Talking With Dr Steven Quay about Covid-19 Virus

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Hello, and welcome to the Victor Davis Hansen Show.

Victor is the Martin and Ely Anderson Senior Fellow in Military History and Classics at the Hoover Institution and the Wayne and Marcia Buskie Distinguished Fellow in History at Hillsdale College.

Today on the show, we have Dr.

Stephen Kuay.

And we'll take a moment to have some breaks and we'll come right back and learn a little bit more about Dr.

Kui.

We'll be right back.

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Welcome back.

Dr.

Kway

is both a medical doctor and a researcher.

He has an MD and a PhD.

He's the founder of Atosa Therapeutics, where they develop therapeutics and delivery methods for oncology and infectious diseases.

So he's spent a lifetime developing drugs to combat disease and save and improve lives.

He has co-authored a book called The Origins of the Virus: The Hidden Truths Behind the Microbe that Killed Millions with his co-authors, Paolo Bernard and Professor Anglish Douglas.

So very welcome to the show, Dr.

Kway,

and I'll let Victor take it from here.

And I should say that Dr.

Kway is also the author of Stay Safe, a physician's guide to survive COVID as well.

And Stephen, when you read your dossier, it's hard to see that one person could do all of that in one lifetime, much less a half a lifetime.

But I had one little unique esoteric question.

So you're the CEO of your company, Atosa.

I was a professor of Greek for 24 years.

Did you pick the name because of that passage in Herodotus where Atosis, the Greek physician in the court makes that little, I don't know if it was a breast operation or mastastitis or what.

Is that what gave you the idea for the name?

It is, Victor.

When I came up with the concept of a TOSA, what I wanted to do was to prevent breast cancer, not treat it.

So, you know, the history of the cervical cancer is that the pap smear doesn't find cancer.

It finds the precursors.

It takes about 10 years and then you can intervene.

12 years ago, I asked a simple question, why isn't there a pap in here for breast cancer?

So in naming the company, then I looked through my history books.

Not the scholar that you are, but yes, Princess Atosa, the wife of Darius the Great, basically, I guess had the largest piece of real estate before the Roman Empire, is the first woman in recorded history with a breast cancer.

They're found in Egyptian mummies, so we know it goes back at least 5,000 years.

but she was recorded to have a bleeding breast lesion.

Her slave cauterized it.

It didn't do very well, but Atosa was established in honor of her as the founding woman in this field.

And down through the ages, millions of women, of course, have had this affliction.

That's fascinating.

We know her in classics because she's a character in Aeschylus's Persians.

She was the mother of Xerxes, and her ghost comes in and talks about the disaster at Salamis.

Before we also begin about the virus, you have a whole nother career that has a lot to do with the virus, but it's separate from it.

And when COVID started, the last thing that you probably thought is that you would be one of the few voices in the wilderness that would use your prior expertise and training to try to adjudicate where it originated.

Did you have any idea when, how soon when the virus was known, did you have worries or did you think that you had to do something or you had to at least sort of be a dissident voice in those early months?

Yeah, actually, Victor, my approach to

SARS was sort of threefold in three stages.

So

if I can walk through that.

Yeah, I'd like you to.

Yeah, I think everybody's fascinated to hear this.

So,

you know,

I'm of an age when

a good weekend for me when I was teaching at Stanford would be I would take home an inch or an inch and a half of publications and would sit on my patio and, you know, have a glass of wine and read through esoteric science because this is just

what has excited me my entire life.

So, phase one was getting the sequence of the virus and looking at a part of the spike protein, the thing that interacts with your lungs, and then looking at its activation site.

So, all these viruses have what I call a two-step verification process.

So, they don't want to waste their precious nucleic acids without knowing that they can go into a cell they can replicate in.

So, step one of the verification is the ACE2

receptor binding interaction.

Step two is cleavage of the spike protein at the furin cleavage site.

And I remember the day I saw the furin cleavage site, it has, it's a very positively charged region of the protein.

Now,

we don't realize this, but proteins are like little magnets sometimes, and they have positive sides and negative sides.

And as magnets do, they attach to each other.

So this has a really, really

strong positive spot on it.

Well, it turns out that my first five years at Stanford, I was studying the toxic component of bee venom, writing really detailed papers.

You know, I had four people in the world reading it, including my mother, but

it was also a positively charged peptide.

And so

my first encounter with SARS was going to my board and saying, hey, look,

I think I can develop a therapeutic for this because I know what this is going to do in membranes.

I know what it's going to do.

And we actually,

I actually developed then a nebulized formulation.

We've done clinical trials in Australia now.

I actually just completed a large safety panel and pretty excited about where this will have application.

So that was stage one.

Stage two was then watching

in a little, you know, and shot, not shock is too strong a word, but watching in curiosity.

a lot of scientists that I respected or had respected making declarative statements about the virus, you know, coming from a market and all that without any data whatsoever.

And I part of me wondered

why they were, you know, talking so much.

And then I started getting into it and then really looking into it.

And so

the third phase was saying, you know, this looks like it came from the laboratory.

And now my mission is to explain that to people and to be sure that we don't have it happen again, because there are worse things than a 1% lethal virus.

In fact, the Nipah virus I found them working on in December 2019, 60% lethal.

So.

Can I ask you two questions before we go into your explanation of the engineering aspect of the virus?

So when you were going to sort of do a parallel line of research about the virus, were you surprised, shocked, not shocked that there would be resistance in the Western world to that line of inquiry and that that line of inquiry that was opposed would have Chinese fingerprints on it?

Did you have any idea how ubiquitous or insidious the Chinese government would be?

Or were they at all?

I don't want want to prejudice your answer.

I expect it, you know, if you're if you're a gain of function virologist, so you go to work in the morning and you gain a function and that's your livelihood and that's your reputational equity, whatever you call it.

I can imagine them, you know, being concerned about,

gosh, could this have come from a lab?

But on the other hand, you also have that, because you have that expertise, you sort of have, to me, a moral obligation to step up and help wherever you can.

And that really surprised me that there is not,

I just don't know how people can look themselves in the mirror in the morning and not be doing everything they can to help people, because that's why we're on this earth.

The second part, though, once you testified before the House, by the time people listen this, they will just have heard your testimony before the Senate.

You've written a book about it or co-authored a book about it.

You've written articles.

You've had a very influential co-authored Wall Street Journal op-ed with Richard Mueller, the physicist, retired physicist at Berkeley.

Were you shocked, surprised to repeat that again about the reaction of the Chinese government or the ability of the Chinese government to make your views eccentric or dangerous or unorthodox?

Is there an effort on the part of China?

to exercise influence about the free expression of ideas, which to me seems crazy.

I mean, we've had 10 million officially die from this virus and probably a lot more.

But are you worried about your research?

Or do you think the Chinese government follows you?

Is this just paranoia on my part or conspiratorial ideas?

Or is it something everybody should be aware of?

Well, I think, I mean, there are aspects of what you said in terms of personal safety and things that I prefer not to go into.

I think that what I have noticed is that

there's a code of silence as much as anything around discussing this topic.

I mean, I have some very esteemed, well, I have some very esteemed friends now, very high places in science, who began together with me, you know, down in the trenches as a resident of the Mass General or at MIT or that sort of thing.

So we have a 40-year history together of doing good science and, you know, and also, you know, having a beer or something.

And these people will not engage me on this topic.

And they're in positions of power within the government or the academia, the academy, that they could really make a difference.

And I do find that very frustrating.

When I've read what you've written and heard you speak, I kind of like to walk us through.

So, you can't find any evidence that before there was a documented human infection, that this particular SARS virus was found in any other animal until after a human was infected.

Is that true?

Yeah, that's true, Victor.

If, if

let me just kind of explain

the way you look at these situations.

So a zoonosis has the word zoo in it.

So there's three things in a zoonosis, an animal, a microbe, in this case a virus, and a human.

And you can look at each, you can find evidence in each of those three

entities that can show you it might have come from a laboratory or it might have come from nature.

In the simplest form, the location of the animal is the answer.

If the animal is from a market, it's a spillover from nature.

If the animal is in a laboratory,

then the person gets infected in the laboratory, and that's how that goes.

So, the lab leak was a pejorative, I think, created by the media or the virologists.

It doesn't leak, it's not a piping, you know, so it's not a piping issue or something.

It's someone who gets infected inadvertently, goes out into the street, goes to the store, etc.,

getting infected.

So, yes, in China, 80,000 animals were tested.

They represented 400 different species,

and there was neither any activirus by the PCR or evidence of infection by antibody testing.

And in SARS-1, the comparison is that 90 to 100% of animals in the markets near the first breakout were positive.

I mean, it was really ubiquitous in the beginning.

When you examined the genetics, the genetic imprint, if I could use that.

you know, layman's term for the virus, were you surprised that it was different than from your experience in natural occurring viruses?

And if so, how was it different?

Yeah, so

it's a nice segue.

So we finished the animal, the animal segment.

Let's talk about the virus.

When a virus,

when a natural spillover occurs, the virus is in the animals in the markets for six months, 12 months, 18 months.

In SARS-1, it was a civet cat.

that is marketed in China.

In MERS, about 10 years later, it was in camels.

So the virus has what we call a molecular clock.

It's basically a very characteristic mistake rate where it makes about two mistakes

in its coding per month.

So it's got 30,000 letters and about every two weeks it makes a mistake and then that mistake is passed down to the progeny.

So you can use the molecular clock to ask the question, how long has this been in animals?

And when you look at SARS-1 or MERS, you see, you know, 27 or 35 mutations in in the first human cases.

Multiple jumps from multiple animals to multiple humans.

So

as I like to say, a natural process loves diversity.

Think of, you know, Victor, you understand this better than anyone, maybe.

Think of a forest next to a farm, where in the forest you have all kinds of diversity and in the farm you have a genetically pure crop of some kind.

So in SARS II, the first 30 patients all had exactly the same genome.

I mean, it looks like a vaccine in terms of its genetic purity, and nature does not do that.

So

that's the second checkbox.

It says this did not come from nature, and it came from a laboratory.

I want to be very careful so I don't try to prejudice the questions or the answers, but What were the traits of the genome or the virus that suggested, if they did suggest, suggest, that it had enhancements.

And I guess the definition of enhancements is either greater propensity for infection or mutation or disruption with the immune system.

Were there things in there that after serious research, you could see what the enhancements, what the trajectory was of them or why they were there?

Or was it just inadvertent?

They're pretty obvious.

So let's, if I could back up and talk a little bit about what gain of function research means and the five different kinds.

Yes, absolutely.

Fine.

So

the overarching purpose of gain of function research is to create

sort of deadly viruses in the laboratory and then figure out how to create therapeutics or vaccines to treat them.

The skeptic would say you're creating something that never could occur in nature,

which has some validity.

But there's five activities you can do with gain of function.

Three of them are accepted by governments and scientists as appropriate gain gain of function research.

Two of them are considered off-limits because they lead to bioweapons properties or bioweapon characteristics.

And they're actually included in biological weapons treaties that China and other countries have signed.

So the three acceptable are to change the animal that it will infect.

So taking a bat virus from a cave and teaching it how to infect human cells in the laboratory.

It's called tropism.

So changing the tropism is one.

Changing the infectivity, which literally means how few uh virus particles do you need to start an infection it's actually not one it's but in sars it's remarkable it's under 10.

so there may be there may be 15 million viral particles in a droplet you can barely see and it takes about 10 of those to cause an infection and then the third is pathogenicity how sick do you get or does it kill you outright The two that are not acceptable are changing the virus in a way that makes it produce asymptomatic infections and changing the virus in a way that makes it evade evade the immune system.

Those two are considered bioweapon properties and are not supposed to be

inside of a virus laboratory.

Did you feel that the latter two were characteristics of this second SARS virus?

I do.

I mean, let's work through the two that are acceptable.

As I said at the beginning, the two-step handshake begins with a receptor on the virus finding a protein in your lungs called ACE2

on the surface of the lungs.

And so, the ACE2 in humans is different from mice and rats.

And every animal has a slightly different ACE2.

Primates are closer to human, other primates are closer to humans.

It's all like the

tree of life.

Looking at the SARS-CoV-2 receptor binding domain, it was phenomenally optimized for for humans.

Let me quantify that.

So there are 200 letters in the genetic code for the receptor binding domain, and there are 20 possible amino acids in each that you could change for each one of those letters.

So a very clever scientist named Jesse Bloom at the University of Washington said, I have a way of testing all 4,000 possible changes in SARS-CoV-2 to see which ones make it a better virus and which one makes it a worse virus.

The standard for SARS-1 was that the first time it touched humans, it only had 15% of the changes it needed to become a pandemic, excuse me, an epidemic.

It was not a pandemic, it was an epidemic.

So, SARS-1 had 15% when it first hit humans and then got the other 85% over about six months, and then it could go human to human.

When the 4,000 positions were changed in SARS-CoV-2, only 17 out of the 4,000 improved the receptor binding.

So,

that's 99.5% optimized for humans.

Now,

in a true validation of Jesse's work, one of the 17 changes led to the delta variant, but he predicted it months before it occurred.

So the receptor binding,

so the other compartment that we didn't talk about was the humans.

In an epidemic, When an epidemic occurs, you can go back to saved samples in the refrigerator of a blood bank.

And once you have an antibody test for the infection, you can say, wow, was this circulating in this community before

we knew about it?

And again, in natural spillovers, they do that.

The virus has to work its way into the human population from the civet cat.

So in SARS-1, 20% of the workers in the market had antibodies because obviously they're working every day with these animals.

About 1% of the general population had it.

In Wuhan,

36,000

blood bank samples were tested, and none were positive for infection.

So we have a virus that is absolutely perfected for human interaction, but it's never seen a human in the community.

Wow.

We're going to take a quick break and we'll be right back.

And I want to mix the questions between science and then health policy and even national security concern, but we'll be right back.

We're back with Dr.

Stephen Quay, our guest.

We're talking about his research that pertains to the origins of the COVID virus.

I had a question.

When we talk about three areas of gain of function or enhancements that are permissible under international accords and two that are not, or they would be by some, I guess everybody, but would be deemed sort of a bioweapon area or territory.

Would the type of research that led to the emergence of this virus would it be permissible to do that research in the way that it was done at wuhan in europe or the united states currently

well am i going from the reverse direction i mean yeah i mean i think you're going from the reverse direction there are two other engineered aspects of sarus-covi2 that i we might want to finish those and then and then we can sort of yeah let's finish these two other ones that you were talking about we we've hit the receptor binding domain it's optimized for humans The next is the furin cleavage site, which makes it very, very infective and actually affects pathogenicity.

This has never been seen in this class of viruses in a thousand years.

So

the SARS-related viruses that led to SARS-2 separated from their cousins about the time

that William was crossing the channel, about 1060.

So since that time,

you can look at the diversity in the SARS-related viruses.

They have never had a furin cleavage site.

On the other hand, we know in the lab,

it's in Ebola, it's in many other viruses.

So 12 times scientists have put furin cleavage sites in in the laboratory, including the Woolly Insta virology, and misspoke, 14 times, and 14 out of 14 times, it enhances infectivity and pathogenicity.

This protein site has never been seen in this particular virus.

And then the code for the protein is a second

layer of unusual findings.

The genetic code of life is a three-letter code.

And the letters in the code for the furin cleavage site of SARS-CoV-2,

CGG, CGG, are very rare in this class of viruses.

And again, there has never been a virus in a thousand years that has these two codons next to each other.

And there's some pretty esoteric reasons why they don't want to put the same ones next to to it.

It basically stalls protein synthesis.

So they never do that.

So

as I say, you have a protein that's never occurred spoken in a genetic language that's never been spoken.

And those three, while acceptable for academic work, are clear hallmarks of genetic engineering.

What you just said, are there medical and scientific journals in China being published where people challenge each of these findings that you're discussing?

Or do they just keep quiet about it?

Victor, I'm just making observations in the codon of the virus and

they're not in dispute.

They're just facts.

They're not in dispute.

Why don't we go on to the whole array that you mentioned when you first, when I kind of interrupted you, we're talking about the five, three of which were permissible and two weren't.

Yeah, so

we've talked about

the two clear indications of genetic engineering, the optimization of the receptor binding to.

By the way, that is done in the laboratory in humanized mice.

That's how you do that.

You have mice.

In humanized mice,

you have a replication of a human lung and a mouse.

They do, Victor.

It's kind of creepy, but

they were doing that in China in the lab.

Well, so it's

here the full story.

So

they're hard to make, but Ralph Barrick at the University of North Carolina managed to make mice with lungs that are humanized, that are human mice,

from a protein point of view.

And in fact, he sent them.

We have the World Courier

shipping records.

In 2018, he shipped them to the Royal Institute of Virology for their work on coronavirus.

But wait, a U.S.

scientist developed this cutting-edge technology, how to conduct

pretty much a facsimile on a human lung within a mouse.

He had this information, this design, this paradigm, and did he have to go through channels?

How could the Chinese have access to it?

You said did he mail?

I mean, was there any restrictions?

I guess as a layman, we were under the impression that there were restrictions on gain of function research after 2017 or something.

Or there wasn't?

Or I mean.

Yes, so there was a moratorium when it wasn't conducted from 2013 until, oh, I want to say May of 2018, and they were shipped after that date.

What the records appear to be is that there was a moratorium because of some very dangerous influenza research in Wisconsin and in the Netherlands.

So under the Obama administration, a moratorium was put in place.

And it seemed like the NIH was simply waiting for a change of administration and they dropped three or four inches of paper saying, hey, we know how to do this now.

We know how to do gain of function research now.

And I think whether whether

whoever was elected in 2016, it would have gone across their desks so fast they wouldn't have necessarily noticed it.

But after that, gain of function research was resumed and the mice were shipped to China.

Could a person argue that without that knowledge in the lab, they probably wouldn't have been able to do the gain of function engineering with the coronavirus that they did?

Was it essential or was it peripheral to this line of research?

Well, it's essential.

They could have made their own.

Not everybody can make it.

It's an art, I guess is the best way to put it.

It's like, you know, it's like making a particular painting it was essential for the work the virus wouldn't the virus wouldn't have wouldn't have killed 15 million people if uh if it hadn't been so wow this is macabre and fascinating at the same time and then i keep interrupting you but i can't help so it's so interesting in a very strange and scary fashion and then we can go on to the areas i i interrupted you on i don't think you were quite were you quite ready to talk about the two areas that under international cores are discouraged or outlawed yes i am and and i think this is really important for your listeners to hear so uh just as a reminder the two areas that are not allowed is is asymptomatic transmission and evading the immune system obviously these would be would be devastating in a virus if it could be transmitted asymptomatic again so backing up to the beginning infectious diseases When a virus first encounters a human for the first time, you know, a true natural spillover.

It's never seen a human before, it doesn't know how to interact.

And we actually have a

powerful brute force, medieval immune system called the innate immune system that is clumsy and can do a lot of even damage to the patient, but it's triggered very easily when a new virus encounters humans.

Influenza, for example, doesn't trigger that, but it's been interacting with humans for 100 years.

So, to my knowledge, there has never been a new respiratory virus in humans that was transmitted asymptomatically.

That's the background here.

So, the third unusual component of SARS-CoV-2 is a particular protein called ORF8,

capital ORF8, stands for open reading frame.

It's down at the right-hand side.

It's the eighth protein from the left side of the virus as it reads from left to right.

So, viruses have two kinds of proteins.

Usually, this is a third kind that they don't usually have.

One protein that viruses have is the, is goes into the shell and making new viruses, you know, going out, going out into the world.

The other protein goes into the cell and takes over the machinery and helps make baby viruses.

This, the ORF-AID is unusual in that it goes into your bloodstream actually before any other proteins are made after an infection, and it does two things.

It turns off the production of interferon and it blocks the development of antibodies against

whatever the infection is.

So it's like your immune system, you know,

on drugs or on marijuana or something.

So part of the innate immune system is a protein called interferon, and it is typically released whenever any virus comes into the body.

It's responsible for the fever, the sweating, the chills that you get when you get an infection.

I think it was highly selected for probably over 30,000 years of evolution.

If someone got a new virus, they would sweat, they would turn red.

You'd put them in a tent, you know, 100 yards away, and if they died, you'd honor their life, and if they lived, you'd bring them back to the tribe.

And so this interferon response is an important social signal of infection and is typically triggered by a new virus.

ORF8 suppresses interferon release, preventing those symptoms.

From 2015 to 2020, two students at the Wuhan Institute of Virology received master's degrees by the first characterizing the mets and bounds of what ORF-8 could do with respect to interfer and release.

And the second, creating a synthetic biology toolkit for manipulating ORF-8.

Those two master's theses were never published in English.

They were never led to a scientific publication of any kind.

I found them in the Chinese deep literature and had them translated for me.

Just as a sidelight, is the ultimate arbiter of the conduct of release of information that comes out of Wuhan Lab, the Chinese military, or is there a distinction between the Chinese government and the Chinese military and the party?

Two data points on that question.

February 1st, a general in the PLA Army took over the Wuhan Institute of Virology.

She was responsible for the vaccine for the SARS-1.

And as far as I know, she is still in charge.

Looking at laboratory records, monthly laboratory record meetings and the like at the Wund Institute of Virology.

I mean, every lab, my labs, you know, for 30 years, we have monthly meetings.

And you talk about the research in the lab, or you talk about an interesting paper, that sort of thing.

When you look at the Wundt Institute of Virology monthly meeting notes, the first paragraph is a party member describing the mission of the Institute, the mission

of the Chinese medical,

helping China be the first country in the world.

So it's very clear that their research effort has a foundation from the Communist Party.

Well, let's continue.

We continue on with this Baroque story.

So we're going to go into the areas that you feel that the virus revealed things that went beyond denofunction research within a normal landscape within, say, the United States.

Well, that's right.

So this ORF-8, which suppresses interferon, so it makes it asymptomatic.

And we now know.

What really killed us was not believing or knowing that there was asymptomatic transmission.

Had the Chinese said that, we would have changed all of our modeling.

We probably would have changed some of our immigration policies.

Some people say 90% of the deaths could have been avoided.

That might be too high, but that's what this is.

You mean by we would have had an earlier quarantine?

An earlier immigration.

From flights to China.

I mean,

maybe you can correct me, but I have a recollection that

some 1 million people in that two or three week period were Wuhan's flights were restricted within china out of wuhan to other cities in china but you could fly directly to jfk i think sfo and lax for that period where they thought there was a problem and therefore air flights were restricted within china from wuhan but not to europe the united states is that correct yeah that's correct it's about a six-day period of time six six days uh and i i mean

I haven't gotten into it too much other than being sure when you think about if you have someone with a foreign passport and they want to leave your country and they haven't committed a crime or have any other reason to be held back,

it might be reasonable to let them leave.

I could imagine a non-draconian theory around that.

Okay,

so

we can continue on.

We're going down this pathway.

I hope.

where we end is not in the ninth circle of hell, but go ahead.

Well,

the other aspect is that ORPHA suppresses the way the immune system makes antibodies.

So HIV is the poster child of this kind of a virus.

And the reason you can't vaccinate against it is because it is constantly suppressing your immune system.

So in fact,

you can't make antibodies against anything.

And the classic is, you know, these patients unfortunately have all kinds of very strange infections because they just, their immune system doesn't work.

Orphate has this same property.

Now,

so if I told you that there was a protein in the virus that made vaccines less effective or made natural immunity from an infection less effective to re-infection, what would you think?

I don't know what I'd think.

Well,

you'd think that you'd seen that

movie before.

And in fact, that's exactly what happens.

I believe I don't have.

So let me just

clarify for the audience.

We're in now the territory that, I don't want to be melodramatic, but we're in in the territory that has affinities with what one would do to make some type of weapon or a bioweapon.

Have we crossed that pathway now?

Yes.

To the extent that there are, yes.

Yeah, I'm not trying to say it is a bioweapon.

I'm just suggesting.

Yeah, and you're not either.

I want to make that clear to everybody.

Dr.

Quay's not, but what he's saying is that there are propensities in the virus that go beyond what we in the West would call legitimate maybe inquiry, dangerous, but maybe defensible in some places.

But now we're getting to places that are too dangerous for normal viral research, I guess, huh?

Well, it's been agreed that of the five kinds of gain of function, three of them are absolutely acceptable in academic situations under proper BSI three, four levels, but that two of them are things you don't do.

And in fact, I've found no scientific papers before SARS-2 of Western virologists working with ORFAI in any fashion.

Are we at the fourth or fifth step?

Or there's one more aspect of it that went to the next one.

No, that's it.

No, that's it.

Let me ask you a question at this point.

When this virus escaped, I don't know if that's the right word, when somebody was infected with it and went out and it spread,

do you feel that the trajectory of research was finished and that this was a completed virus?

Or was it a work in progress that had a trajectory into areas that might have made it even worse?

Do you you have any speculation, or does anybody know?

Was it just a finished virus?

And they said, you know what, we've got this virus.

We ended it.

We did everything we wanted to know to learn and do to it.

Or do you think that had that leak not occurred when it did and had it occurred, say, a month later, there would have been even a more frightening aspect to it?

Well, I don't really think that's the case.

I mean, I believe that it was an inadvertent escape.

You know, if they wanted to do a deliberate release, they'd.

No, I don't mean it was deliberate, but I'm just saying that I don't think it was deliberate, not that I would have the expertise to be authoritative, but I'm just saying that when somebody unknowingly was infected and then unknowingly spread it,

that version that he spread, was that

a completed research project at that point and it was in storage?

Or were they actively working on it, do you think?

I believe it was somewhere in the process of being worked on.

For example, it doesn't look like it had ever been tested in animals other than the humanized mice based on

a particular finding.

So

soon after it went into humans, it required an additional change that occurred of position 614, it's called.

D became G at 614.

And that occurred on January 10th in a couple patients.

And now 99.7% of all the viruses in the world

have that particular change.

So it had an inherent instability

in the very first 30 or 40 cases.

We're going to take a quick break and we'll be right back with Dr.

Stephen Kway and his research explanation and enlightenment to all of us about the origins of the COVID-19 pandemic.

We're back.

Dr.

Kway,

at this point, I'd like to ask another question.

And so we have this virus, and all of our initial expectations, and these were made by some of the world's top virologists, that when we had the Pfizer or the Moderna, the RNA vaccines, there was this sense that we were hearing 95% effective, 96%.

There was some caution about mutability.

But is it your impression that the scientific community

was kind of caught unawares that a virus could come out of nowhere and would be able to mutate so quickly and so successfully against vaccines or would be able to trick the immune system in ways that we didn't anticipate?

It just seems that given their body of knowledge and their use of that body of knowledge to contain or prevent infection, there was a, I think, a window somewhere between September of 2020 and right after the election when there was a sense of euphoria almost.

And our politicians of both parties were sort of saying we conquered it.

And then people were very, you know, and you got, and then people were saying, well, even if you didn't get the infection, if you've got Delta or the original alpha variant, you're going to have immunity.

And we didn't even have in our vocabulary for a while long COVID.

Was there a sense that we just were caught unawares of the complexity and the insidiousness of the virus?

Well, let's start with what we should have expected.

Viruses respond to environmental pressure by making genetic decisions.

Now, they're much faster than we are.

The typical person will have 100 million viruses produced during a typical infection.

So if you do anything to put pressure,

selective pressure in that patient, the virus can respond very quickly.

And so this is where the concept of

vaccinating a population during an active pandemic is,

by definition, an experiment to prove that Darwin's theory of evolution works.

You are driving selection of vaccine variants by the very process.

So I think there should have been some cautionary discussion around this.

I mean, one of the little blogs I did when the Delta came out was: I said, okay, look, we now know that the vaccine doesn't recognize the whole spike protein.

It recognizes what are called eight epitopes.

So just think of the spike protein as a ball, and there's eight spots on the ball that the vaccine that your immune system recognizes as being foreign and that you make antibodies against.

Delta had gotten rid of two of those.

But as I put in my blog, 75% may be a C in a classroom, but for stopping infections, you know, you have to get below 20% to really have a serious problem.

So what happened is the more you vaccinated, the more the variants ticked away at those eight, seven, six, five, four, until Omicron, we were at zero.

I think a lot of our viewers, I think they're frightened about the origins of COVID or they're perplex, as I said.

But where are we now?

We're trying to vaccinate as many people as we can.

I know so many people who are so disappointed because I had the two Moderna vaccinations.

I know a lot of colleagues that had them plus two boosters, and yet they still got Omicron.

Is there a danger of a person

to the person particularly

or into the collective population in general about mutability when a person, let's say, you get two of the initial vaccines, you get two more boosters, and then we just keep boosting and boosting and boosting and boosting.

Does that in itself, in terms of virology, does that accelerate mutability of the virus?

Well, let me start by saying what I think is really important.

Medical decisions like whether to vaccinate, whether to get boosts, and that sort of thing are very complex questions, and they should always be done in consultation with your own personal doctor who knows you, knows your family, knows your situation, knows the details of that.

That's absolutely critical.

And so nothing I would say should ever be interpreted as medical advice

for that reason.

So point one, moving on.

When the opportunity to get a booster became available, one of the questions you should ask your healthcare provider is how far from the structure of the virus in the vaccine is the virus that's circulating in the world?

I see.

So for example, I mean, I wouldn't give you a measles virus if chickenpox was in your community, right?

Because

different, different proteins.

So, very

from Omicron on, I mean, one of my most difficult challenges was the vaccines were covering the virus that first came out in, you know, January 2020, and it no longer was really

didn't recognize Omicron.

So, you had a theoretical reason why it probably wouldn't work very well.

You can get the peripheral T cell stimulation.

I mean, you know, so it's not zero, but it's it's certainly not what you'd want.

I noticed as a philologist, I was looking at the language that emanated from our federal health authorities.

It started from surety and then to advantageous and then to preferable to not to the alternative and then preventing death or serious hospital.

But it was downgraded as we went through.

these various letter mutants and I don't know where it is now.

Is the status now that if a person has say two vaccinations and two boosters or do they give a greater degree of protection even from Omicron than not being vaccinated or not being boosted?

Is there any hierarchy or it's just too confused now because the virus is changing so quickly?

It's very confusing and the virus is getting more infectious but also getting much less pathogenic, much less, much less deadly.

Where do you think will be, I know that's an unfair question, but are you optimistic about the natural course of the virus or the ability or the ability of science to combat it, either with therapeutics or with vaccinations?

Is it going to devolve into something like the annual flu vaccination and the annual mutated flu virus?

Or was there something that, because of the unique circumstances of its birth and origins, is there a chance that it could veer off somewhere and then not follow the typical trajectory of a virus?

Yeah.

So, I mean, I think it's going to become endemic, which means it's widely spread.

The virus loses when it puts you in the hospital, when it puts you on a respirator, when it puts you in the ICU.

It stops being able to transmit easily because everybody around them is

in a PPE.

So it's optimized

if it can spread quickly, do a round of reproduction and move on.

The thing we all liked about influenza was as bad as it could be, you know, it was seasonal.

So you had two two months, two seasons you worried about it, and two seasons it was down in the southern hemisphere.

And we use the information of its circulation in the southern hemisphere to inform the new vaccines each fall.

But this doesn't seem to have much of a seasonality, as far as I can tell.

No, that was the initial hope.

You remember where everybody was saying that we've got over the original winter seasonal aspect of SARS, and now we're going to be, and then all of a sudden it took off in the summer.

Yeah.

The advantage of being optimized 99.5% to to human receptor is it doesn't have a lot of canvas left to paint on.

You know, as I mentioned, Delta took one of the 17.

The other ones have picked up some of the others.

I don't know the exact number, but I think about half of the mutations have already been used up.

So

it's going to come to terms with humans.

I think it's going to be, you know, a much less than 1% lethal virus, which, you know, many influenzas can be a couple percent in a bad season.

So, but it's going to be with us for a long time.

It's so strange because I'm out in veritable nowhere in southwest Fresno County, and I'm meeting people who are doing work on a remodeling house.

And I can't tell you how this thing that originated in Wuhan has affected so many people, that just random people.

I've had an electrician, and he's still nine months after he was infected and recovered.

He's had problems tasting.

He has no energy.

And I've had another.

carpenter whose wife was very ill for a while, but extended.

And, you know, I was infected on May 1, and I'm still not back.

The symptomology, I've never seen a disease where you'll see somebody say, I'm losing my hair.

You think they're crazy?

And then you look it up and they are, or they're losing their taste, or their tongue is crap.

It's got this ability to cause so many autoimmune responses.

It's just incredible.

There's two reasons for that.

Backing up.

Another piece of information about the origins.

So in 2018, a grant proposal was written by U.S.

scientists in in North Carolina and New York and the Wuhan Institute of Virology to purposely put a quote human-specific furin cleavage site, end quote, in a bat,

in a virus of bad origin.

And of course, SARS-CoV-2 is a bad origin virus with a furin cleavage site on the doorsteps of the Wuhan Institute of Virology three years later.

The importance of that is twofold.

importance and problem of that.

The reason this virus is so ubiquitous with its problems is it not only is highly optimized for humans, but the furin enzyme, which it's taking advantage of to cleave it.

So, furin is a human enzyme.

It's found, guess where?

In the lungs, in the heart, and the liver, and the blood vessels, in your brain, in your ears, in your hair follicles.

So, the virus can go into all of those cells.

It can go into any cell that has a furin.

And by the way, most organs in the body have a furin on their surface.

So, unlike SARS-1, which is a a respiratory virus and didn't go into your bloodstream, et cetera, this has the ability to cause a viremia in the bloodstream and then attack organs.

And that was what was,

yeah, that was what I had an initial cough during the acute phase when I was testing positive, but very quickly I didn't even consider it a pulmonary problem at all.

I had no problem, but I started to get neuropathy and muscle soreness and brain fog and all of these other things that we didn't associate necessarily with the acute lung version.

And that was what was so surprising to people.

And the idea that they don't even have a definition.

Can I just ask you, do you think your optimism seemed to me somewhat predicated that the virus, the mutations, as you said, they're using up their canvas.

Do you see hope at all in therapeutics or vaccinations coming?

in the fall or next year?

And do you have any idea which would be more effective?

It seems to me that we sort of erred in the initial euphoria about vaccinations that we didn't put enough emphasis or emphases on therapeutics, but maybe that was just my own speculation.

But do you see that there's a hope for a therapeutic or a vaccination?

Well, so look at this, as C ovatosa therapeutics, I have a vested interest in that question because I developed a nebulized formulation of some drugs that in animals and in the laboratory block the entry of the virus into into the into the lung.

So I do think there's a role for therapeutics now.

Some of these oral therapeutics, I think are going to be very effective because again,

you don't need to kill it or sterilize it with it.

What you need to do is slow it down enough.

So even though the immune system doesn't recognize it as exactly the same as the one three months before, it can make some adjustments and hit it.

Basically, you need to keep the patient alive and well for seven to 10 days the first time around.

And then the whole purpose of the immune system is the the second time you see it, you only need to tamp the virus down for three days or four days.

It becomes a race.

And that's what the therapeutics can do nicely.

So,

you know,

if I had a patient that was going to travel or something, I'd write them a prescription.

They'd put it in their luggage and they'd have it.

So they don't even have to lose one day

without.

That would be wonderful.

We're running out of time.

And I don't want to put you on a spot, but if you looked at the reaction of the federal government, whether it was the elected government or the Institute of Allergy and Infectious Diseases or the CDC or the National Institute of Health, what in retrospect, I know it's unfair to them because they were working in the dark, but what it seems to me that we were monolithic, that it was important that everybody be on the same page and that we didn't pay attention to people like you and others that were, whether they were advocating some therapeutics that were drugs that may or may not have been effacious, but they had a safe record, or we were on mask or quarantines.

I know that you're a former professor at Stanford, and I'm there now.

And when you think that one of the signatures of Stanford Medical School had been these wonderful immunologists and epidemiologists like Jay Bacharia or John Yannidi, it seems that we were afraid of dissonant voices, or we didn't see that as an advantage.

That was my perception.

Is there a way you can comment without getting in trouble on that?

I think so.

Look,

first of all, you know, a retrospectoscope is 2020,

and it's always dangerous to use it.

Neil Ferguson is the Imperial College in London, and he's one of the earliest modelers around this virus.

And look at it, it's a coronavirus.

So, what happened the last few times we had a coronavirus?

Well, we had SARS-1, which is about 9% lethal, and MERS in the Middle East in camels, which is 30% lethal in humans.

So, if you run those numbers through your model,

you have, it looks really, really bad.

By the end of February, however, there was an 80,000 patient study that I had out of China that showed that it was 1 to 2% lethal in the overall population, but it was only the people over 60, 70, and 80.

People under 20 is almost, you know, didn't touch them at all.

And a group that ended up with me and about 700 other signatures called the Barrington Declaration

was a pretty reasonable approach that was either discarded or never considered.

I wasn't in the room, so they said.

Yeah, I remember when that, there was a lot of hope for that declaration because of the people who signed it and their commitment to open discussion without

restriction.

We know now through Freedom Information that the highest people at the NIH and

Dr.

Fauci were quite disturbed about it and

were doing things to not have an open debate about it.

Yeah,

and those initial emails that were released that were redacted, that was a whole nother question that Rand Paul got into in his initial discussions with Fauci.

Just to finish in conclusion, are you worried?

Say that we get through this, and I think we will, especially after Harry, I think you've been very optimistic.

It really is encouraging, but could this happen again?

given the situation at that Wuhan lab or others like it or have we learned anything?

It seems to me that this is a very dangerous place, this level four biology lab.

And it's almost as if it's, to me, it's much more dangerous than a

centrifuge in Iran that we don't know much about.

Is this going to happen again or could it happen again?

Or could it happen to a greater degree again?

Well, yes, yes, and I hope not.

I recently made an analogy between the plutonium in the second atomic bomb in Japan, which weighed about 13 pounds, and the entire SARS-CoV-2 that has infected the planet in this pandemic, which is also about 13 pounds.

Remarkable how, you know, one was devastating, but only in a 10 square mile area.

And SARS-CoV-2.

This was much worse.

I think Fat Man was 18 kiloton.

Well, this is much dangerous.

Yes, much more dangerous.

What can we do about it?

Our people in the government, we're in a nadir right now with China.

We're almost, especially with this Pelosi visit, we're almost in a state of Cold War, if not worse, but it seems that they will continue this type of research.

Yes, and I'm going to be making recommendations that I believe would put us on a much safer footing with this kind of research.

The simplest thing would be simply to ban dain function research, but that may be a hill too high to climb.

but putting it under institutional review boards.

So people in the community whose blood and treasure are going to be spent if it gets out of the laboratory, they are given the authority of whether to authorize the research or not.

I mean, that's what an institutional review board is for human research.

So you simply take that same legal structure and drop all gain of function into it.

Can there be some type of embargo?

That's a tough word, but there couldn't be some kind of restrictions on the transmission of expertise from labs in the West to the Chinese

that we do with Iran.

We don't seem to have any.

And then

I'm just thinking of the Lancet investigation that Peter Zasek and Echo Health ran, and they almost demonized their opponents who challenged their inability to get transparency from their Chinese host.

And then everybody who objected to it, I know, scientist or not, was attacked.

And then we learned that Lancet is almost, I guess they have disowned the results of their own sponsored investigation.

Yeah, I mean,

as it turned out, I want to say two-thirds or three-fourths of all of the people there had conflicts of interest with respect to funding and that sort of thing.

I don't think we've ever been there before, Stephen, when we've had a national crisis like this.

But every time you pick up a paper or you read an op-ed or you look at a corporate CEO's declaration or you see a federal official or you see a prestigious medical journal, you feel that there's a chance that they have been recipients of Chinese leverage money, et cetera.

So there's no they're there anymore.

There's no security, no reassurance that everybody's disinterested.

That's correct.

I mean, the Chinese have certainly played the long game of

creating influence with money primarily, but sometimes with prestige.

I mean,

there are named institutes with famous American scientists' names on the top of the building in China.

Sometimes the university barely knows about it.

But I think that is definitely there.

I also, you hit on one.

I'd like to see export controls

around

the sequencing machines, because at least at this point in time, Western, primarily UK and US sequencers and synthesizers are the state of the art.

And so all of this work requires these machines.

And as a minimum, we should know where everyone is and they'd be registered.

I think there's ways to make the data that they generate.

uh available to law enforcement under probable cause and a warrant to allow that if that was in place for example you'd be able to look inside the machines at the Wuin Instruology without ever setting foot in China.

I did that.

I did that for five samples, and that's where I found their work on the Nipah virus in December 2019, gained a bunch of research on the Nipah virus, which is 60% lethal.

Wow.

It seems that an ending that one problem is that when you were discussing the functions of the virus in general, that you were drawing on 50, 60, 80, 100 years of careful research, objections, retractions, advances, discussions, debate, that whole scientific sturm and drag that gets us progress.

And this was going on and on.

But when you abort that and you just take the finished result and you transform it to China or a group that has not had that tradition until recently, then it seems like you're almost giving an adolescent a very, very sophisticated body of knowledge, but not the common sense that can only be found by slow and deliberate research over decades.

That seems to me really scary.

Victor, that is exactly, that is so well put.

We have the situation where the father of all coronaviruses, Michael Lee, a Taiwanese doctor in

USC, has Ralph Barrick as one of his first postdocs.

SARS-1 happens.

Michael goes back to Taiwan.

Ralph goes into North Carolina.

But so these people have now had 20 years and they had 10 years before that.

So 30 years of working with this virus, you know, in many, many

different ways.

The folks in China have less than a 10-year experience with this virus.

And we're giving them the fruits of 30 years of work, which is one issue, but also the, but we're giving it to them and they don't have the experience.

So yes, I guess it's like giving your new 16-year-old a you know a 450 horsepower car and not being surprised when he crashes it.

Yeah.

Do you have any final observations about this whole catastrophe, this human tragedy, or what it tells us about this supposedly sophisticated 21st century world?

None of us thought that it was this fragile.

And from what you said, it seems to be that we're almost fortunate that the gain of function could have been much worse.

It could have, Victor.

You know, the Black Plague killed about 20% of Europe and

it set the standards of living back about 250, 300 years.

So anything like that would break the back of civilization.

I'm not sure where we would stop going back in time, but it certainly wouldn't be in the 1700s even.

So we are, we're very interconnected.

We're very fragile.

Every death is a tragedy and all of these sort of unnecessary deaths.

It's quite remarkable.

I know so many people that have died or been ill or disabled.

It's tragic.

And with that, I want to thank you so much, Dr.

Quay.

I can't express my admiration for you, what you've done.

You've been a voice in the wilderness.

And I hope all of our listeners appreciate it.

And I hope if there's anything we can do to let people read about your book, whether it's your work on how to survive COVID or the origins, let us know.

We'd like to have you come back.

Well, I'd like that, Victor.

Thank you very much for having this opportunity.

Thank you.