. It's a lab that collects viruses from around the world on behalf of the USAID and other U.S. organizations. So this is a multinational issue, in my opinion, that it came from a laboratory.

So it's very important, excuse me, for me to be sure that we understand this is not a China problem. This is a peoples of the world problem where our multinational scientists have gotten together and they're doing some things that could be potentially extremely dangerous. With the assumption that it may have come from the laboratory, what I believe we need to do is to put regulations, you know, different kind of regulations around gain of opportunity and gain of function research. Again, gain of opportunity, collecting weird viruses from the middle of nowhere and bringing back to a lab in the middle of the city, a gain of function. We could go into it if you really wanted to, but there's three kinds of experiments that you can do,

serial passage, pointed point mutations, and then recombination, you know, big, big chunks of DNA. But these things, we need to change the way they're regulated. And that's almost a misnomer because they're not regulated literally at all now. And so we need to regulate them. There was, you know, there was a moratorium placed on gain of function research. The history here is really quite fascinating. In 2014, some Dutch scientists take an influenza virus that's maybe 90% lethal but can't transmit airborne. And they do an experiment where they put ferrets in cages in a room. They put the cages apart. They put a fan blowing from one side to the other, basically.

They infect ferrets with the influenza in the cage upwind, and then they see if the ferrets downwind catch it. You know, they do it over and over again for a few months, for a few months. And lo and behold, they create an airborne version of influenza. That's 90% lethal, 80% lethal. The nerd in me says the interesting thing is it only acquired four mutations. So the thing is 30,000 letters long, it required four mutations. So that shows how scary these things can get. But anyway, they wrote up this paper.

They sent it in for publication. And the world said, oh, my God, we shouldn't publish this because maybe it'll teach people, you know, nefarious things about this. So there was, there's a huge discussion about whether it should be published. It was ultimately published. Some of the details were redacted. But this public discussion, it got into the journalism, it got into the media, led to a very public discussion. And gain of function research was placed in a moratorium by President Obama, executive order, basically saying that if money was coming from the NIH, you couldn't, you couldn't fund gain to function research from, you know, henceforth in 2014.

Now, there was a, there was a checked and balance system set up inside of that, which was supposed to allow certain kinds of research that was of national interest. You know, so there was a system that was put in place. Now, in 2017, right after President Trump took over, four inches of paper were produced by the NIH saying this stuff is really safe. And in May of 2017, the Morton was released. And there was a big, there was a big symposium of the U-WIN Institute of Rology. All the players were there.

There's a big picture of, you know, like 100 scientists on the steps outside, smiling, you know, into the camera. Because they were celebrating their, you know, they're back in business in 2017. So we know that the checks and balance system doesn't work. So what is my solution? It's really quite simple. I've invented seven drugs that are FDA-approved. I've done about 50 clinical trials. And so we learned very early on that doctors experimenting on humans was a problem.

We learned about it during World War II. We learned about it during Tuscany where we were infecting folks with syphilis and not treating them, watching what end-stage syphilis and death from syphilis look like. So really bad, bad experiments, bad people experiments. So what we put in place was what's called the Institutional Review Board system. So it's a very simple system. It's a panel of lay people. So you can have a religious person or a nurse or somebody from the community, not involved

with the research, not at the institution where the research is being funded. So they're financially independent. They've got no state. And for me to do an experiment on one human or two humans or even clinical records, I have to go to them and I have to explain the benefits of the research and the risks of the research. I have to get their permission. And 90% of the time, they say, well,

sometimes I say you can't do the experience at all, which doesn't really happen. They say, well, you can't do it the way you plan to. You need to add this and this and this. You need to check back with this. You know, they put checks and balances into it because they're not comfortable with me doing it, you know, out of the box with the design you start with. That system is now part of the legal structure. It's part of the, you know, even China does all of their clinical trials with an institutional

review board review because it works. so well at being an ethical challenge. Because if you think about a patient, you have cancer and this doctor has this thing that they say, you're going to cure your cancer. You're not a neutral person in terms of taking that drug. You want to live no matter what. And so the ethics committee that doesn't, hey, you know, they're not related to you. They can say, you know, there's really no evidence that's going to work and you really should try something more traditional. That's what the checks and balances does. I am proposing that the NIH put in place institutional review board process for all gain of function research. So if you want to put new genes into a coronavirus,

you want to play with NEPA virus, 50% lethality in a laboratory, you've got to explain it to your neighbors, the ones you see in the grocery store, why this is worthwhile. You get a one-year license because that's what you do in clinical trials. You know, you get to work for one year and then you come back and tell us what you did. And that process alone would be, I think, an immense contribution to allowing the people who's, I mean, it's the world's blood and treasure that is paid for this for this experiment. Could you imagine that SARS-CoV2 began in a vial this big, and now we have probably one out of seven people on the planet, going to be seven out of seven, infected with something that started with one person in one vial, in one lab, in one afternoon. They did something wrong.

They walked into a subway, and the rest is what we have. So that's one of my, major checks and balances that I'd like to put in place. Are there financial incentives either to not have this discussion or to not head in the direction where we would have an independent board review this gain of function research? Yeah. So, I mean, part of my proposal is, you know, sometimes the perfect is the enemy of the good. So what a lot of people are calling for is let's stop. gain of function research. And what that does is that, you know, that's the, that's the lifeblood of

these 20 or 30 or 40 or 50 people. And they include some very powerful people. Dr. Fauci is, you know, he is a strong, strong believer in the value of gain of function research. I could argue with him. I could probably win an argument with him. I'm not going to go there. But nonetheless, so he's a very strong proponent of this. So he's going to fight to the death on principle that this. That should be conducted. The other 30 to 50 folks who are doing it, you know, it's their paycheck. So they either have to, you know, find another line of work, flip burgers or something, or they need to fight to the death on this. So my proposal is say, okay, look, I hear you, let's continue maybe. I mean, if it was my druthers and I was in charge and had a magic wand, I would just

stop it. It's never, gain of opportunity, gain of function research has never contributed to public health policies around pandemics or epidemics. Just hasn't. And that's the truth. We've now done it. We're doing it for about 20 years, 25 years. So we've kind of baked in a lot of data. And there's no evidence it works. That's, you know, it's an interesting reminder because, you know, you go on some of these organizations website as I did in preparation of this podcast. And very clearly on the homepage, it's, you know, a lot of talk about the mission around, you know, where's the next pandemic going to come from? And yet if we don't have an honest discussion that maybe some of the same organizations, that are looking into it contributed to it, we may not be able to answer that question honestly. Give us your current view of where all things are with coronavirus, the new variant, and just whether or not your feelings are that we're headed towards endemic. And whether you feel at all through your advocacy going on different shows, podcast, radio stations,

anybody who will have you, whether or not you feel that the origin conversation is getting more attention or less attention in the current state of where all things COVID are. Yeah, let me sort of finish with that and then I can go back to where I think we're headed. But the public interest in these kinds of discussions has a half-life. you know, and even something as dramatic as imagining how 20 million people died, you know, you can talk about it for a couple weeks or months. And then, you know, people want to move on. I think most of the world has decided they want to move on from the origin conversation.

I think for the folks that don't want to have any regulation, this is convenient. And, you know, maybe it's, you know, it's purposeful. You sort of buy time and you let the news cycle flow through and you take your hits. and then nothing happens. That's actually been written up in some emails from some of these players basically saying, hey, let's just ignore it. They're making a lot of noise out there about it,

but it'll go away. We just ignore it. It'll go away. So that's one aspect of it. And I think it's misguided because, you know, we're all here on this earth for a purpose, right? And the idea, I think the simplest idea that the Twitter version of what we're here for is we came, we lived, and the world was a better place when we were when we're not living anymore, which is going to happen for all of us. So doing something to make things better should be what you get up in the morning every day to do.

And so ignoring the fact that this might have come from a laboratory and ignoring what you would do then to do a better job of making sure it doesn't happen again, I mean, if you're not going to take your talents into that space, if you have them, I don't know. I don't know what's more important you could discuss. And that's why I did this. It's my spare time. It's my weekends. My wife, you know, wants me to finish it as soon as possible so I can get back to, you know, a normal life. But I do feel it's absolutely critical that I put down on paper for, you know, what I think are the next five to ten steps we need to take to be sure this never happens again.

and then I'm going to put it out there. And then it's like a relay race. You know, I was in high school. I was in the track team. We broke a 25-year mile relay record because there's four of us. We passed a baton. And so I want to pass the baton here to the next group of folks that will take it. But we really need to be responsible ourselves for where we put our money in this research.

Otherwise, we're going to have this again, and it might be worse. It actually could be worse. Okay, where are we with this process? Knock on wood, because this thing has disobeyed so many different aspects of virology, the Omicron variant has the combination of being the most infectious virus we've ever had. It's more infectious as Delta, and it's more infectious than measles, which before was the Guinness, you know, 10 patients per patient infected kind of R0 of 10. this thing might be 11, 12, 13, 14.

There's a story of a dinner in a restaurant in Norway. Just for Christmas, they're having their celebration. One person out of 180 was in South Africa where the virus was really catching on, goes to the restaurant, everybody's vaccinated. 179 of 180 people in the restaurant got Omicron variant. So that's an R&Ot of 179. And I don't know what the one person did who didn't get it. Maybe they left early or something.

So it's going to infect all of us. And that's kind of what everyone is realizing and, you know, kind of adjusting to the new normal around that. I might have this wrong. In fact, I probably have it wrong. But there was a discussion that I think that you were part of recently about were there any gain of function, research going on with the new Omicron variant. Was there some topic that was discussed recently that you were involved with around that? Yes, there was. I have to look at the data. I have to look at it, right? So what's Steve Quay's rule? Data and then conclusion. So three things about

Omicron are weird. Number one, I call it Rip Van Winkle because it disappeared. So this background, this background mutation rate of one mutation every two weeks, it doesn't have that. It's kind of frozen in time for most of its genome around July of 2020. And then it pops up, you know, October, November, 2021 in southern Africa. So it's missing about a year of evolution. Number two, its favorite host is not humans. Its favorite host by a long shot is mice. It likes mice about 200 times better than it likes.

human. And the final thing is, it is amazingly built to resist every antibody that anyone's ever made against those, you know, those vaccines or the infection over the course of time. So, each of us have a different immune system, but we sort of have families of antibody cells, antibody making cells, and they're kind of classifications, epitopes that we can, we all sort of to recognize. And this virus had the remarkable ability of having been mutated around every single epitope in the human race. So one way to do that is to incubate the virus with convalescent plasma. So you take, you take, you know, 20 people with the infection, you take their serum out, you've got antibodies from 20 different people, you pull them together and you

have this nice cocktail of antibodies against SARS-CoV-2. If you take the SARS virus and you you try to infect cells in the presence of that, what is the virus going to do? It's most of the time going to fail, and then there'll be a random mutation that gets around and it'll start to grow. And if you do that over and over again, serial passage in the presence of convalescent plasma, you get an escape virus. If you grow it in mice, you're going to get an escape virus into mice. So in the spring of 2021, I remember having this, oh my gosh, you know, hitting my forehead moment when there was a paper out of South Africa where they were doing experiments, where they were, they were seeing if some of these variants could get around the convalescent plasma.

You know, what is the next phase? Because, again, they were trying to think, how can I get ahead of this virus? And I put that away. I mean, I just said, that's really dangerous gain of function research. And then the thing shows up the end of 2020 in South Africa. So three weird things about the virus that all would be consistent with coming from a laboratory and are hard to explain from nature. I'm not going to run stats around it and math around it.

It's, you know, it's, I mean, it's very much worth knowing about. But those three things are quite weird for a natural virus. Are there any aspects of the virus, whether it had mutated on its own or whether there was laboratory involvement in the mutation? Many people are looking at the new variant, Omnacon, and are looking at it as a sort of nature's vaccine, right? Nature's vaccine, quote unquote, that is now making a bunch more people in a milder way have longer T-cell and B-cell memory to be able to fight off, you know, potentially future variants. What are your thoughts on that? Yeah. So, I mean, I want to get back to

it, it stimulated a conversation around, you know, this, to me, crazy. public conversation we've had around the fact of comparing natural immunity to a vaccination immunity, right? So I think you learned in college, you definitely learned in medical school ad nauseum, the natural immunity is a much stronger immunity than vaccinated immunity, just by definition. With a spike protein, we're immunizing with about 11% of the virus. There's another 90% of the virus that's important. And this virus actually does some very crazy things. It puts some proteins into your bloodstream that mess with your immune system. So this thing called ORF8 suppresses your interferon response. Orph 3A messes with T-sale presentation of antigens. So I think we would have

predicted from medical school kinds of things that natural immunity would be a much stronger, more robust process than vaccinated immunity. And yet we're not having that discussion. And there is discussion around it. And so doing, for example, antibody tests. People say, people have asked me, you know, should I get a booster in us? What's your opinion on that? And I say, well, if you really want to do good science, you'll go and you'll get an antibody test and you'll see what your antibody levels are. If they're sufficient, you know, maybe you don't need it. You know, that kind of thing. I mean, I don't practice medicine, you know, remotely, but you always want to get information from your own doctor. But those kind of things. But we aren't focusing on that. I mean, there was a

wonderful study out of the UK where they've nationalized this, where they show that something like 98% of people between 40 and 80 have antibodies. And it's either natural or vaccinated. You know, they're measuring antibodies. They don't care. And that's a really good thing. But we failed to have that conversation. And, you know, treating the American people like they're, you know, in third or fourth grade is just, I think it's just wrong. It's just ethically wrong. And so, you know, the idea that, well, we can't tell them the natural immunity works because we want to push the vaccines, that, you know, that kind of concept. Lay the vaccines out there, talk about their benefits, talk about their side effects, let people make informed decisions based on their own

life, their own whatever. That, that, I think, would have been a better approach to this. So I'm not sure I got off on that. So Omokron grows about three or four times faster, more abundantly, in the nose and the back of the throat. So if you sneeze, if you cough, I mean, it's the cough for around the world because that allows it to spread. That's why it's more spreadable. It doesn't grow as well, about 1-6 as well in the deep lung. So it's not going to cause the bronchitis and the pneumonia, which gets you in the hospital, gets you in the ICU, gets you on a ventilator, kills you eventually if you're not careful.

So that's a nice combination. The other thing that's really strange about it, scientifically, so what is the scientific data that they're calling strangest. SARS-CoV-2 has this fur-insite on its spike protein. Never seen in a thousand years in this branch of coronaviruses, never once in nature in a thousand years and it shows up here, 11 times we've been put it in the laboratory, because we know every time you put in the laboratory,

it makes it more infectious. So that's why fure-insites are put in the lab 11 times since 1992. So when SARS shows up with a fure-insite, that's never happened in a thousand years ago, okay, well, I think I know where that came from. Anyway, Omicron has a fure-insight. it's now done things to protect it. It's not cleaved.

So Omicron's fear in sight is not cleaved. Now, what's the implication of that? The site of implication is really, really powerful. One of the other things that SARS-CoV-1 original did was when the spike protein is cleaved, the back end, so it's spike protein SP, and then the cleavey site, to the left of it is called S-1, where it binds to your cells.

The back part of it is called S-2, where that's the part that punches the hole in your cell. It's like a hypodermic needle, if you could imagine it. So having the Furencite cleaved in the cell in the original SARS-CoV-1 allowed it to do something called form a syncyum, which means instead of coming out of the surface of the cell going into your air or lungs or bloodstream, it went sideways into the cell next door, and it causes cells to fuse.

So when you look at it out of the microscope, what you see in an autopsy or, you know, person with pneumonia is you'll see this huge pancake-shaped cell, which may be with 20 or 30 nucleuses. It's a crazy big cell. The virus replicates in 20 cells without ever coming out, and then it bursts. The whole thing just explodes,

and you get a 20-times dose. So that requires the cleavage at the S-1-S2 site of the furen site. So SARS-1 did that, And that was one of the really nasty things about it because you'd get it in the lungs and, you know, you wouldn't be doing a lot of production or sputer or something for maybe a day or two because it was growing sideways sort of under the rail, like tunnels, like tunnels in a war zone. And then it would burst out. The Omicron variant can't do that.

And so it's not going to be, it's not going to form these sensations. And that's part of the reason it's not as pathogenic. So, you know, I like it in the. in the context of being a virus that is going to be low risk for most people. Comorbidities are the key question of sort of any infectious disease, but in this coronavirus and omicrous, that's the thing to think about. So comorbidities, obesity, you know, diabetes, cancer, immunocompromised, you know, AIDS, HIV, autoimmune diseases.

is people that see a specialist doctor are sort of by definition someone with a comorbidity. My friends with children say, well, how do I know if my kid is going to get a serious infection? He says, well, are you taking them to a university hospital once a month for care for something? No, I'm not. Well, then they don't have the kind of comorbidity that's going to be serious. Because, you know, the Omocron variant in California, the Kaiser system did a study of 52,200-something people. they had one death, one Omicron death out of 52,000. So this is definitely something we can live with and manage.

As much as every death is horrible, we're used to 60, 70, 80,000 deaths a year with influenza never makes a news. You know, we never talk about it. We never close schools. We never do anything at that level. So, you know, and the question is, well, could it become more pathogenic? I suppose it could. But remember, this virus has only one goal.

and that's to infect as many people as possible. Once somebody goes in the hospital, it's sphere of influence. The virus is limited, right? It's got the person in the bed next to you and it's got the nurses and doctors. You go in the ICU, you've got your own room. Virus does not like that situation. So evolution-wise, those viruses that do that don't tend to pass on very well. It's the ones that can stay in the community that, you know, you can spread it asymptomatically.

You don't even know you have it and, you know, you still go to work, or you go in the subway or you, you know, you go to a restaurant. So knock on wood, Omicron or the next variant, because there will be another one, will continue to be as infectious or, you know, I don't know how it can be more infectious, but as in the same kind of pathogenicity. Let me pivot here as we wind down in our interview. And I just want to say thank you again, Dr. Quay, for coming on and walking us through all that in your work and advocacy.

Again, all this is around, how do we get prepared? around the next pandemic and have an honest conversation around that and really step out of any sort of tribalism for the betterment of the human race as a whole. Are there any topics here that we didn't get a chance to cover that you wanted to touch upon? No, I think we've, you've done an excellent job. And together, we've kind of walked through some of the major issues that happen with Cyrus COVID-2. And I think my solution around, you know, putting this under the drove the people in the community. It's sort of like a jury system, you know, where we have the Institutional Review Board is a middle ground that I think, it would be very hard for me to imagine

a gain of function jockey, as we might call them, gene jockey, objecting to that. You know, they might complain behind the scenes, but they'd be hard pressed to do it in public. So that would really make me, allow me to sleep a little better at night, because again, my work showed that the wind instrument of virology is doing gain of function research with the NEPA virus, which goes sort of straight to your brain is 50 to 80% lethal, always trying to compete with Ebola on its lethality. And they're quite public about working on it. They did a symposium where, you know, Dr. She, the lead scientist,

the witness virology, has a presentation around her work on the NEPA virus. So the fact that she was doing gene manipulation, I don't think was publicly known, we revealed that. We were able to get inside some raw data that she had published and tease out the work that was going on in the laboratory. It's basically a way to forensically go into a laboratory and see everything they've done for the last two years because this gene research is so sensitive. If you do one experiment two years ago, the machines will still have evidence of that two years later. It's quite remarkable. So we were able to do that. But no, I think we've covered most of the aspects of this.

We all would like to get, you know, back to a normal life here where kids are in school and there aren't masks and we're just, you know, living our life. Well said. How can our audience keep in touch with you? You know, you have a few places that you're semi-active on. I would love to mention that for anybody that wants to continue to follow your work. And you wouldn't mind mentioning, you know, your company and also you've written a book with another one on the way, it sounds like. We'd love to get those resources mentioned. Sure. Yeah. Well, I have a website

at www.DR-Qua-Y dot com. Email is Stephen at Dr. Quay.com. So we'd love to hear, you know, comments, suggestions, anything I can do to help. You know, my COVID-Stay-Safe book was written primarily to help people before the vaccines were out there. I'm a, I'm a strong advocate of at least the first two vaccines. So, you know, I'm not sure it has legs anymore, but it does have some good tips around things you can do to mitigate against the infection or things you can do if you get the infection. I have a chapter on how to not die from COVID. It's probably my most read chapter just by the title there. But I really think that one of the things around exercise and intercostal muscle strength is a surprisingly strong correlate with

whether you get pneumonia from COVID and whether you die from COVID. And there's some specific little devices you can use to get the exercise for those intercostal muscle. Well, lots of tips around how to stay healthy. You know, because wellness, they don't teach that in medical school, but, you know, 80% of staying, having high quality life is staying healthy, not getting, not getting over getting sick. And there's a lot you can do before you get healthy with diet and exercise and lifestyle habits. Well said. And we'll have a link to all those inside of the show notes. Dr. Stephen

Quay, thank you again for coming on. I really appreciate it. No problem. Enjoyed it. Thank you.