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We've been hearing a lot about H5N1 avian influenza in recent months.

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Should you be afraid?

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And how does this relate to recent testimonies surrounding gain-of-function research?

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What kind of gain-of-function research has been done on avian flu?

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And what are the possible implications?

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And of course, this is all in the context of a looming World Health Organization vote

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that could give the WHO unprecedented powers over global health policy,

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all in the name of pandemic preparedness.

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Join us for this week's Fallout Truth Ball.

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Hello, everyone, and welcome to Fallout with Dr. Robert Malone,

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and myself, Jan Jekielek, Senior Editor at the Epoch Times.

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So, Robert, let's talk about H5N1.

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This has been in the news where, of course, we're talking about avian influenza.

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A lot of interest, some alarmist language.

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What's your take?

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Well, basically, the truth is we are all going to die at some point.

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Are we going to die from H5N1?

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I don't think so.

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If we do, it's going to be a rare person who probably has preexisting conditions.

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And there has been a lot of fear promoted around this at an odd time when there are various agendas in play.

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So H5N1, or avian influenza, has been around for decades, if not centuries.

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It's endemic in birds, particularly migratory waterfowl.

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What that means is that it's been infecting birds for a very long period of time,

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and it's pretty much present in all migratory waterfowl.

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So that's ducks and geese and things that are along the flyway here in the United States.

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And these waterfowl produce enormous amounts of influenza virus in their stool.

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So then anybody that's drinking or any cattle or other animals that are drinking from water sources where there have been ducks or geese pooping virus

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are likely to be positive in terms of nucleic acid sequences in their gut from having consumed water

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that had these avian influenza viruses in the water from the ducks and the geese.

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So let me see if I've got this straight. It's been around for a long time.

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There's quite a bit of it in, frankly, most water sources that haven't been treated or something like that.

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And so why is this a big deal now?

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From the perspective of the U.S. Department of Agriculture and the FDA,

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the FDA and the World Health Organization.

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Technically, their position is that we've had an outbreak of avian influenza beginning in February of 2022.

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That caused death of a lot of poultry flocks, chickens.

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And there's a particular variant of that, a clade.

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There's four major clades or groups of these avian influenza H5N1 flu viruses circulating.

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But there's one in particular that seems to have become more pathogenic in birds, particularly in chickens.

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Recently, the FDA has implemented a policy that involves sample testing of other livestock, in particular cattle, for the presence of H5N1.

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And it's been determined that this currently circulating, more highly pathogenic H5N1, more pathogenic to birds, is infecting some cows.

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Not clear how many, not clear how significant that is, because they just recently implemented the testing.

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So, you know, if you don't test for something, you don't find it.

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And when you start to test for it and you find it, then you're not really sure if this is a new finding or something that's been going on for a long period of time.

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But the USDA is raising concerns.

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They are insisting that cattle that are transported across state lines be tested for the presence of avian influenza.

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And if they're sick, they would have to be culled and potentially the herds from whence they came would have to be tested then and potentially subject to culling.

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And let me jump in again. So testing, does that mean that the virus exists in that animal or that animal is somehow symptomatic?

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Because those would seem to be quite different things given that they're drinking all this water, right?

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So what the USDA in its guidance that it's put out speaks of is that they absolutely want to test animals, cattle, that have symptoms.

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But they also now are requiring testing of asymptomatic potential carriers would be the implication.

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Unclear whether that symptomatology really confers any significant commercially meaningful disease.

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Does that have any implications for human health?

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That hasn't been demonstrated.

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H5N1 historically is very poorly transmissible in humans.

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It doesn't infect humans very well.

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In fact, the study for the incidence of H5N1 in China since 2005, big country, lots of influenza.

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Since 2005 for H5N1, there's been a total of 54 cases.

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So not very transmissible in humans, even in these kind of high intensity farming environments.

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And it would probably be someone that's somehow immunocompromised and gets like a giant viral load or something.

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So good point.

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And that's a really important consideration when you listen to the language coming from the FDA and the World Health Organization

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and the European Medicines Agency, ECDC, that's their version of the CDC.

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When they put out publicly that H5N1, when it infects humans, has a 50 to 60 percent mortality rate.

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Now that sounds pretty scary.

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And it's being amplified in current American corporate media.

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50 to 60 percent mortality for H5N1 sounds pretty scary.

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But think that through.

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We've all seen this movie before with coronavirus, where we were told early on that it had a 30 plus percent case fatality rate.

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And the problem is sampling bias.

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And as you say, if you think through who's going to present to a medical specialist with a clinical infection from a influenza virus

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that is not easily transmitted into humans.

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So what's the setup here?

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Well, the people that are going to be presenting are people that have pre-existing conditions, like you say.

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Or they are getting a massive load of virus in their initial exposure.

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But otherwise they wouldn't have gotten infected because most people don't.

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H5N1, like other influenza A variants, is an RNA virus.

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The big difference between influenza is many subtle differences.

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But the big one is that influenza has a multi-segmented genome, whereas coronavirus is a single RNA.

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So a multi-segmented genome means that if your cell gets infected by one influenza virus and then another influenza virus, the same cell, their genomes can mix.

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This gives rise to something that's called shifting in influenza biology.

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And it's why you have this designation, this abbreviation, H5N1.

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What that relates to is that there are many different hemagglutinins, that's the H part, which controls the ability of an influenza virus to infect classically different species.

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So H5 is a hemagglutinin, which is kind of like the spike protein.

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It's on the surface of an influenza virus, controls binding to cells.

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And H5 typically is evolved to infect bird cells.

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Now we know it can infect some cattle cells also, but not evolved to infect human cells.

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And to the extent that it does, it's a very rare event.

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The fear is, of course, that H5 would evolve in some way, it would be selected, or somebody would engineer it, to make it more infectious in humans.

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We don't really know what the true case fatality rate would be if H5 was to jump or evolve, or drift is the word used in influenza research, to where it would be more readily infectious in humans.

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But that's the fear.

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It was actually gain-of-function research into influenza way back when, I think it was 2012, 2014, that caused the moratorium or ostensible moratorium with a lot of caveats on gain-of-function research during the Obama administration.

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You know, there's been a ton of discussion about gain-of-function recently.

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You know, there's been all these hearings.

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Actually, I was just reading through the Francis Collins testimony, the transcript.

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It's a very wide-ranging definition of gain-of-function even described.

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Piano playing could even be gain-of-function.

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How does gain-of-function work with viruses?

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So, the common understanding of gain-of-function is based on the words themselves.

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It means that you have a virus or a bacteria or a fungus, for that matter, that normally has certain functionality, abilities to infect or aspects of its biology, and somehow it acquires a new ability to do something.

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Now, the truth is that you could say all of recombinant DNA research involves gain-of-function because it involves the use of either a bacterial virus or a plasmid circular DNA that is put into a bacterial cell that gives it new abilities to produce a protein, to express antibiotic resistance, a number of different things.

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This is done by undergraduates on a routine basis at thousands of universities all across the world right now.

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So, you can appreciate there's a gradient.

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And then there's the alleged events that occur at the Wuhan Institute of Virology with the Bat Lady and others potentially involving EcoHealth Alliance, purportedly, in which there is research performed involving specific recombinant DNA events that are engineered into a bat coronavirus,

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that otherwise doesn't infect human cells very efficiently, that enables it to infect human cells very efficiently.

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Okay. So that's kind of on a spectrum with transferring genes into a bacteria as part of routine recombinant DNA research, and yet it's fundamentally different because we're now conferring the ability to infect humans that wasn't there before.

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And so the NIH apparently has come up with a, we might argue, a extremely precise restrictive definition of what is gain-of-function research.

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Of course, this all relates to the famous confrontation between Tony Fauci and Rand Paul.

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When Rand Paul says, does NIH do gain-of-function research or are you sponsoring gain-of-function research?

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And Tony Fauci adamantly denies it and turns it back on Rand Paul, basically questioning why he even thinks he has the expertise to ask the question.

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So it appears that Fauci was relying on a very precise and restrictive definition of gain-of-function research which consists of modifying a pathogen which is highly infectious in humans and has high pathogenic potential to alter it in some way that might modify or augment its pandemic potential.

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That's one definition of gain-of-function research that has to do with potential pandemic pathogen or PPPs and the modification of those PPPs to confer further functionality or risk in humans.

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So when Dr. Daszak was testifying recently to the Senate Select Subcommittee in the House, he took the position that the Wuhan Institute of Virology was working with a virus which was not, at that point in time, highly infectious in humans.

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And so therefore, it fell outside of the restrictive guidance for gain-of-function research because it wasn't, at that point, a potential pandemic pathogen because it wasn't highly infectious in humans.

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You've studied, stated unequivocally many times today in private testimony publicly that EcoHealth did not fund the WIV to conduct gain-of-function research.

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This has been directly contradicted by witness testimony.

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Dr. Tabak testified that while your research did not meet the definition to be regulated by the P3CO, it did fall under the definition of gain-of-function.

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And Dr. Barak, who is a world-renowned coronavirologist and expert in gain-of-function, testified that the work described in your Year 5 progress report was, quote,

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absolutely a gain-of-function phenotype.

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And he went so far to say as, quote, you can't argue with that.

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You would disagree with them.

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Well, I have a letter from NIH that says our work is not gain-of-function.

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You have testimony from Dr. Barak, who says absolutely it was.

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Both are out there.

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I mean, I tend to go with the regulatory authority on this, which is NIH.

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Now, they were engineering it to make it highly infectious in humans.

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So this is wildly confusing because it seems like a much bigger problem, frankly,

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to be taking something that isn't highly transmissible and making it so than taking something that already is transmissible and making it a little more transmissible.

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Or a little more pathogenic.

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Or a little more pathogenic, sure.

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Yeah.

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So both are bad, right?

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But wasn't the original ban on—I mean, did I have this wrong, right?

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I have always assumed we're talking about taking something that can't infect humans and making it capable of that.

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It's so much more than that.

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And the original ban, quote, ban—let's just backtrack to that.

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Sure.

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Okay.

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What that was was a restriction on federal funding of research to provide additional functionality to a pandemic pathogen, basically.

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Okay.

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And so the restriction was only on federal funding.

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It didn't prevent or prohibit the private sector from doing this.

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It didn't prohibit a hostile nation from engineering something on U.S. soil.

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That wasn't prohibited.

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It was only restricted to federal funding.

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So taxpayer-funded gain-of-function research was restricted for a brief period.

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By the way, by the same committee managed that, that is now issuing slightly modified—they're marketing it as more restrictive—guidance for gain-of-function research under federal funding.

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According to recent testimony from Lawrence Tabak to the select committee of the House concerning the coronavirus origins.

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But that increased restriction is still limited only to federal funding.

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It has nothing to do with commercially funded research, which is wide open in terms of gain-of-function work.

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And has the clause in it that it can be overturned, that restriction, and required additional oversight.

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It can be overturned at the advice of the White House, the White House Special Counsel on Science and Technology, the Department of Defense, the Health and Human Services in general, and the Department of Homeland Security.

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So basically, if the government decides that they want to allow a gain-of-function study to proceed, they've got multiple pathways and multiple agencies that can do so.

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That means that basically if the government determines that they think it's in the interests of national security to allow gain-of-function research on any pandemic potential pathogen in order to determine what modifications would be required to make it more infectious or more pathogenic in humans,

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they can go ahead and proceed to do so.

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So it's not really a restriction at all.

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It just creates yet another level of bureaucratic authorization required to proceed.

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Well, and let's go back to H5N1 here, because this is kind of our focus here.

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From what I understand it, we actually know because of that research, gain-of-function research that was done with H5N1,

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we actually know how to make it particularly transmissible to humans.

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So this is something that isn't generally known by the public and isn't discussed in corporate media.

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But as we covered earlier, the whole genesis of the restriction on gain-of-function research or federal funding of gain-of-function research that was put in place during the Obama administration was triggered.

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It was triggered by two publications.

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The two key authors, senior authors, are Fouché and Kawaoka on separate papers independently, performed gain-of-function research on H5N1 on a very similar clade to the one that's currently circulating.

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They were able to show and published in 2012 that there were four specific point mutations.

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These are four amino acid substitutions in H5.

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The hemagglutinin enables H5N1 or other H5 influenza viruses to efficiently and reproductively infect mammal cells.

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And in particular, it was selected by the laboratory in Wisconsin, Kawaoka, that did this work, to more efficiently infect human cells.

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Then it was, in both cases, they verified the ability of this new gain-of-function H5N1 to reproducibly infect animals using a ferret model.

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Ferret is the common animal model, small animal model for doing influenza research.

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So they showed that with these four-point mutations that would confer greater infectivity in humans, they could demonstrate that they could get ferret-to-ferret transmission efficiently, reproducibly.

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And they published this.

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What that means is that virtually anybody, certainly anyone with a graduate-level molecular biology and virology background, can readily engineer a highly pathogenic, highly transmissible H5N1.

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And that, I think, is a concern.

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That H5N1 has been existing for decades, circulating in waterfowl, and it has no evolutionary pressure right now to jump into humans.

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But we now know because of this gain-of-function research, it could jump if it acquired these four separate point mutations, which, by the way, in terms of frequency of genetic events, would be a relatively rare one.

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Difficult to occur in a natural environment, but it was forced.

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In one case, it was forced using serial passage.

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What is that?

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So you can think of serial passage as kind of like animal breeding with viruses.

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What you do with serial passage is you take the virus and you place it under a restrictive condition.

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It could be the presence of some antiviral in cell culture.

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So you can passage it from cell culture to cell culture to cell culture under different conditions.

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You can do it by taking a mouse, engineering that mouse so that it had human receptors on its cells.

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So this is recombinant DNA transgenic technology.

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And then creating a lineage of those mice.

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So basically a whole lot of cloned mice that are all genetically identical that have this human characteristic.

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And then serially passaging a virus from one mouse to the next mouse to the next mouse.

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What that means is that when the virus is replicating, it throws off a whole lot of mutants, particularly an RNA virus.

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And so somewhere in those millions to billions of viruses, there might be one that'll be more infectious.

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And so you take a sample of the lot, the swarm, put it into the next mouse.

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And then when you passage it to a third mouse, the only viruses that should still be living are the ones that are able to replicate in that second mouse.

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Okay.

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And so you do this again and again and again, and you get a virus that is adapted for whatever those conditions are.

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You're basically breeding it to be more infectious.

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The more modern approach is that you use recombinant DNA technology and potentially also including the CRISPR-Cas9 system, which allows for very powerful selective directed mutations.

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So let me see if I've got this right.

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So two separate labs did this.

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Using two separate methods.

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Using two separate methods and they came up with the same four point mutations.

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Basically the same.

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I don't know if they're the identical four point mutations, but in both cases they found, I believe it was only four mutations were necessary.

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Okay.

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So now we're in a situation in which that knowledge is public.

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The knowledge that would be necessary to engineer an H5N1.

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And so that I think is something that is worth concern.

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Is it worth the level of concern that's being promoted right now?

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That's debatable.

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Is there anything that's particularly changed since 2012 and now in terms of H5N1?

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Well, we had that outbreak in 22 of a more highly pathogenic in birds H5N1.

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Right.

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But it's not more highly pathogenic in humans to the best of my knowledge that we don't have documentation to support that.

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That's why I said since 2005 in all of China, 32 dead out of 54 cases.

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Not much.

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The question that this raises, right, the kind of the obvious question, I think, is it seems to be, at least in this case, relatively easy for someone to do this.

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And so, you know, there are millions of people around the world who have the ability, right, to do this.

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Absolutely.

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So I agree.

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You know, I don't know what the policy response to that is in a situation where there's crazy people.

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There's people filled with nihilism.

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There's, you know.

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All kinds of motives.

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All kinds of motives.

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You know, there's people that are, you know, into depopulation.

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I don't know, right?

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There's just a lot of crazy people, right?

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Well, and then there's the, rather than calling it a conspiracy theory, let's call it a fear.

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That there could be an agenda of promoting a crisis, a public health crisis, to advance a variety of agendas.

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And then we have the complications of what's going on geopolitically in the infectious disease area, having to do in particular with the World Health Organization upcoming vote concerning the pandemic

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accord or treaty, depending on which version, and the international health regulations.

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And there's the appearance that promotion of fear around avian influenza certainly could contribute to greater acceptance of the logic that the World Health Organization should be given more power and money to coordinate global

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global responses to an infectious disease outbreak.

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And whether or not there is such a surreptitious agenda, but it's certainly something that a lot of people are concerned about right now.

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The thing that strikes me here through our conversation today, well, first of all, no need to fear H5N1.

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In its current version.

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Sure.

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But that's important.

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But number two, we're in a strange brave new world, aren't we?

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Yeah.

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Yeah.

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One of, in which bad actors have the ability to create material, biologic material, that can impact on all of our lives.

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Right.

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And that can really destroy economies.

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Anybody with a reasonable amount of training, basically graduate level training, can create a highly pathogenic virus.

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We're assuming, by the way, that a human engineered, human, highly infectious H5N1 would be highly pathogenic.

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So I have colleagues that are very active in this sector that are really skeptical that we've ever been able to engineer a more highly pathogenic virus with pandemic potential.

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There's been a lot of talk about it.

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Right.

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But the truth is that even with this H5N1 gain of function research, there was not a demonstration that those ferrets were dying, whereas they weren't dying before.

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The end point was, it was just more transmissible.

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Right.

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More readily infectious.

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And we had all this fear about the SARS-CoV-2 coronavirus being highly pathogenic.

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So even if somebody was to put in those four point mutations, we don't necessarily know that the engineered H5N1 would create this level of disease

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disease that is being discussed by the FDA, World Health Organization, ECDC of 50 to 60 percent case fatality rate.

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That's probably a gross overestimate of the risk.

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Well, and I think that's the other, you know, lesson for me here in our discussion today is that, you know, when you hear a number like this, you need to understand the context.

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Absolutely.

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Because numbers are brandished about these days in all sorts of ways and, you know, to elicit a particular response.

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Absolutely.

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Right.

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I think we're going to have to look into this further.

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I think the whole story of gain of function research and the federal response, or I believe inadequate federal response, is something that we should continue to monitor here on Fallout.

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So with that, we'll see you all next week on Fallout.