We have heard on other podcasts here, that experts think the pandemic began in the Wuhan Institute of Virology.
Now Back Story Host Dana Lewis interviews Dr. Steven Quay, a scientist who has run statistical analysis that seems to indicate a lab leak was almost certainly the cause of the pandemic.
And Quay and many other scientists believe that Covid19 wasn't a naturally occurring virus, but came about through controversial science called 'Gain of Function' experiments, and that the virus must then have escaped.
We have heard on other podcasts here, that experts think the pandemic began in the Wuhan Institute of Virology.
Now Back Story Host Dana Lewis interviews Dr. Steven Quay, a scientist who has run statistical analysis that seems to indicate a lab leak was almost certainly the cause of the pandemic.
And Quay and many other scientists believe that Covid19 wasn't a naturally occurring virus, but came about through controversial science called 'Gain of Function' experiments, and that the virus must then have escaped.
Dr. Fowchee. Do you still support funding of the NIH funding of the lab and Wu Han Senator poll with all due respect, you are entirely, entirely and completely incorrect that the NIH has not ever and does not now fund gain of function research in the Wu Han Institute. Do they fight Eric? We do not fund your barracks gain of function research. Dr. Barrett does not doing gain of function research, and if it is it's according to the guidelines and it is being conducted in North Carolina.
Speaker 2:Hi everyone. And welcome to another edition of backstory. I'm Dana Lewis, that was Dr. Anthony Fowchee and Republican Senator ran poll squaring off over the origins of coronavirus. Paul accusing the national institutes of health of funding, risky Chinese research into bat coronaviruses in Wu Han. The research is called gain of function, which turbocharges viruses to spread to humans. The idea being that scientists can then anticipate the next pandemic outbreak in a laboratory it's risky science because there have been numerous lab escapes of the viruses on this backstory was COVID 19 created in the[inaudible]
Speaker 3:Lab. Did it escape? Did the Chinese cover it up? All right. Joining me now all the way from Taiwan is Dr. Stephen Quaye. Hi, Steven.
Speaker 4:Hi, Dana. How are you doing great.
Speaker 3:Before we launch into the theories of the origins of COVID-19, let's just establish who you are, because it's important, right? Because we're talking about science. So you are part of the Paris group, which as I understand is a couple of dozen, just over a couple of dozen scientists with, um, some of them are mathematicians. They're not scientists, there's a lot of different disciplines in there, but that group was formed because, and what is its raise on Detra?
Speaker 4:It's mainly a curiosity around the origin. Um, everybody has, you know, pretty busy day jobs of, of one form or another, but we've committed to meeting once a month, uh, by zoom, um, for about four hours. And we usually have someone in the group where we have a group, someone outside the group present, uh, some scientific aspect of it. Uh, and then we have discussions. I mean, we've, we've put out two letters, uh, publicly to, um, support the who into, into support investigations, further investigations. And that occupies some of our time, uh, the logistics of getting those letters done on the sword. But, uh, and
Speaker 3:You are a doctor of what and what is really your specialty and your
Speaker 4:Strength. So, uh, I have an MD PhD, PhDs in chemistry, uh, taught at Stanford medical school for about 10 years. Yeah, it's a, it's pretty good school down there in the mid peninsula of California. Uh, my, uh, uh, residency was at the mass general at Harvard and I was in a Nobel prize winners laboratory at MIT. So during the day I was learning to be a doctor and at night I was doing photochemistry across the river at MIT. You're not a geologist. I know I haven't, I've invented a treatment for, uh, for a particular, uh, influenza, uh, using sir. And a, so I have 87 patents and I've invented, uh, seven drugs that are FDA approved, including the gadolinium that's used for MRI contrast. So, uh, about 80 million people have used that drug. So, uh, I'm, uh, I'm, I'm a really nerdy scientist. This is probably the core of Steve cuase. Uh, back in the day, 20, 30 years ago, I would take, take home an inch of before the internet, an inch of scientific papers that I xeroxed. And that was my sitting on the patio with a drink on Sunday afternoon. Uh, this is the way I spent my weekends. So fast-forward, I now do it on the internet.
Speaker 3:Let's talk about the origins of COVID-19 because you were also, I understand a signatory to this letter, um, from again about 26 scientists. I don't know if they're the same as the Paris group. I know some of them overlap, um, which essentially essentially says to the, who look, your investigation was flawed from the beginning, the, the membership, uh, that Chinese demanded in terms of the scientists that were on that panel essentially gave the Chinese government a veto and your findings. You tell me how you want to put it diplomatically, uh, just don't hold water. And we need to start
Speaker 4:Again. Uh, yes, that's essentially what the letter says. And, um, you know, there was a second letter that actually tried to offer a blueprint of, if you are going to start again, th these are the people you need. This is, these are the skill set of the people you involve. These are the steps you should take, et cetera, et cetera. So tried to lay it out pretty clear. Um, so with any sort of impetus, they have, they have the tools they need to do it right. A second time,
Speaker 3:The lineup on the theories, there, there is one that says maybe it was in bats and then it jumped to another host, and then it became, um, you know, it was then transmitted to humans and, and, uh, was able to replicate in humans and grow the other is a lab escape.
Speaker 4:Yeah. So, um, I've written a basing analysis of what, uh, of those two theories. Uh, I uploaded it on Zanotta. I think in the end of January, it's been viewed 140,000 times. So just for perspective, I written about 360 publications, scientific publications on various fields in that, uh, this one is one or two orders of magnitude, better than anything else I've ever written. The Bayesean
Speaker 3:Is kind of, um, of statistical math formulations on what are the odds, right. And, and I understand that you think through your Basie and calculations, um, that a lab origin was 99.8% possibility.
Speaker 4:Yes. Uh, in the legal standard is called beyond a reasonable doubt. So, um, basically it is a three-step process. You, you establish a prior probability based on whatever, you can get your hands on, you do an experiment and you see which way it leans. You drop it into base equation, which is a very simple bit of math. My eighth grade daughter does it routinely. And then you get a new unit to get a new outcome. So 26 pieces of evidence were run. My starting hypothesis was 98% probability. It came from nature. But as you said, I ended up, uh, greater than 99% from the laboratory. Okay. So let's
Speaker 3:Kind of walk through this a little bit. Um, first of all, in terms of hosts, if you go back after an outbreak of a pandemic, you generally find patient zero, and then you, uh, or patient number one or whatever it's called. And then you go back and you find the animal hosts. Um, in SARS 2003, there was an, an immediate host. So that was a, that was
Speaker 4:A cat. Yeah, it's called the civic cat. It was found four months after the first year patient.
Speaker 3:Then in 2013 with mirrors a camel,
Speaker 4:It took 10 months, but you're exactly right. It was the Campbell's SARS. We're more than a year into this 16 months, eight 80,000 samples of various animals around China. I mean, one of the biases is that you, you absolutely know China has to be motivated to find it in nature, right? I mean, I think that's an intrinsic either bias or preference, but so after testing 80,000 animals and not finding a single case of it, um, to me, that's one of the most screaming pieces of evidence that came out of the, who study that really needs to be addressed.
Speaker 3:Chinese would say they just never came from China that you need to go look in Thailand and Thailand or somewhere
Speaker 4:Else. One of the, one of the problems with any of this theory is the, the, the virus keeps a clock or a calendar or a diary. However you want to describe it, but basically you can use mutational analysis and phylogenetics to say which virus came before, which virus and therefore put them in chronologic order. Um, that is one of the important things I do in the Basie and analysis is the, the genetic patient zero. I don't believe it's patient. I don't believe it is the actual patient zero cause it's December 20th, thereabouts, but what's from a PLA hospital, every patient and every specimen from the seafood market is downstream from that. Uh, every, every
Speaker 3:Patient close to the Wuhan Institute of virology, by the
Speaker 4:Way. Yes. I mean, I, I actually did a separate investigation where, which concludes what I call the line to COVID conduit, which is, is basically looking at which hospitals where the December patients wind with the assumption that they went to the nearest hospital for where they live kind of, and then which, which of the nine subway lines they were near, all hospitals were along line too. And that is a, like a 180,000 probability,
Speaker 3:Right? Why is it important? Where does line to run to and
Speaker 4:From, I have some very unique features. So it's the closest station to the one in sort of neurology. So, uh, if, if a, if a, an asymptomatic worker came out and took the subway and they would go downstairs, it carries 1 million people a day in normal times, you know, obviously back then before that. So that's, so if you imagine it's a back and forth for people from the suburbs going to work as a half a million people, and that's probably coincidentally, but nonetheless, the number of people have infections. They said they had an in, in Ruan was 500,000. It also has the wet market as its closest, uh, is it's close to subway station. And in fact, the who said they had a map of the infections inside the wet market and they're they're asymmetric. So the west entrance has more infections than the east entrance. And it's the west end entrance that is closest to the line to subway. Now it gets really cool for amplification because the next station from the, from the, from the wet market is the station where the high-speed rail goes. So from that station, you can go to any corner in China that the high-speed rail services in a matter of hours, if you continue to the end of line to your, at the international airport. So you can literally go from the oneness neurology downstairs, never go outside again and come out doors in London or Paris or Dubai or Houston, um, being entirely indoors. So, uh, I'm, I'm really looking for someone to help me with an analysis show, how much amplification that subway connection probably had, because it's independent of whether it came from the market or the lab. It satisfies both of those, but carrying a half a million people a year and having those two major conduits inside of China and into the world, it probably is part of the reason this thing spreads so aggressively, where do you
Speaker 3:Think COVID-19 began? Some people trace it back to, uh, a bat cave, um, where several minors became sick. Uh, I think three of them died and those samples were later taken to the Wu Han lab, uh, where they were doing work on them, trying to understand the bad viruses. And if an indeed it came from a bad at all, it came from a cave.
Speaker 4:Yeah. Yeah. So, so we know that that again, after 16 months and literally thousands of animal testings looking for closest relatives, um, the closest relative is inside the came from inside. The one is a virology, a bad call, a bad virus called ROTG 13. It was collected in 2013. Uh, in those in they'll say minds with the miners were sick. Um, there were, uh, there were literally hundreds of samples collected and there, there are eight really critical ones that we would love to have the sequences for because we've seen phylogenetic tree. So Dr. She has, you know, done done presentations and she's, she's teased us with these other seven that are very, very close to our 13, but no one in the world knows outside of the one Institute knows what their sequences are. Uh, I think a lot of us suspect that probably a closer relative in the actual precursor to the gain of function research that led to SARS cov two is one of those other seven. My take is RTG is too far. Uh, you've got to come up with 1100 changes to get from RTG to deciders Coby to, I can do about 600 with kind of two quick things in the lab, but the other, the other 500 are, are too difficult. We know
Speaker 3:That that lab at one point was doing gain of function, which is essentially a scientific, uh, scientific term where you scientists and it's very controversial. It was banned in the United States at one point where scientists work with viruses and they try to strengthen them and try and determine when they may through mutations, jumped to humans and thereby head off the next pandemic. And then, you know, there's been a lot of denials by the Chinese that they were doing gain a function. And yet it, it was published at one point that the, the bat lady, the woman who ran the lab essentially was indeed doing gain a function, but did that lead to COVID-19? So you, do you want to, you want to try and string some of that together for me?
Speaker 4:Well, there's, uh, look a doctor, she, Dr. Barrack have worked together. Uh, they are either they're one and two, and you can, you can pick, which is which it depends on the day and in the year probably, but they're the number one and two coronavirus, uh, scientists in the world, uh, doing synthetic biology, which is gaining function, which is basically taking them apart, putting them back, back together, mixing, mixing pieces from different species of viruses,
Speaker 3:A backbone or element
Speaker 4:Well, well, with, with, with, they're always, they're always a bad virus backbone. So, so this Corona virus, no matter where it ends up, started at some point in time in bats and whether the intermediate host is a, is a camel or a civet or, or something else, uh, in this case, we think it's probably a humanized mice. Um, but nonetheless, and, and then, and then it jumps to humans, but what's
Speaker 3:A humanized mice mouse.
Speaker 4:Yeah. It's a little, it's a little scary, but so you take, you take a mouse embryo and you put human genes into the embryo. Um, so that when it's born, it's a, it's a mouse, but it has human lungs, respiratory system. So if you want to test what will happen precisely in humans, uh, it's, it's a great model for that. Now, Dr. Barrick developed that model and he, his mice physically went from North Carolina to, to the one Institute that's documented again and in publications where she, she thanks him for his mice. It just sounds
Speaker 3:Like dark arts, quite frankly, but I'm not a scientist,
Speaker 4:You know, it's well, it's, it's, it is. Um, and by the way,
Speaker 3:I mean, I'm not, I'm not altogether naive either because I've talked to, I, you know, I, I was based in Russia covering biological, chemical, uh, warfare, the dismantling of the former Soviet union's, um, incredible programs and, uh, an assistant secretary of defense, not a Republican or Democrat in that case under the Obama administration told me that, um, the gain of function research is highly controversial and should be banned and was banned. And, uh, it's high, high risk, you know, again, a dark art in, in, uh, in essence.
Speaker 4:Well, it absolutely is, again, in my basing analysis, I talked about the fact that it's, it's absolutely published for 30 years. There has been on average 0.9. So that rounds to one, one laboratory acquired infection per year in Asia. So, uh, these are, these are Cyrus, COVID one, uh, you know, other viruses one a year. So, um, you know, you're just playing Russian roulette with, uh, the 7 billion people on the planet.
Speaker 3:There is no good explanation. Uh, I'm reading this, this, this was written by Nicholas Wade, who I interviewed about a week ago. There is no explanation of why a natural epidemic should break out and Wu Han and nowhere else, there is no good explanation of how the virus acquired. And I'm hoping you can explain this it's furin cleavage site, which no other SARS related beta Corona virus possesses. What does that mean?
Speaker 4:Yeah. So it's one of my five facts that I, that I talk about that are not in dispute. So there, there are five facts about this event that every person, every scientist agrees to, but they, and they all lead to the conclusion that came from a laboratory. So one of them is, is this unusual fear in sight? Okay. So the spike protein is how the virus gets into cells. It's basically like a key and the lock that the cell has is called[inaudible]. So it's a protein on the surface of your lung cells and the spike protein binds to it. And then a second step has to happen where the other part of the spike protein makes a hole in your membrane and injects the RNA, and then it takes over the cell and then it makes a million of its own copies. So in order for this, so th this, this, the spike protein is one big protein. So in order to do that physical process of injecting the RNA, it has to actually physically move and, and the, and the, and the, the, the binding part, you got the binding parts of the ACE two, and you've got the other Proctor. This part has to physically move like a hundred nanometers, which is a huge distance on a molecular level to get the, to get, to let the RNA go into the cell. So the spike protein has to be clipped. So most spike, most beta coronaviruses clip it at a place called[inaudible] one, there's only a couple enzymes that will clip it there, which means there were only a couple kinds of cells that it can go into. So we've known since 1992, 11 different laboratories have done a new doctor, Dr. Barrick and doctor. She had the willingness to dos since 1992, 11 labs have put fear in, in coronaviruses and 11, 11 times it does one thing. It makes it either more, in fact, more transmissible or more lethal or all of the above. Uh, and the reason is it, it gives a new way of activating that spike protein with, uh, with an enzyme called furin, which is our enzyme. So basically the, the virus is very economical. It doesn't bother having an enzyme to activate itself. It knows with this, with this new, pure insight, uh, that we'll be able to get into a cell.
Speaker 3:You've never found fear in cleavage sites in natural occurring, uh, proteins, or what do you want to
Speaker 4:Call it? So, so look at the virus. Kingdom is very big. So influenza uses them all the time, all the time. Um, certain other viruses use them all the time, beta coronaviruses and never seem to use them. So, so we've, we have over 2000 sequences of beta Krone viruses from nature. And the number of Ference sites is zero. It was one is, so I was going to be too. So there's no natural fear on site, in any beta coronavirus. That's just, I mean, look at zero out of 2000, you asked a statistician what the incidence in the population is, and it's, it's, you know, under a 10th of a percent,
Speaker 3:It tells you, it tells you what about COVID-19 that fear in Cleveland site?
Speaker 4:So it has, it has it, but,
Speaker 3:And it tells you what about the fact that it has it
Speaker 4:Okay. So if there's, it doesn't, it tells you it was lab created well, yeah, so basically, yes, it's never been found in nature in that class of viruses and in, in, in 11 virus, in Landon laboratory, since 1992, it's purposely been put in, uh, including coronaviruses to make them more effective. So that's one layer of the, of the fear site, which makes it special. I call it the, the immaculate immaculate cleavage site, because it literally has to be if it came from nature, um, the next level is the genetic level. So the, the, the fear inside is four amino acids in a row. Now I worked with golden Cron at MIT. You've got the Nobel prize for the genetic code. So there's three basis in the code for every amino acid. So it's, it's redundant. So, so your genetic blueprint that makes proteins has three nucleotides, one amino acid, three one three one three one. So there's six different three letter words for one of the amino acids in the Ference. I call our genie there's six different words for the same amino acid. It's redundant humans, like a particular letter word CGG bad. Coronaviruses hate CGG out of the 64. So if there's four nucleotides and three letters in a coat on, you know, that's, that's, you know, that that is 64 different possible codes. So the least popular code on for Corona viruses is CGG they hate it. They absolutely hate it. And yet here it is, here are two of them together. Now I've looked at 580,000 Cotons in beta coronaviruses with the help of a computer. And there are not, there is not a single example of, of the, of the two together. CGG CGG next to each other,
Speaker 3:Back to Nicholas Wade last line, where he says the natural emergence theory battles of bristling array of implausibilities.
Speaker 4:Yeah. So, so I've been, uh, you know, I've been working with Nicholas for about six months weekly, uh, with, uh, with, uh, you know, some of the science behind, behind some of his writing. So, yes. Um, so that, that's a very that's, that's absolutely weird. Now, why, why would the flip side of that is, is there a, is there a laboratory reason why you'd put CGG CGG in, because if you think about it, if you've got six possibilities for the first Argentine six for the second that's 36 combinations, right?
Speaker 3:I mean, why would you, why, why as a scientist, would you put
Speaker 4:It in? Yes, exactly. Why is a scientist? Would you put it in? So we know that nature is never going to put it in in 580,000 code ons. It's never appeared there before. So nature hates it. Why in the heck would a scientist do it? If there's 36 possibilities, it's very simple. There's a, there, there, there is an old technique where if you, if you inserted something genetically and you want it to follow it in your experiments, you would put in what's called a restriction site. So you'd put in a set of amino acids that gets clipped by a, by an enzyme. You can buy off the shelf. And then when you run a gel, if the protein isn't, if it's still in there and intact, the protein runs very high on a gelatin. And then if it's been cut accidentally or it's been lost or something, you don't see it. So it's, it's a very common laboratory technique. The one in suits that they've been doing it for years, where you, you, you know, when you do an assertion, you purposely put in one of the restriction sites, so you can follow it in the laboratory. Uh, that's the only one of the 36 that has a restriction site like that. So a lot of motivation for putting that in there.
Speaker 3:Well, the allegations have been that, um, the us national Institute of health provided funding for gain of function, experiments, and move on. And then you had this very telling, uh, Senate intelligence committee investigation last week, where a representative, um, Republican Senator, sorry, ran poll then, you know, gets in this, w what looks almost like a court examination with Dr. Fowchee, um, who was the head of the national Institute of health, um, were you in front of this group kind of categorically say that COVID-19 could not have occurred through serial passage in a laboratory Fowchee? I do not have accounting of what the Chinese may have done. I'm fully in favor of further investigation of what went on in China. However, I'll repeat again, the NIH and the NIH aid category, categorically had not fund funded gain of function research to be conducted in the Wu Han Institute of neurology. Does that ring hollow?
Speaker 4:Um, I think it does. I mean, it may be, you know, in a really lawyerly court, like way, you know, there's a technicality. So what we have is we have the grants that EcoHealth was funded, and we have the subcontracts to, to sort of Realogy inside those grants. So we know exactly what was expected of the WIB inside the grant that EcoHealth got from NAA ID, which is funky cheese, uh, Dr.[inaudible], uh, work it's clearly, it's clearly a gain of function research. Now, the money didn't go from, from an NIH to Han and went from NIH to eco health, to Wu Han, if that really is what he's relying on, it's, it's disappointing, but, um, I don't have another explanation. Now, he actually also said during that interview that there was no gain of function research being done. And I think on the face of it, the document, the not on the face of the documents that are available to the public, uh, you don't have to even do a foil request. You can just go online in the NIH. You can see, uh, they're describing Ghana function research in the five-year grant that was funded the fund of the one Institute. They don't call it, gain a function. We don't call it, gain a function, but to describe, but what they describe is gain of function. So the gain of function is a very broad definition of just increasing the, the, the transmissibility lethality, uh, or infectivity of a, of a, of a virus in human, in human population, uh, and using humanized mice and, and improving in purposely causing testing to test for spillover potential is exactly that the, the, I mean, it's, again, I will try to pretend to be interested in what they were doing. So the idea was, can I deal with how close to SARS cov one, so we know Colby wants spilled over, and then we know that there are these virus that are 60% similar in 70% and 80% of the 9%. Literally what they were saying is what percent doesn't have to be like SARS Coby one. So we know it spills over, and then we can use that number to go out in nature and say, well, here's a virus that's 85. So it's not likely here's one that's 92. So it's likely giving them the benefit of the doubt. That's probably what they were trying to do. But, um, we know we know what the outcome is.
Speaker 3:Steven, just a couple of quick questions as well, before I let you go. The, um, the data that was online, some of it from the Wu had labs, some of it that you required a password. I understand all of this appears in September, it's taken down in September. So October, November, you know, some three months before the official outbreak, although a lot of people think that they already had cases well into November. Um, what, what do you make of that? And how important is that data
Speaker 4:Critically important? I mean, uh, 3:00 AM, September 19th, the server that was available for the world for most of it. And it also did have a password protected carbon, but, you know, Steve quake could have gotten on it the day before, but it's taken offline. Uh, now they, they slept up and they said, well, it's taken offline because of hackers around the COVID infection. And then they realized, oh my gosh, this was in September. So I'm not sure. They're still saying that's a pretty big slip up. Well, it's, it's, it's out there. I mean, that's, that's how it is with cameras anyway, but, um, it's not available to this day. So I asked Peter dash Jackie in a, in a public forum here, uh, maybe two months ago, uh, where if, uh, if he would provide access to those files, uh, and he literally said, it's, it's on the record there that, um, he knows what's in them. He's looked at them and there's nothing there of interest. Uh, and that I, then that that's the basis for not providing them
Speaker 3:And show him, show him to the world, because right now that lab is under look. I mean, I, I think you, you tell me if this is an overstatement, but it seems to me that there is a consensus amongst the scientific community. Now that at the very least there are huge gaping, uh, gaps in the China, Chinese official story on that lab. So if you want your lab, if you really want to support your, your suggestion to the world, that it didn't originate in the lab, then make all the data available. That's the best thing that they could do right now to the who or
Speaker 4:Whoever agreed, uh, whether they would do that or not as is a political question.
Speaker 3:Right. Okay. So we we've, but that, that it does still exist. We think,
Speaker 4:Oh, I hope so. I hope so. Are we ever going to get to the bottom of this? Well, see, it's an interesting question because, um, with my analysis, all of my evidence is circumstantial, but I remind people that, you know, uh, there are many sort of murder trials in which all of the evidence is circumstantial. And yet we quite routinely can determine, uh, the guilt of, of someone with a proper process and adjudication and, and, and, and getting to beyond a reasonable doubt. So despite it being circumstantial, I believe it's, it's strong enough at this point in time to conclude, uh, again, beyond a reasonable doubt that it came from the laboratory that the, the key thing to remember with, with, uh, these coronavirus pandemics is there's three components. There's the intermediate is there's the host, the animal hosts, the humans and the virus. This is the only one in which it's a singularity that is, there seems to be only one animal because we can't find any in nature. So there's, there's one animal. Um, all the, all the human cases go back through one patient at the PLA hospital in muon. So when president Trump got it, you can follow the mutations to his virus back to the PLO hospitals. So there's a single area there. Um, and, and the, and the, and the sequences inside the virus. Uh, so, and I'm sorry, the, the patient there's absolutely no patients before December who had any hint of this, of this, uh, infection. So it is a true singularity,
Speaker 3:One animal, one patient, one virus, one animal, because normally it takes a virus time to become more and more transmissible. There should be a trail of patience.
Speaker 4:Oh yeah, exactly. And again, they, so in my basing analysis, I looked at, at, at stored specimens, uh, in Taiwan, in China, I had about 2000 of them in the public record. None of which had SARS COVID two. So the, who has actually updated that. So they, there are 10,000 specimens, um, in that they reported on their, in their report with zero, uh, serial conversion before the first date. So nobody out of 10,000 in an archive specimens had had SARS COVID two, what is the MERS or SARS Coby, one history they're one to 4%. So that means a hundred to 400 samples should have seen. It should be. There should be evidence of Cyrus. Kogi two in a hundred to 400 specimens out of two, out of a 10,000, there was zero.
Speaker 3:The reason why we just spent 30 minutes talking about this and why you're spending part of your career studying this and why so many other scientists are looking at it is because in order to understand the next pandemic, you have to, you need to trace back the origins of this one. Can I ask you something that occurs to me? And you can tell me whether it's ridiculous or not, but in trying to fight this pandemic and come to terms with what COVID-19 is, is it important that we understand it was created in the lab? Does it make it a very different pandemic and a very different fight?
Speaker 4:Uh, he has one, it seems to me it has one, um, one aspect of the design of a virus that escapes that causes a pandemic, uh, that I think is, is interesting and worth talking about. So the downside is that it is clearly pre adapted for humans. So when SARS Colby one first jumped into humans, it had only 17% of all the, the, the, the ch the mutation changes that needed to cause that initial epidemic 17%, uh, this one has 99.6% at the get-go. So the downside is it was very pre adapted. So it spread very quickly, very widely. And that was the first wave of it. There actually is an upside to that, which is, it has very little genetic runway, very little movement to improve. So in the spike protein, there are only five, uh, five positions that it could mutate at to get better at, uh, from, from it's from the initial case, it turns out what we called the UK strain that the British strain that was, you know, started in the fall and spread. That was one of the five. So, and now
Speaker 3:About the very end, that's
Speaker 4:Another one. So it's, so it's used up two of the five possible improvements, uh, in the spike protein in terms of binding. So, um, that's somehow to me, encouraging that, this thing, uh, that we've seen the worst of it, and these variants are not going to be able to, um, to have much impact. Uh, I did another analysis and theirs looked like there's, there's eight, uh, epitopes. So the, the human immune system sees eight separate things on the spike protein when it sees this virus. So it makes eight different kinds of antibodies. And at this point in time, the Indian strain has only gotten rid of two of those eight. So we still have 75% of the epitopes are the same. Uh, you know, when I was teaching at Stanford, 75 was a C, but in, but in immunology, that's a pass fail, and that's a strong pass. You probably have to get well below 50% to do have an issue
Speaker 3:There, roadmap on where we will be in a year or three from now, with this virus.
Speaker 4:No, I said a year ago now, unfortunately, 7 billion people have to either get the virus and get the vaccine. Um, and I'm afraid I haven't changed that tune yet. We're years away from that. That is unfortunately, that's the analysis, Steven,
Speaker 3:Last word to you. And I thank you for your time on, on all of this, just wrapping it together.
Speaker 4:Well, you know, I think that, uh, my belief is that as a gain of function research project, uh, my belief is that there is a way forward for gain of function research to be done on a different structure. Uh, I'm going to be pro proposing that publicly in the next few months, uh, when I put together a consortium around how that should be conducted. Um, but I think absent that we're just going to do this again with another virus in, uh, in another decade or another few years,
Speaker 3:Or just ban gain a functional together.
Speaker 4:We could, that, that would be the easiest. Uh, I'm willing to, to find a middle road if that, if that is, uh, is possible,
Speaker 3:Steven CUI from Taiwan, Steven, great to talk to you, thank you so much for taking all that science and trying to make it as digestible as possible. And I appreciate
Speaker 4:Very much thank you, Dana, for focusing on this. It's an important issue.
Speaker 2:So why was there a scientific split on using the term gain of function in the[inaudible] lab? Why do we hear Dr. Fowchee say there was no gain of function? Well, I'm no scientist, but Dr. Richard E. Bright, a professor of chemistry and chemical biology at Rutgers university and a biosafety expert contested Dr. Anthony[inaudible] testimony before the committee saying that felt she's claim made during the exchange with ran poll that the national institutes of health has not ever, and does not now fund gain of function research in the Wu Han Institute of neurology is demonstrably false. According to Ebrary, at least some of the NIH funded research conducted in Wu Han equivocally qualifies as gain of function e-brake was quoted as saying he bride claims that the work being conducted at the Wu Han Institute using us funds a pit of Mises gain of function research, and is the exact kind of research that led the Obama administration to conclude that gain of function was too dangerous to continue domestically. And it was in fact banned in the U S in 2014, following a series of lab accidents. And after a petition signed by 300 scientists, demanded a moratorium on gain of function. The ban was later lifted after a review by a secret government panel in gain of function, experiments were allowed to go forward. The Obama administration's ban was lifted in 2017 under then president Trump. That's our backstory and the origins of COVID-19 subscribed to our newsletter. If you like Dana Lewis dot[inaudible] dot com, and please share this podcast so that others can listen. I'm Dana Lewis. Thanks for listening. And I'll talk to you again soon.
Speaker 5:[inaudible].