It doesn't matter much at all what you believe about vaccines until we invent really important ones, you know, until we have a pandemic that's killing everyone, you know, and, you know, it's, it's not, it's, you know, measles plus, you know, okay, I can tolerate what you think about measles.
Cause you know, not that many people die from it.
It's, it's just a big hassle in the end, but no, when, when we have this.
So what I argued, I believe I can.
It doesn't matter much at all what you believe about vaccines until we invent really important ones.
Whoa, cyber attack.
Until we have a pandemic that's killing everyone.
Sorry about that.
And it's measles plus.
I can tolerate what you think about measles because not that many people die from it.
It's just a big hassle in the end.
But no, when we have this new pandemic that has got 75% mortality
There'll be no pretense of being polite in the face of these beliefs.
It'll be a moral emergency, because it has to be.
Jonathan, who's going to talk about his latest distillation of what the pandemic means to society, to biology, to science, and to democracy, and to the whole kind of idea of empiricism and integrity.
And then each of us, this incredible preeminent panel that we have, each one of you is going to get a chance to comment
I think truth is good for kids.
We're so busy lying, we don't even recognize the truth no more in society.
We want everybody to feel good.
That's not the way life is.
So what I argued, and I believe I came up with this independently, but I believe Peter McCullough has mentioned something similar, as has Jonathan Cooey.
If you think about it, you know, if we're defining vaccine really liberally, and these COVID vaccines are vaccines, the flu vaccine is vaccine, okay.
But actually, they're kind of cheating when they're calling these things vaccines.
And, you know, anything with really rapidly fading efficacy, such that you need shots within a year, you know, Canada's saying nine months, is as actually J.J.
Cooey's insistence, and I think he's right, on calling them transfections rather than vaccines.
But you can tell if someone's lying.
You can sort of feel it in people.
And I have lied.
I'm sure I'll lie again.
I don't want to lie.
I don't think I'm a liar.
I try not to be a liar.
I don't want to be a liar.
I think it's really important not to be a liar.
Now, Dr. Gallo and Dr. Fauci talked a lot about isolation and purification.
Can you tell me what the difference is between the two?
Isolation, what was it?
Isolation and purification.
Of the virus?
Yes.
Well, you isolate a virus by finding the virus which causes a disease.
You purify a virus by making a lot of, I mean, just by purifying it so you get a pure virus.
I don't understand what the issue.
Well, they interchanged the two and I wasn't sure if it was the same thing or if it was two totally different.
No, it depends on how they used it.
Okay.
Can you explain the process of HIV isolation?
Well, didn't Dr. Gallo do that?
I mean, he actually isolated it, so... I mean, why should I do all of this?
This is all textbook stuff you're asking me.
It's literally turning into a worst-case scenario.
The latest data tells us that we're dealing with, essentially, a worst-case scenario.
rules protect yourself at all times follow my instructions keep it clean touch gloves if you wish let's do it sweaty palms this is so crazy like these bumps this is so crazy i feel so nervous like what in the world man
He's scheduled for 60 minutes next.
He's going on French, British, Italian, Japanese television.
People everywhere are starting to listen to him.
It's embarrassing.
Hello, everybody.
Sorry to be late.
I wanted to be on at 1.13 today, but I'm not.
I'm here now.
It is, again, one of these days where we're trying to get a different start, a little quicker.
This is the home of the high-resistance, low-noise information brief called Gigaohm Biological.
It's the 23rd of July, 2024.
Today, I wanted to do something a little different.
I want to do a study hall session, and I want to look at
a video from just at the start of the pandemic and a video from a couple days ago so that we can try to learn a little bit about the pandemic potential of coronaviruses from none other than, um, Ralph Baric.
And I think that's a really, really good idea because, um, this is the kind of sort of biology that as we move forward, we're gonna be able to... Let me just get this... at the right...
level there.
And yeah, so don't forget that the basic premise of this show is that weaponized piles of money and the people that that get their comfort and fame and and fortune from those weaponized piles of money have used social media and mainstream media to convince us that it's worth arguing about where this virus came from.
And
It's by participating in this argument that we have accepted the existence of the novel virus.
We've been governed by a theater that spans from mainstream media, all of these social media platforms and podcasts, and the intellectual dark web is just a small, front-facing example of all of these crafty little things that are going on with sponsorships and things like locals and this kind of thing.
I think it's really important to realize that still after nearly a year and a half of challenging people to just address these things, if you want to address Jonathan Cooley, why not just start with these three statements and see if you can whittle them down to something a little better.
Intramuscular injection of any combination of substances with the intent of augmenting the immune system is dumb.
Transfection in healthy humans was always criminally negligent and RNA cannot pandemic.
That last one you might express with a little more nuance and elegance by saying viruses are not pattern integrities, but I think any way that you look at it, these three statements are statements that no one seems to want to talk about.
Everybody wants to talk about
I don't know, a whole bunch of other things other than the biology we are pushing.
And when I say they, I'm talking about these people.
I do want to give you a little positive information.
Oops, that was not the right cut.
I wanted to cut here and then there.
Hello, everybody.
Yesterday I showed this graphic and I suggested that this was a team being loosely orchestrated by Robert Malone.
And if you look at this graphic carefully, you'll see that I'm kind of implying that maybe I need to be a little skeptical or we need to be a little skeptical of Denny Rancourt.
And it was with intention that I put him over there because I want to show you that all of the purple frames there are people that aren't American.
And although I think that when I've spoken with Denny Rancourt and when he's spoken with other people, he's very clear that there's no evidence of spread, there's no evidence of a pandemic at the beginning when it was all supposed to be starting in 2020.
He seems to also kind of be okay with the fact that a lot of these people on this side of the diagram are very happy to point people to Denny's work without saying that.
Instead, they will point to Denny's work and say that, wow, it's really great, and look at how many people were killed by this shot.
Look how many people were killed by the double-stranded DNA contamination of these shots.
Look how many people were killed by the rush.
Look how many people were killed by the lockdown.
But never really quite get to the fact that Denny actually shows that it's tantamount to murder.
And that nuance there is starting to become frustrating because Denny could just put his foot down and say, hey, I think it would be better if you guys would point out that the whole justification for rolling out potentially billions of transfections made in many different places around the world by all the same processes of recombinant DNA, molecular biological techniques,
rather than saying that that whole impetus for that is based on a lie, they keep staying focused on the shots.
And I think this is a problem, although there is some sunny side to this.
Denny recently showed on Substack that Michael Yeadon is making the argument
that we only need to focus on one of his observations.
You can see that right here.
Mike focuses on one of our observations in particular that there was no excess all-cause mortality prior to the WHO declaration and that is a brilliant argument.
Now I think
This is maybe the first step in first, you know, giving credit where credit's due.
Mike Eden has been saying that for quite some time and trying to do it as succinctly and generally as possible.
I think Mike Eden agreed with me on my show and liked my portrayal of the idea that if we call the police,
We don't have to have a reasonable explanation for the motives of why the criminal has invaded our house and why we're calling the cops on the criminal at two in the morning.
We just have to say there's a criminal in our house and he shouldn't be here.
And in this case, I think Mike Yeadon saying that there's no evidence of a pandemic, so all of this stuff is bullshit, is I think one of the best tactics.
And quite frankly, I really feel as though that's what this slide is all about.
I really think that saying it this way and choosing to try and succinctly express our position in short,
statements is what should, in theory, open any dumb ideas or any preconceived notions of biology that doesn't exist.
It should open any of those potential things to ridicule and correction and critique.
But instead, the only thing people do is ignore this slide.
And that, I think, is kind of the same thing as what people are doing when they tend to ignore the fact that Denny Rancor has shown for really four and a half years now, since May of 2020, that there's no real evidence of the thing they're claiming that's happening.
And he went on to show it over and over and over again.
And eventually he got invited to go to Romania of all places and present on stage with some of those people over there.
And then those people all came back to the United States and said, Denny Rancor's presentation was amazing.
17 million people have been killed by the shots.
And so that again, started to run, it ran out another quarter.
It ran out another half really.
I mean, we're talking about over half the game being run out because from November 2023 until now, we haven't made any useful progress since Robert Malone and Meryl Nass and Jessica Rose met Denny Rancourt for the first time in Romania in November of 2023.
saw his presentation live, probably had breakfast with him at the hotel, and then came back to the United States and didn't tell us anything about that first observation which he first made in May of 2020.
And so the only reason why I had Denny over there is because I find it so strange that of all the people who've made all the observations early,
Denny doesn't seem to insist that everybody acknowledge that he keeps making, he made that observation and he keeps fine tuning it and sharpening it and all arrows point to yes, you know, and demanding that those people over there who don't want to talk about 2020 make the admission that it's all murder and lies.
It doesn't appear to be a, a,
it doesn't appear to be a spreading pathogen.
And this is really crucial to see that this is where I'm pushing.
And while other people might come up with different terms for what this is, a gigaspiral or a purity spiral, no, this is very objectively looking at what people said and when they said it
and comparing that to when they first talked to me, how long they talked to me, and what I was able to, in my opinion, adequately express to them.
Some people haven't heard my pitch.
Some people haven't heard my pitch over coffee.
Some people have heard my pitch over Zoom, over Signal, over
over dinner, over a rental car ride.
So there's lots of different, you know, doses of KUI that you can get along the way.
And not everybody has spent hours and hours listening to me on my stream.
Not everybody like Brett Weinstein has had me at his fingertips on a signal chat for six or eight months.
Not everybody has hired me as a consultant for a book like Robert F. Kennedy did for a whole year.
Not everybody has hired me as a staff scientist like Children's Health Defense did for six months this year until I stepped on Meryl Nass' or Robert Malone's toes.
So I think it's important to point it out, but we're gonna keep that stuff for Mondays.
I'm sorry, I just wanted to give you a little positive note there that we keep seeing Denny Rancourt giving a shout out to Mike Eden, who's, you know, understandably Mike Eden is done.
Like he's too little butter spread over too much bread at this point in time.
In 2020, he was already,
complaining about this stuff in front of the parliament in UK.
And so, you know, either he has been an operative since the very beginning, or he's been an outspoken critic of everything that this pandemic has been since the beginning.
And my chips are still on the ladder.
So let's try to make some headway into the pandemic potential of coronaviruses and how this concept, right, because that's a concept, pandemic potential of coronaviruses, how is that
created.
And I think you're going to find that if you go into the literature and look, there are very few people to blame for this.
And from the perspective of, let's say, mentor chains, the mentor chains basically start at Ralph Baric and end after Ralph Baric.
In other words, everybody that trains with him is familiar with coronaviruses.
Very few people go on to work on coronaviruses further.
A notable postdoc of Ralph Baric that went on further to work on coronaviruses, at least in terms of writing reviews about them, is Alison Totura, who went on after her postdoc with Ralph Baric to write a review with Sina Bavari that all of you should read, and that I included in Bobby's book, which is about a coronavirus pandemic that would come from a bat cave or camels, and that remdesivir would be a hell of a useful drug to start with for.
And so I think that one of the things that I'm trying to challenge people to consider is the idea that this whole thing is a sort of manufactured biosecurity narrative that has been laid down over many years, primarily by funding Ralph Baric's lab.
And so as long as Ralph Baric passes students through and is able to bamboozle them with the shell game about what infectious clones are, and that infectious clones are essentially what we find in the wild, just conveniently replicated by modern molecular biological techniques so we don't have to work so hard culturing.
And that's a lie.
Transfection and transformation in cell culture is not virology.
It is transfection and transformation in cell culture.
And doing the same in animals is not virology.
It's just transfection and transformation.
And so working on self-replicating RNA constructs is not virology either.
It's synthetic biology.
It's synthetic manufacture of DNA and RNA and its application in cell culture in animals.
And so what I want to do is listen to these two
discussions about the biology of coronaviruses and I want you to listen specifically for, specifically for clues about methodologies where the elusive nature of coronaviruses and their reluctance to subject themselves to culture is contrasted by the
the sort of mythological biology of coronaviruses that they can evolve very rapidly.
And they are a very stable genome that can shift gears when it needs to, to adapt to what I guess Geert van den Bosch would call infectious pressure, but Ralph Baric will call evolutionary pressure.
I don't know.
These people are all just using words to enchant us.
So let's start with the first video.
which is Ralph Baric from 2020, right at the beginning of the pandemic, just trying to make sure that everybody starts out on the same page with regard to the basic coronavirus biology.
And so let's check this one out.
Hit escape here.
No, that's not what I said.
I said escape.
My keyboard might be dead or something like that.
I'm not really sure what's going on there.
And let me move my brain for a second.
Get this arrow up here.
February 26, 2020.
This is very close to the first time that a lot of these people, uh... It's very close to the time when Kevin McKernan started joining podcasts when, um...
when Addy Adds and Paul Cottrell and Kevin McCairn decided that they needed to hit the airwaves as well to get the word out about the worst case scenario, a Red Dragon event or something like that.
So this is Ralph Baric and the public facing version of this
giving a presentation at the University of North Carolina, Gillings School of Public Health.
That also may just be where he's affiliated, but I do think that's where he's presenting as well.
Here we go.
Here with them, people wearing masks, as is happening right now.
And most of the new emerging coronaviruses that we've experienced in the 21st century are derived from bats.
And in general, there are 1300 different bat species, and each one has somewhere between seven and eight
different coronaviruses.
And so this is, in essence, a reservoir of viruses that occasionally spill over into human populations and cause big outbreaks of disease.
And I'm going to try to talk to you about how this occurs, why it occurs, why it appears to be accelerating.
and what we need to be prepared for in the future.
biological dark matter that the founder of MetaBiota, Nathan Wolf, was selling us a few years before that.
So this is a very consistent biosecurity narrative with very little biological data to substantiate these kinds of claims.
And now again, remember, we're focused on methodology, but I will pause it occasionally to say things like that as well.
So who knows how long it's going to take to get through this, but it's only about a
30 minute presentation.
In the context of this new SARS coronavirus 2 novel coronavirus that emerged three months ago.
So just on your right-hand side of the slide, there have been four major respiratory viruses that have emerged in human population.
A lot of this is what I said on my bicycle on JC on a Bike.
Some of my first pandemic videos are exactly this.
I'm just going to check the notebook camera.
Since the beginning of the 21st century, starting with SARS in 2003,
the 2009 H1N1 influenza virus strain, followed by Middle Eastern respiratory coronavirus in the Middle Eastern Kingdom of Saudi Arabia in 2012.
That outbreak is still ongoing.
And then just a few months ago,
the SARS-CoV-2 strain or 2019 novel coronavirus or COVID-19, which is the disease.
So what I'm going to talk about is talk about what the drivers are of emerging coronaviruses in terms of how they jump between species to cause outbreaks of human disease.
talk about the context of the 2003 SARS outbreak and why we were able to control that and why this is gonna be so different, so much more difficult to control the 2020 outbreak strains.
And then I'm gonna talk a little bit about countermeasures that we use in our lab.
So, coronaviruses, nidoviruses is a bigger, larger group of viruses that include the coronaviruses.
And these viruses have a tendency to traffic easily between species.
So there are four common contemporary human coronaviruses that we've all been infected with, probably in the first five years of life.
They originated between 120 and about 800 years ago, mostly from bats, rodents, or cattle.
to cause human outbreaks.
They then colonize the human population.
They cause mild disease, respiratory tract infections in children primarily.
Over the last 25 to 30 years, there have been a variety of new... Now, it's interesting.
I don't know why I took myself off the screen there.
It's interesting that he, these are the things he starts with, right?
Nidoviruses are a larger group of viruses that include coronaviruses and traffic easily between species.
No real data to substantiate that, just that's an assumption.
Another assumption that was built in there was that all
Humans are infected by these four endemic coronaviruses in humans.
They're infected in the first five years of their life.
And that's just said.
As a matter of fact, that's the way it is.
Now, think about that very carefully in the context of this new coronavirus that supposedly none of us have any immunity to.
Because that's part of the illusion here.
It only works, the only way that argument works is if the only correlative immunity you care about is antibodies and the ability to detect them with a given
commercial product or specific methodology.
So in other words, they are going to make no effort to describe to you that we don't really understand how the complex immune memory to, let's say, RNA signals occurs during the first five years of the life of a child, but we kind of assume that it happens.
And that's what he should be saying, that we assume that in the first five years of life, that any of these signals that are endemic to our environment are going to be things that our immune system reckons with in such a way to build sort of a symbiotic or, you know, ignore kind of pattern with the environment that we find ourselves in.
but instead they're hyper-specific and they say that kids are infected with the four human coronavirus strains in the first five years of their life.
And that already is a massive simplification of, and a massive level of specificity that they absolutely do not have.
If that's the case, then why don't we have hundreds of thousands of sequences, never mind millions of sequences of these coronaviruses, and why haven't we been monitoring them so that we understand how they change and don't change?
There was already an experiment to be done.
20 years ago then if these coronaviruses have been in the background the whole time and somehow or another we're supposed to believe that the biosecurity state that's concerned with pandemics wouldn't have characterized that background that all of us apparently are developing a lifelong immune memory to or at least an immune tolerance to for the rest of our lives come on guys
This is the kind of of incongruency that I saw already very early and was frustrated with.
And it was available in 2020.
This contradiction right here was already available in 2020 because we don't know how we build an immune memory and immune tolerance to the
RNA signals that are in our environment.
But the assumption is, is that we build a tolerance to them over time, and especially in our development, in during a childhood.
We probably should assume that breastfeeding has some role in bridging the gap between a naive immune system and an immune system that is appropriately adapted to some of the antigenic challenges in their surroundings.
None of this stuff is discussed.
They walk so carefully around it.
Or they do this, where they just tell you some ridiculously simplified cartoon about the immune development of a child.
Coronaviruses have caused major outbreaks in domesticated species of economic importance, like pigs and cattle.
The most notable one here was porcine epidemic diarrhea virus that killed about 12 million piglets in the US in 2012.
And then since the beginning of the 21st century, there's been accelerating cross-species transmission movement, starting with SARS about 16 years ago, MERS about seven years ago.
The SADS coronavirus emerged in China
two years ago, to cause outbreaks in pigs.
It's notable because it replicates efficiently in human cells of the lung, and so it has all the potential features that could make it an epidemic strain in humans.
And then we have SARS-Coronavirus-2, which is a kissing cousin of SARS that emerged three months ago.
There is gonna be some science in this talk, but I'm gonna try to keep it relatively
You understand that the lockdowns haven't occurred yet, right?
There's not this super panic.
I don't even know how far off we are time-wise.
If this is the 26th of February, I don't know how far off we are from Sohomish County, man.
It could even only be a week later.
What are the drivers of coronavirus evolution?
Why are they moving between species?
So here is the regulated fidelity thing.
This is the fundamental problem or obfuscation that occurs with the use of infectious clones.
So we're just going to take many stabs at this all summer long and all fall long and all winter long until people actually get it, until it sinks in, or until I'm able to figure out
a very short ladder for people to climb out of this hole.
But understand that one of the illusions that needs to be created, one of the biological problems that is created when you're using RNA, and especially single-stranded RNA, as your genetic material, is that it's hard to copy single-stranded RNA with high fidelity.
And that high fidelity is revealed in the behavior of and the instability of the smaller genomes that we have understood as similar entities before the discovery of and the description of coronaviruses.
And so now here, Ralph Baric is going to describe how coronaviruses have evolved, apparently,
a better enzymatic solution to copying RNA.
And that's why they are able to sustain these large genomes despite the usual downside of RNA, which is copying can be terrible.
And he's going to say in this talk that it can be an error every 1000 bases.
coronavirus has 30,000 bases in its genome, that would be 30 errors per copy.
30 errors per copying.
We're not even talking about recombination.
And he says recombination rates are high.
And we're going to talk about why recombination rates being high is not a good thing for the infectious cycle model that they want us to teach our kids.
So let's just listen to Ralph first.
Well, these viruses have the largest RNA genome in nature.
It's 30,000 nucleotides in length.
And to maintain a genome of that size,
They have a polymerase that has a fidelity function.
In other words, it fixes errors when the virus replicates.
Most RNA viruses, like flu or HIV, make a mistake every 1,000 nucleotides that they synthesize, they make a mistake.
Or every 10,000 nucleotides, they may make a mistake.
RNA viruses, like flu or HIV, make a mistake every 1,000 nucleotides that they synthesize, they make a mistake.
Or every 10,000 nucleotides, they may make a mistake.
In a big genome like coronaviruses have, if they can't repair that, they go into what's called error catastrophe and die.
So I've just told you of a potential vulnerability that if you can develop drugs to knock out that activity, the virus will go into error catastrophe and eventually burn out.
So novel enzymatic functions in the virus
that can be taken advantage of for therapeutic intervention.
And of course, what drug is going to target XON and the replication fidelity of coronavirus?
It will be remdesivir, of course.
And drugs that interfere with this are going to be a target that they all get very excited about.
What they're not going to tell you is the reason why that would be exciting is because these enzymes, even if XON, non-structural protein 14 there in his diagram, even if this protein is real and it does contribute to a higher fidelity of copying,
It doesn't change the fact that the fundamental model of the infectious cycle involves these sub-genomic RNAs and the regulation of sub-genomic RNAs, the packaging of full genomes or not full genomes.
It involves recombination rates.
If the recombination rates are 25% during mixed infections, the vast majority of recombinations are gonna be error catastrophe.
They're gonna be not error catastrophe.
They're gonna be a catastrophe error.
and you're going to cross over and then you're going to recombine with another transcript that inevitably knocks out a gene or deletes half.
You're not guaranteed to jump from one transcript to the other and have the story be continuous.
That would be like saying, well, you're copying one book, and then you're going to jump over to another copy of the book.
And hopefully you'll start at the exact page and the exact sentence that you need to start at, so that that recombination doesn't matter.
But instead, you might go from chapter 14 to chapter 2 again.
And what consequences does that have if that genome with that kind of redundancy gets packaged or vice versa?
You might go from chapter two and jump to chapter 14 and finish the book in two chapters and then that's your genome.
And so the rates of recombination being this high suggest they want you to believe and imagine in your head that these are all bonuses.
These are all things that give superpowers to
to coronaviruses when in reality these are all things that make their model of what's supposed to happen even more complicated and even more unlikely to occur as simply as they want to claim it is.
Now this regulated fidelity can also vary depending on environmental conditions.
So the virus, if it needs to increase its mutation rate to adapt to something or to a new change, it will modulate that activity.
And so- And so if you're going to claim that the virus can modulate its ability to be high fidelity or not so high fidelity, does it also modulate where it makes that mutation?
And where will it make those mutations?
It'll make those mutations presumably in those subgenomic transcripts, which are the highest abundance.
That's what you'd presume.
That's what they presume, but they don't really talk about that.
He's just going to say that in general.
They can modulate it depending on conditions.
Think about the fact that these are not pattern integrities.
These are supposed to be single chain, 30,000 base pair long, single RNA molecule genomes that can modulate the way they copy themselves depending on conditions.
but he doesn't need to explain it to you any more than that.
No more biology needed there because you should just take his word for it that these things, if I told you that an insect could, that bees could adjust whether or not their venom was really stingy or it actually kind of tickled a little bit and it all depended on conditions, wouldn't you want a pretty good explanation for how the hell did they do that?
What are the conditions?
How does it change what's in their stinger?
So as a biologist, the question that should come to your mind is he just showed you earlier here, a picture of some, some, I'm going to go back so you can see it.
He just showed you a picture of some proteins that are all lumped together and supposedly making copies of, of, uh,
RNA and he's telling you that these little machines here can adjust their error rate depending on whether you need more errors or whether you need less errors.
That's a pretty bold claim to make about a cuckoo clock whose parts you still don't really understand.
That's a pretty bold claim to make and just hand wave around it.
The cool thing about coronavirus is they can adjust their fidelity to depend on conditions.
This is a deep state national security narrative that Ralph Baric has very nervously been creating himself on behalf of Tony Fauci, NIH, and the rest of these people who want to enslave our children
that want to take our children and turn them into voluntary experimental animals.
Or maybe get our children to give their children as voluntary experimental animals, like maybe Sasha Latupova did to her daughter.
You know, just experiment on my daughter.
See if you can make her go viral.
Give her some scripts.
Help her make some videos.
So we can have some idea of how to make people go viral.
We can have a list of people that we could use to create chaos in the United States.
Sure, have at it.
My daughter would be great.
It's all the same thing.
It is one giant national security narrative.
And as long as all the postdocs that study these enzymes go through Ralph Baric's lab, they're all working on synthetic constructs.
They're all working on DNA and RNA produced synthetically.
None of it is derived from the wild.
None of it is derived from culturing viruses.
And it's just ridiculous.
He is the sole distributor of SARS Urbani, the infectious clone made from SARS-CoV-2 or SARS-CoV-1.
Well, these viruses have the largest RNA genome in nature.
It's 30,000 nucleotides in length.
And to maintain a genome of that size,
They have a polymerase that has a fidelity function.
In other words, it fixes errors when the virus replicates.
Most RNA viruses, like flu or HIV, make a mistake every 1,000 nucleotides that they synthesize, they make a mistake.
Or every 10,000 nucleotides, they make a mistake.
In a big genome like coronaviruses have, if they can't repair that, they go into what's called error catastrophe and die.
And so it's weird to even be talking like it's the virus because the virus is the genome.
That's it.
The genome goes into your cell and it makes these enzymes and now the enzymes are responsible for this.
But the enzymes aren't the virus.
The enzymes are not in the virus.
The enzymes are made by your cells.
And yet he attributes all of these things, all of these ideas, all of these processes, all of the supposed selective pressures on the virus, even though the virus doesn't have these enzymes.
These enzymes are only present when it's infecting something.
And so once your biology is sophisticated enough that you can listen and hear it,
These people are just telling a story.
That's just a mythology that has been very consistently curated by a few people like Peter Daszak, Nathan Wolf, Tony Fauci, Ralph Baric, and maybe Mark Denison.
That's it.
That's all you needed.
They took Stanley Perlman out of the equation a long time ago.
And Stanley Perlman, of course, is the guy who made his whole career showing that it was T-cells that were the important and crucial
crucial part of the immune system that responded to a respiratory virus and created the immune response and governed it.
Yeah.
So that's why we don't talk to Stanley Perlman very much anymore, but we talk to Ralph Baric.
Just told you of a potential vulnerability that if you can develop drugs to knock out that activity, the virus will go into error catastrophe and eventually burn out.
So, novel enzymatic functions in the virus
that can be taken advantage of for therapeutic intervention.
Now, this regulated fidelity can also vary depending on environmental conditions.
So the virus, if it needs to increase its mutation rate to adapt to something or to a new change, it will modulate that activity.
And so the viruses are quite clever.
They also undergo recombination at high frequency.
Well, what is RNA recombination?
Well, remember that I mentioned that up to six, seven to nine coronaviruses exist in a bat.
If you have a co-infected- So 1,300 species of bat and seven to nine coronaviruses in each bat.
Now, are they implying, are they just saying it right here that bats make coronaviruses?
We don't make coronavirus, but bats make coronaviruses, and each species has between seven and eight or six to eight coronaviruses unique to them.
That's an interesting statement to make.
It's possible that bats, because of their biology, signal with self-replicating RNAs more than other species.
That's totally possible.
Why not?
They live in huge, dense colonies that might require a methodology, a mechanism by which the cells of the immune systems could communicate in such a way to keep them in sync.
I don't know.
I'm just saying that
that it's an interesting thing to say here, because again, it's very Nathan Wolf and Metobiota-esque.
It's very EcoHealth Alliance and Peter Daszak-esque.
It's very Tony Fauci-esque to say that there are 1,300 species of bats and he says between six and eight unique coronaviruses in them.
And then when they're replicating, they can cross over and recombine.
And that's a further complication in the pandemic potential, further
data to edify pandemic potential when that's not true.
That means it's more likely that you're not going to make a successful copy of the genome.
It's more likely that you're going to make erroneous recombinations.
It's more likely that you're going to make erroneous recombinations that result in truncated genomes.
And so the whole idea of this creating more
more potential is just wrong stop lying action with a blue coronavirus and a green coronavirus when the blue coronavirus is being replicated this polymerase complex up here can fall off bind to the green template and make a chimeric it can fall off this super high fidelity proofreading
proofreading RNA-dependent RNA polymerase can fall off and go on to another transcript that just happens to be right there.
You see what we're talking about?
The inside of an infected epithelial cell, presumably, which is not a small space relative to the size of these RNA molecules, and more importantly, relative to the size of these proteins.
One cell could have hundreds or even thousands of ribosomes.
It's extraordinary the level of bullshit that they've thrown at us and how hard it has been to extricate ourselves from it.
So in other words, they've genetically mixed their components so that you have something new that didn't exist before.
And this happens about 25% of the progeny of a mixed infection.
will be recombinants.
Flu does reassortment in about 25% to 30% of the progeny from a mixed infection are resorted viruses.
And this drives pandemic outbreaks of flu disease.
So coronaviruses have their own trick like flu.
But it's not the same because flu, supposedly, according to their biology, number one is a negative strand RNA.
Number two are small little segments of that RNA.
And the segments are what get reassorted.
But every flu virus has to be packaged with a number of these little pieces of RNA.
And then also, what?
It needs an enzyme.
It needs the RNA dependent RNA polymerase because a negative strand RNA, we don't have that.
We can't do that.
We can't use those.
That's what I think you should realize from the perspective of the flu versus.
So a flu virus, if I just draw a cartoon of flu virus, the genome would look like this.
It might have, let's just pretend it has four parts.
This would be flu.
And then a coronavirus genome is supposed to be just one long genome that's 30,000 bases, yeah?
And so maybe the genomes are equivalent size, but this one is broken up into some kind of segments.
And these segments, during replication, are what get reassorted.
So if you call these segments 1, 2, 3, 4, 5, and then you have another flu virus with 1,
two, four, six, and seven, then you can imagine a scenario when you're copying these two viruses that you make all of these, you know, you're making all of these little RNAs and then the new package might have a one,
a 7, a 4, a 3, and a 2.
And so this combination will be unique to the infection, right?
That's what he's arguing.
But here's the key.
Because flu virus is a negative-stranded RNA, then you also have to have the enzyme inside.
If you don't have the enzyme inside, then you don't have an infectious particle.
That's not a problem for coronaviruses because coronaviruses are positive-stranded RNA.
And so again, what I'm just trying to show you is that this is a pretty fundamental difference between the way RNA flu viruses are purported to create and maintain an infectious cycle and the way that coronaviruses are supposed to
initiate and maintain an infectious cycle.
It's very, very different.
And the recombination mechanism by which the RNA is done, remember what I'm saying is if this is a 30,000 base pair genome, and this is a 30,000 base pair genome, and you get this far copying it,
and then you jump down here to a random spot on another genome, the odds of you ending up with the equivalent of an entire genome over here when you're done are almost zero.
Because you're gonna be jumping from a very specific spot on genome number one to a random spot on genome number two and the resulting
It's not going to be great most of the time.
You can just do it in your imagination, but it's also statistically provable.
Recombination doesn't help the infectious cycle with infectivity or with replication competence.
No, it doesn't at all.
And it further complicates this admission of Robert Malone in 2021, where he said the vast majority of coronavirus particles during infection are not replication competent.
That's a huge problem.
And it suggests a different biology is involved here.
And indeed, it could be that our normal
exosomic communication is being hijacked by a foreign RNA for a brief period of time.
That's possible.
But in that scenario, none of the limitations of that are acknowledged because if they would be acknowledged, then they would undermine the illusion, which is, well, of course, pandemic potential, right?
We're trying to create the illusion of pandemic potential.
So we got to get rid of all of these complications
which would, by any biological estimation, in reality, it would just make pandemics a ridiculous notion.
RNA can't do that.
They also can undergo modular evolution.
That means genes can be shuffled, or critical virulence motifs can be shuffled between strains.
Okay, so they can change quite quickly.
And then if you look at the virus particle, you see these projections on the surface that give the particle a corona or a halo-like appearance in the electron microscope.
That's the spike glycoprotein.
It's a large glycoprotein.
This is the actual structure of that protein.
And it tolerates high rates of mutation, and I'll show you a picture of the amount of variation that exists within the SARS-like viruses in a little bit later.
There can be big deletions, over 100 amino acids can be removed and the virus spike genes can tolerate it.
Parts of the protein can be recombined into other coronavirus spikes.
And the shuffling of sequences regulates host range, tissue tropism, transmissibility, and to some extent, virulence.
Now it's interesting because this data would all be derived from PCR data.
So they would PCR and sequence and find variability most often in the spike protein and then claim that that's evidence that it tolerates the variability.
But if you go back to the fundamental observation of whatever these RNA viruses are doing, they end up producing a lot of subgenomic RNA.
And the most abundant subgenomic RNA by several orders of magnitude is the spike protein.
Now, again, roll back.
Make sure that you have all the tools in the toolbox in the right place.
we're still copying RNA.
So if you're making lots of copies of the spike protein RNA, number one, I don't know how that's regulated and why that occurs, but that's what happens.
You get hundreds of thousands of copies and all of those can potentially have errors in it.
Now, is the evidence that the spike protein gene tolerates a lot of errors the result of their observation that there's a lot of this RNA and it's very variable?
I think that's the most likely solution, the most likely assumption here.
And instead, he's again trying to create the illusion of pandemic potential out of every observation that we have.
And the observation that we have all of this subgenomic RNA dominated by spike protein
is being misconstrued as a biological evidence of a phenomenon where the viral spike protein can tolerate lots of mutations and deletions, and we can substitute different parts and blah, blah, blah, and it all seems to work.
It's extraordinary, because he's not telling you that certain parts of the spike protein need to be conserved.
He's telling you that other parts of the spike protein don't need to be conserved.
aren't so tied down.
And of course, this comes from many, many, many years of research that spans all the way back to Robert Gary.
who was making small proteins that could inhibit these, these, I don't know what you want to call them.
At the time he called them fusion proteins, but that wasn't, that wasn't aggressive and weaponized enough.
So now they call them spike proteins, but Robert Gary was calling them fusion proteins and fusion proteins are a general, you know, phenomenon in biology recognized across a lot of different viruses and certainly across all Corona viruses.
And there's a, there's a common protein motif there.
And so if these phenomenon are a background signal that we become tolerant to by the age of five,
and some of these stories of virology are real, it is that some of these phenomenon are generalized, like the fusion protein.
Of course, if exosomes are something that we are shedding actively as a biological signal, or as a biological repellent, or as a biological screen or filter, then it's gonna have some shared mechanisms that'll work, that can allow that to happen.
this all would make sense, a lot more sense than portraying these signals as RNA hijacking our cells and making them do something they don't already do.
So a lot of capacity to change themselves in natural situations.
Now, I'm going to talk a little bit about SAR, capacity to change themselves
in natural situations.
Now, I'm going to talk a little bit about SARS.
I don't know how many are familiar with a phylogenetic tree, but this is just a way to look at the relatedness between strains.
The state of knowledge before 2019 was that there are a few out there in the bats.
That's it.
That's all we got.
And the 2003 epidemic basically did this, I guess, which is extraordinary.
It's pretty extraordinary.
I don't know, where is the, oh, this is the 2003 epidemic in yellow.
And these are bat coronaviruses that have similar potential.
Let's let him talk.
So SARS coronavirus emerged in 2003.
It came from bats.
And it circulated in open markets through civets as an intermediate, which were used as a food source in China.
All of these strains here in yellow
are strains that were associated with that 2003 outbreak.
Human strains, civet strains, raccoon dog strains.
That's what was circulating that was involved in infecting 8,000 people.
Over the next 17 years, we sequenced coronaviruses in bats.
And we found the dark red ones up there and the light.
Well, that was a weird way of saying it.
We sequence coronaviruses in bats.
How many did you sequence?
Why didn't you sequence coronaviruses in kids since the kids are all infected with these by the time they're age five?
Why don't we know more about the endemic coronaviruses?
Why are we paying attention to these SARS viruses when apparently,
There are four endemic coronaviruses that are infecting little kids before age five all the time that we could be studying their evolution or lack of evolution.
Like, wow, it's extraordinary to me.
Red ones down here.
The dark red ones are strains that are about 10% different.
than SARS, but can grow in human cells, they can use human receptors, and they have all the properties that would make them pre-epidemic strains, or strains that could immediately flip over and infect human populations.
The light red ones down here can't, and I'll show you how that is tested.
SARS-2 also originated from bats,
But it's nowhere on this list.
But he says that recombination during a co-infection is 25%.
of the viruses produced.
So if the bats that have between six and eight viruses in them are constantly recombining, then even a phylogenetic tree like this is but a very short change snapshot of whatever is actually going on.
If you just go to the logical conclusions of their claims, it's so extraordinary.
You really got to be a gap mouth
drooler and just absorbing what this amazing man says and not questioning or thinking about the implications of it at all in order not to hear how much bullshit is coming out right now.
Tree.
I'll show you where it is later.
It's a totally different clade of SARS-related viruses from anything we'd seen before in the past.
And it also was associated with open markets, but that's debatable.
So SARS, there are two models to explain that outbreak.
The closest strain is a bat virus called WIV-16, which is about 98% identical.
In other words, about 600 nucleotide changes across the 30,000 nucleotide genome.
It could have transmitted directly to humans in the open market, which then spread to civets and then back to humans.
And as it went back and forth and back and forth, you selected for strains that were about 99.5% identical that were associated with the expanding outbreak.
The other model is that bats could have infected the intermediate host, then those could have infected humans, and that set up a transmission cycle.
Coulda, woulda, shoulda.
Both are possible.
What you hear the Chinese say about the SARS-CoV-2 outbreak is that there had to be some intermediate host that transmitted to humans.
And that's not actually the case.
It could be direct bat to human transmission.
So you're supposed to hear somebody who's at the center of a debate trying to understand a biological phenomenon, and that is at the heart of the illusion.
That whole idea that Ralph Baric is at the cutting edge of understanding an ongoing biological phenomenon that we've just scratched the surface of,
is the illusion that this national security operation is dependent upon.
If that illusion and the whole career of Ralph Baric didn't exist, then there would be no reason to have the biosecurity state that we have.
None at all.
Even though I think whatever they say was there was before they said it was there.
And we were fine not knowing about it.
Now that we know about it, the national security state exists.
And how do we know about it?
Really because of Ralph Baric.
There aren't very many other coronavirus biologists that work on their pandemic potential.
Not even Stanley Perlman.
It's extraordinary.
OK, so it's really just Nathan Wolfe, Peter Daszak and Ralph Baric, who are probably just three sides of the same national security narrative curation team.
They work for them.
That's it.
And as long as those three guys agree to this, do the same shtick.
And as long as Jikki Leaks decides that those are the three guys we have to focus on, it couldn't possibly be Robert Malone or Pierre Kory, then this is gonna go on forever.
The SARS coronavirus outbreak went extinct around 2003, 2004.
But is it extinct or is it still present in bats?
And what's the relative threat level of these bat viruses that are SARS-like?
Are they dangerous to human health?
And so one of the things that we do in the laboratory is called reverse genetics.
So coronaviruses have an RNA genome.
You can make a DNA copy of that genome and then change it however you want and then recover the virus in the laboratory, okay?
So in this case, you can remove a copy.
And so one of the things that we do in the laboratory is called reverse genetics.
So coronaviruses have an RNA genome.
You can make a DNA copy of that genome and then change it however you want and then recover the virus in the laboratory.
Okay?
Recover the virus means transfect or transform cell cultures and collect it.
That's what it means.
So you make a molecular clone using recombinant DNA, reverse genetics,
And then you recover full length virus by making synthesizing full length genomes, you see.
And yet he just got done explaining to you that synthesizing full length genomes is actually something that coronaviruses are very specialized in doing and can adjust their fidelity of, of, of synthesizing full length genomes, depending on whether they need more mutations or not.
And they even can recombine up to 25% of the time and still make full length genomes.
That's where Kevin McKernan comes in.
That's why Kevin McKernan had to stream with me a few times before he finally had to block me on Twitter and call me an idiot.
Because this is the trick.
This is the secret.
That you can't get full length genomes in quantity any other way.
Not if you had a whole cave full of bats and then fed them pure virus.
from extracted from their feces, you could never get full length viral genomes in a pure quantity ever.
Never, ever, because of recombination, because of the lack of fidelity of copying RNA, and because of a million different other reasons, you just can't.
They've never been able to do it.
But one of the things we do in our laboratory is we make synthesized full-length genomes and then use those to recover full-length virus.
It's ridiculous.
They're telling you right here.
It's transformation and transfection to synthesized full length genomes that we would have no other way of obtaining and no other way of producing in a quantity that we could detect.
And so, yeah, do viruses exist?
We don't know.
The best we can do is detect short sequences with PCR and then synthesize them assuming they're full genomes.
That's all they can do.
And if you realize that they're talking about signals that are made by the bats, they're talking about signals that are made by us,
then that's where this lie becomes extraordinary.
Are they dangerous to human health?
And so one of the things that we do in the laboratory is called reverse genetics.
So coronaviruses have an RNA genome.
You can make a DNA copy of that genome.
and then change it however you want, and then recover the virus in the laboratory.
So in this case, you can remove the spike glycoprotein of the 2003 SARS strain, and drop in spike genes from these other bat strains, and then ask the question, are any of these capable of replicating in human cells?
And the answer is, the top three, WIV1,
SHC014, these two up here, and another one called WIV16, can grow just fine on primary human airway epithelial cells.
Now, what these are is the transplant recipients.
The discarded lung is taken.
You can take the cells out of the conducting airways and grow them in the culture.
So it's, in essence, a replica, as close as we can, of what the human airway looks like.
And then you can ask the question, can that virus grow in it?
And these viruses replicate in those primary cells, which are shown right here, just as well as SARS can.
They also use the human receptor, just like SARS, and they can use the bat and the civet receptors.
So there's no reason why those strains couldn't actually spill into humans and cause an outbreak of disease.
Now the question is, should we inspect those papers to find out if they're just transfecting a cell culture and passaging, and then at the end looking for signals that indicate that the transfection made it to the passage eight or whatever?
or three, because that's not evidence of replication.
That could just be evidence of ongoing transfection.
and it's not evidence of infection, it's ongoing transfection and whether or not that RNA can replicate itself to enough to be found over there or whether the dilution occurs.
No quantifications are being made to show you the relative fidelity of replication or the relative rate of replication.
None of those measurements are being made, just proxy measurements that show the presence of something.
And that's how they did it with AIDS as well.
The presence of reverse transcriptase activity was sufficient to indicate the presence of HIV.
And here we have a scenario where a lot of these gain-of-function or pandemic potential papers are using molecular correlates that don't really adequately differentiate between
the resultant of transfection or transformation to these cloned molecules, or the bona fide replication of those molecules, packaging of those molecules, and then the repackaging of those molecules by other cells, which is a very, very different thing.
Well, their strains are not viable, so they're dead.
So in reality, what's happened, the situation in nature is as follows.
We have a reservoir of SARS-like bat coronaviruses that exist in bats.
And this heterogeneous pool can be up to 35% different.
Don't forget that this is just a very complicated molecular biological story that is exactly the same as the story told in Man and His Future, the book and the chapter written by Hilary Kaprowski.
That it's the exact same thing, viruses from bats, before we even really knew a lot about it.
This is just a continuation of it.
The exact, I mean exact same story that was told by Alison Totura and Sina Bavari in their 2019 coronavirus review.
And you can believe if you want to that that has nothing to do with a national security state that would like to enslave our kids.
You can believe it has to do with the genuine biologists and virologists of Nathan Wolf and Peter Daszak and Ralph Baric and Tony Fauci or
You can pull your head out and realize that it only takes those four guys agreeing about this and using slides like this, and they are just part of a continuous intellectual chain of bad ideas that starts at Hilary Koprowski and goes all the way through to Ralph Baric.
And somewhere in that tangled mess of intellectual vines, you can find people like David Baltimore, and Bob Gallo, and Murray Gardner, and Judy Mikovits, and Rischetti, and Malone, and all of them, all the way down to Paul Offit.
The brick wall is visible and the smell that you smell is wet bricks.
They're right there.
Like if somebody hits you in the back of the head, you're going to break your nose.
That's how close we are to the brick wall right now.
And that's why it's useful to go back to 2020 and see what Ralph Baric said and didn't say, because the narrative is right here for you.
It is a national security narrative.
It is not real biology.
Some of those are high risk, some of those are low risk.
In 2003, SARS emerged and caused 8,000 cases and about 800 deaths with a 10% mortality rate.
The prediction is that these high risk strains could emerge in the future to cause future outbreaks.
I'm going to speed it up a little bit.
In 2019, SARS coronavirus 2 emerged, which was 22% different than SARS.
It has caused 81,000 cases across the globe with 2,700 deaths in over 40 countries.
There is ongoing human-to-human transmission.
It's been stopped in the U.S., Thailand, Japan, Vietnam, China, Iran, Italy, and South Korea.
So it's moving towards where we would call the definition of continuous spread.
It has caused 81,000 cases across the globe with 2,700 deaths in over 40 countries.
There is ongoing human-to-human transmission in Germany.
It's been stopped in the US, Thailand, Japan, Vietnam, China, Iran, Italy, and South Korea.
So it's moving towards where we would call the definition of continuous spread.
on two different continents, which is the definition of a pandemic.
I think I gotta slow it back down because I want you to hear that the way it was.
Now, keep in mind that this is 22%.
There's still other strains within this pool that could emerge in the future.
That was extraordinary, actually.
It has caused 81,000 cases across the globe with 2,700 deaths in over 40 countries.
There is ongoing human-to-human transmission.
in Germany, it's been stopped in the US, Thailand, Japan, Vietnam, China, Iran, Italy, and South Korea.
So it's moving towards where we would call a definition of continuous spread.
It's stopped in the United States.
I don't think he feels very comfortable with what he's doing.
His glasses are falling off of his nose because he's sweating.
Vietnam, China, Iran, Italy, and South Korea.
So it's moving towards where we would call a definition of continuous spread on two different continents, which is the definition of a pandemic.
So we're approaching that.
Now keep in mind that this is 22%.
There's still other strains within this pool that could emerge in the future.
Even if SARS-Coronavirus-2 goes away, we will still be at risk for these kind of viruses.
And so you need to think about it like, I know people don't do encyclopedias anymore, so I apologize.
But you have to think about it like an encyclopedia of volumes that have 0% variation to about 35%.
So now again, we're focusing exclusively on the spike protein, the spike glycoprotein, one of 30-odd proteins that
that virologists like Robert Malone will tell you that each one of those proteins has like four different functions.
And so the spike protein was characterized very early on by people like Kevin McCairn and Walter Chestnut, who's been on my stream multiple times as being this crazy sort of Swiss army knife protein toxin kind of thing.
And here Ralph Baric is exclusively focused on the spike protein before any of that nonsense started, before McCairn had said that it's going to be neurotropic, that there were HIV inserts according to an Indian paper that got retracted or whatever.
Like all of that stuff is coming still.
And already we're focusing on the spike protein because broad-based vaccines are based on the spike protein, even though it can tolerate so much variation.
Human monoclonal antibodies and antiviral drugs all focused on the spike protein, even though he told us in the beginning that one of the interesting targets would be the XON gene.
and replication competence of the RNA-dependent RNA polymerase complex.
It's interesting.
It's really interesting that we fool around with the spike protein over and over and over again, that the gain-of-function protein that supposedly would be insertion of a second fear in cleavage site, according to the champion Charles Rixey, is what resulted in it being the most infectious virus in human history, and insisted on it
And so there's a narrative being curated here that focuses on the spike protein exclusively.
And that narrative is then picked up and ran with by people like Kevin McCairn, Charles Rixey, Richard Fleming, Jessica Rose, Walter Chestnut, who all wittingly or unwittingly by being encouraged by each other or by a few meddlers to focus on the spike protein as evidence that this was a laboratory virus.
And so here we are,
We're on that train, we're going on the Scooby-Doo together.
And it shouldn't be very surprising that alongside all of these meddlers was the king meddler, king clone himself, Ralph Baric.
Some variation.
Some of these volumes are high risk.
And they're shown there, SARS-WIV-16, WIV-1, SHSCO-14, and the 2019 novel coronavirus.
They all have high-risk features.
They use the same human receptor to infect the lung.
High-risk features is just an enchantment.
What does that mean, other than to scare the audience and to think that there's just yet another concept that you aren't sophisticated enough to understand?
But thank goodness we have experts like Ralph Baric.
That, of course, people like Jiki
And Robert Malone and all of these lab leak people want you to believe is the bad guy responsible for these molecular techniques.
Stop lying!
They all grow great on primary human cells.
They cause ARDS, acute respiratory distress syndrome, which I'll show you a picture of what that looks like, which is what is killing people.
Acute respiratory distress syndrome can also be very easily inducted using supplementary oxygen at too high of a level.
And that is well known.
And the ones that are boxed or in animals, the ones that are not.
If you are older, you are at much seriously increased risk for disease.
The over mortality rate for SARS and MERS was 10 and 35%.
But if you're over 60, the mortality rate goes to above 50 and above 75%.
And especially males are vulnerable.
So I don't know whether to be glad I'm studying this or whether I feel kind of like I'm a sentinel or something.
But anyway, this is the threat level.
These are the strains.
And one of the things that we're doing in the lab is by resurrecting these strains in our laboratory, we now have a platform to test broad-based vaccines, human monoclonal antibodies, and drugs that not only protect against the bookends, the human strains, but anything that might emerge in the future.
Solar Fire, I would say to you that coronaviruses aren't the only virus with spike proteins because viruses aren't real.
Exosomes are real.
And exosomes all have the requirement of a fusion protein.
They have to have a fusion protein or they wouldn't be able to send the signal that they're sending.
And so you shouldn't see it
as a generality across viruses, what you should see is that if this was a packet communication system that is utilized by all eukaryotes and maybe plants and animals alike,
then that system would have a universal mechanism by which you cross membranes or get membrane fusion.
And although there would be variation across species and even across conspecifics, you would expect there to be some general mechanism by which a small membrane-bound organelle could bind with a larger membrane-bound organelle.
And that universal mechanism is definitely real.
The issue is whether that constitutes virology or whether that constitutes exosomal communication and endogenous biology of our own.
Now, it's not just specific for SARS.
If you look at MERS coronavirus that is currently causing an ongoing outbreak,
with 35% mortality in the Kingdom of Saudi Arabia in the Middle East.
We have MERS at one end of the encyclopedia and a Chinese strain called 422, which is 35% different in its spike glycoprotein.
It can still use the MERS receptor for docking and entry.
It grows fine on all the primary human cells that MERS targets.
Although our intervention strategies are focused on MERS,
coronavirus emergence in human populations.
The classic model for viral emergence was that you had this tsunami.
Remember, we're talking about these cartoons in the context of 1,300 bats with six to eight variables.
And those variables recombine at a 25% rate during co-infection.
And there's an error rate that's controlled by exo-AN.
But then now, here we go.
Here we can make an even more simplified cartoon about how they change and how they get back to humans or whatever.
And this, again, is just bamboozlement.
It's just enchantment.
This is not real biology.
It's not real science.
I mean, he's using little circles and arrows.
Come on.
I just want to get to the point where we...
He might mention something.
Oh yeah.
So here's the story about, you know, we got five isolates here.
Um, person to person spread identified, uh, in January, you know, this is really seeding the narrative of the pandemic to come.
It's going to keep going here.
I don't, I, maybe we should listen to this.
I don't know.
Farming communities in close proximity to bat hibernacula.
could have been infected with a bat, coronaviruses.
It's the outbreak.
So there's a couple of different hypotheses floating around, which- What's a couple of different hypotheses that would include a lab leak if you guys weren't covering it up?
That's the narrative that's gonna be fueled right after this.
You see how enticing it is?
So he's justifying the market.
are used in certain delicacy dishes, and also used in medicinal medicines.
Oh, yeah, bushmeat, just like Brett Weinstein said.
So, you know, he's giving you the natural side.
And so there's a kissing cousin of SARS.
I'll show you where it sits in a minute.
They publish each respective nation.
Around the 20th, they reported a major, I'll talk, the major characteristics of SARS, MERS, and SARS coronavirus 2.
It's a good way for you to understand
why this thing is so much larger in scope than anything we've seen in the past.
Oh, so now he's going to explain why the past ones didn't make it, but this one, this one's going to be a lot bigger.
So the first, let's just look at the number of countries involved.
There's over 40 countries affected with SARS coronavirus two, about 28, 29 with MERS and SARS coronavirus.
The number of cases for SARS-Coronavirus-2 far exceeds both the SARS outbreak and the MERS outbreak.
Mortality rate is about two to 3%, and I'm gonna talk about this in a minute.
There are currently about 9,000 cases that are under critical care, meaning that they're probably getting some form of respiratory support.
It's about 18 to 19% of the people develop really serious disease that require respiratory support.
About 83% of the cases are mild or asymptomatic.
It means you can be infected with this virus and not know it.
And that makes it difficult to control.
Asymptomatic spread.
I don't know how loud that is.
That's all right.
Asymptomatic spread.
Unbelievable.
The mortality rate bounces around depending on who you talk to.
2 to 3% is probably not a bad estimate, but the mortality rate in Wuhan was about 4.1%, 2.8% in a different part of the country.
It's 0.17 to 1% in different areas of the world.
Probably the best way to get an estimate of the mortality.
Prion proteins supposedly don't change when you heat them, and they cannot be sterilized away with autoclaving.
That's what they say.
I don't have any personal experience to verify that, but that's one of the magic features of proteins, of prions, is that they are proteins that are so stable that you can't use, you can't denature them.
It's extraordinary.
The rate of this virus is from the Diamond Princess cruise ship.
where 3,600 people were sort of locked in a closed container with a highly contagious respiratory virus that could undergo fecal spread as well.
So in that case, right now the mortality rate is about 0.6%.
That is about 750 people that have been infected.
Most of the epidemiologists I've talked to expect somewhere around 50% of the people will be infected, will have been infected in that cruise ship.
About 36 are still under critical care.
So whatever that number turns out to be is probably a pretty good estimate, keeping in mind that there's an age skewing toward older individuals on the cruise ship.
So again, this is an example of a disease where it's good to be young and not so good to be old or male.
The incubation period is two to 14 days.
This is a real problem, because now if you're quarantining people, you have to keep them in quarantine for 14 days.
SARS and MERS were much more limited.
The RO rate, or the number of people that get infected from one infected person, for the 1918 flu, for example, was about 2.2 cases per every flu-infected individual.
SARS was about 1.8 to 2.5.
MERS is low.
SARS-2 is around three.
That means on average... Something is really wrong with this thing.
I have to change something here.
Reconnect.
Hopefully it'll reconnect.
Yeah, there we go.
Let's see if that works.
One person will infect three people.
Wow, it's so bizarre.
Something is really wrong with my keyboard here.
And this makes it also difficult to control because you have to reduce that.
Asymptomatic spread never occurred.
Never occurred with SARS.
It does occur with MERS, and rarely, and that's one of the reasons why
How do we know that?
How do we prove that it didn't occur with MERS or SARS?
Who were they testing and how did they prove that?
You see what I mean?
That's extraordinary because the assumption that SARS-CoV-2 spreads asymptomatically is thrown out there with an equal lack of data.
Public health officials in the Kingdom of Saudi Arabia have trouble getting this thing under control because there's chains of transmission they can't track.
But it's probably common.
with SARS-2.
Why is that?
We don't know.
Most likely the virus is replicating in different individuals, either in the lower or the upper respiratory tract or in the nose.
And this could allow for more efficient transmission.
Oh, it's just, you know, the trend, it's all about replication and replication.
We just, he just explained to you how it works.
And so if it's replicating in the wrong place or too fast, then that's how it happens.
And this was the biology that we were all supposed to argue about in 2020.
And we did, I argued about it and read about it and read about it and read about it and read about it.
That's how I became an armchair expert in basic immunology.
How I discovered Stanley Perlman's work.
How I realized that T-cells were paramount.
How I understood the order of activation of the immune system was all because of videos like this where I was like, wait, what is going on here?
If you were a mouse, I could tell you in detail why that is working.
But nobody's a mouse here, so I can't tell that.
The attack rate varies depending on the situation.
But still, requiring temperatures above 900 degrees Fahrenheit is a very, very exceptional attribute to a protein.
900 degrees Fahrenheit is several,
you know, steps above the boiling point of water.
Proteins are supposed to be a biologically organic molecule that does its thing in water.
So for me, it's, yeah, it's pretty amazing.
I mean, we should harness this for some industrial applications where an incredibly heat-stable protein would be useful.
But we don't do that now, do we?
Now that should already say something to you.
20 to 30% is probably pretty common.
So those are the basic features of this.
I guess there's 57 cases in the US, just to keep you updated.
And I don't have the full state list shown, that's not correct.
Okay, so why do people die?
The major cause of death with SARS-2 is from acute respiratory distress syndrome.
Imagine your lung as a set of tubes that go from big tubes to smaller tubes to smaller tubes.
And they end with a balloon on the end of it.
And that's your alveoli.
It looks like this.
And normally the alveoli is open and oxygen air is flowing back and forth.
And oxygen transfers across the single cell layer into a capillary bed.
Imagine a capillary bed on the top of that balloon that you've just blown up.
And oxygen is picked up by the red blood cells and so that oxygenates your tissue.
So what happens with SARS and MERS and SARS-2 and high path avian flu strains, these viruses kill these cells that provide the support around the balloon on the surface and it perforates them.
And so fluid pours across this capillary bed
into the alveoli, and so the immediate acute cause of death is by drowning.
Your lungs fill up and turn into a water balloon.
Okay, so remdesivir can cause that to happen?
because they decrease kidney function and so you can get water in your lungs and that can happen.
And it can also happen because you use high flow oxygen inappropriately.
So there are multiple ways to get to this general condition.
It can even happen if you use a contaminated vaping product.
It can happen if you put
Apparently, according to, I won't even say, I did see something on Twitter the other day about using ice in smoking devices, and that can also cause ARDS.
So, I mean, you're really here talking about a general phenomenon that he is trying to attribute exclusively to these viruses, and he's not being precise about it on purpose.
He's not being precise about it as a, let's say, physiological stress point that a human can reach from a variety of different causes.
But he's trying to tell you that ARDS is actually something that we specifically call the disease progression that's created by these respiratory viruses.
And that's definitely not true.
Now, in the repair process, hope this isn't too graphic.
Might as well know.
In the repair process, you end up going through what's called a profibrotic response, and you start laying down fibroblasts along this balloon to repair the perforated holes.
But in some people, it doesn't just lay down a few, it continues to lay down more and more layers.
And so now you have a thick layer of cells and the oxygen can't diffuse through and you suffocate and you can die from this months after the virus has been cleared.
So some of these patients will probably be on respiratory care for a couple of months.
So this is a pretty brutal disease.
Now you can imagine a scenario if they transfected your lungs with an immunogenic protein, the same exact thing would happen.
If they sprayed a inhaled toxin into your lungs, the same thing might happen.
It's just simply the breakdown of the alveolar epithelial layer and the leaking of liquid from the blood into the lungs.
That can be caused by any number of things.
Probably also in extreme cases, it could be caused by allergens that you're allergic to from plants.
Why not?
This is the fundamental lie that's being told here.
He's trying to bamboozle the people that are listening and see this talk into believing that this is a series of symptoms that's very specific for a series of very specific viruses instead of a general phenomenon that can occur in a variety of situations where the lung is compromised.
Do you see what I'm saying here?
1918 flu does this.
About a million deaths per year.
The federal government has spent millions of dollars trying to figure out ways to treat this illness.
not only from viral infections, but mechanical things and others.
So it's, it's just a, um, a very devastating end stage lung disease.
There.
He almost said it actually.
He almost said it.
Not only from viral infections, but mechanical things and others.
So it's, it's just a, um, a very devastating end stage lung disease.
It's a very devastating end stage lung disease can, that can be reached within a few hours using high flow supplementary oxygen, nevermind high flow oxygen on a full mouth nose mask.
He should say that because I think that's the way a lot of people were murdered in America.
And the way that the progression of the disease in hospitals was essentially created under the priority of a national security narrative that needed to be accepted so that we would get maximum compliance when transfection was rolled out.
perhaps transfection to the very immunogenic protein they claimed to have found in Wuhan and in the Sohomish County man in Washington State.
Okay, so why could we control SARS?
Well, SARS had three drivers to the outbreak.
The first was he had civets and raccoon dogs in the marketplace that were infected that transmitted virus to people.
Okay, so we're going to skip out of this now because I do think that we'll hear more of the same in this talk.
And I do want to get to this keynote presentation, which is from two days ago.
I don't think there are more than a hundred views on YouTube of this one.
And so this one will be very interesting to hear.
Scheduled for what?
What would it say?
I'll go back and pause it.
July 13th in Los Angeles, see?
So it is now the 23rd.
I think it was only put up on YouTube where I got it two days ago.
So let's listen to this.
Hello everyone and welcome to today's keynote webinar titled SARS-CoV-2 Rapid Response Platforms for Pandemic Virus Control in the 21st Century.
This webinar is a part of the Coronavirus Virtual Event Series, the seventh in the series.
I'm Antonina Salcedo of LabRoots, and I'll be your moderator for today's event.
Today's educational web seminar is presented by LabRoots.
Now let's get started.
Before we begin, I'd like to remind everyone that this event is interactive.
I encourage you to first participate by communicating with other attendees using our new live chat feature during the presentation.
You can find the live chat located at the right of your screen.
You can also participate by submitting as many questions as you would like during the presentation.
To do so, simply type them into the Ask a Question box and click Submit.
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And then it's a pleasure to be here to speak this morning.
about pandemic virus control measures.
On the left-hand side of the screen is a snapshot of the... I already have the energy of a tired old man who's tired of having to do this job.
Tired.
not happy that finally his work is taken seriously, not happy that finally he's justified in not having wasted his life on coronaviruses, but just exhausted.
Gilling School of Global Public Health at University of North Carolina, where I hang out somewhere in this complex.
Obviously, I'll be talking about SARS coronavirus, which is sort of a schematic picture on the right-hand side.
And again, I want to mention my collaborations
interact with the elderly in the 14th, 15th century, it's called the Triumph of Death.
And he painted the Flemish countryside.
And in this particular... What an interesting quote to choose here.
The single biggest threat to man's continued dominance on the planet is the virus, Joshua Lederberg.
And I think that's also at the beginning of Outbreak.
The movie Outbreak also starts with Joshua Lederberg's quote.
It's interesting.
He's showing the impact of the bubonic plague on a small village.
And as you can see, a large amount of death and destruction is coming into the village.
Villagers don't really know how to prevent or control this pandemic outbreak of disease, but are doing the best they can with the tools they have at the time.
Obviously, 500 years later, we're much more effective at dealing with new epidemic and pandemic viruses.
But again, this slide illustrates a common event that has evolved just right along with human civilization over the past 2,000 years and will continue to threaten humanity in the next 2,000 years.
The 21st century has seen a rapid resurgence in new epidemic and pandemic and outbreak viruses.
In the backdrop of this slide, you can see some number of the 240 some emerging or reemerging viruses or newly emerging viruses that have occurred since around in the 21st century.
Three epidemic pandemic human coronaviruses, starting with SARS coronavirus in 2003, the MERS coronavirus in 2012, and the cases are still occurring in the Middle East and in Africa.
And then in end of 2019, we've had SARS-2 reemerge causing COVID-19.
What most people aren't aware of is that in the context of this 20-year interval, there's also been three new swine coronaviruses that have caused epidemic or pandemic diseases in these animal populations with devastating consequences.
So the coronavirus family in general is a group of highly and rapidly evolving emerging viruses that threaten both human and animal populations.
In addition, we've had pandemic alpha viruses like chikungunya, pandemic influenza viruses like the 2009 H1N1, as well as sporadic avian influenza virus cases of H5N1 or H7N9 that have been sampling human populations for the past 20 years.
The flaviviruses include West Nile virus and Zika virus in the backdrop of about 300 million cases of dengue virus each year globally.
And then we've had several filovirus outbreaks like Ebola in 2014-16, 2018-20.
And not shown here are the four
norovirus pandemics that have occurred since 2002.
Four norovirus pandemics.
There are also norovirus pandemics that we just don't talk about.
Like, that's just crazy talk.
They do not have evidence for that.
That's what's so extraordinary.
They're adding things to the list all the time.
Human suffering.
It's been a global catastrophe.
There have been over 500 million cases and 6.2 million deaths that have been reported.
If you look at
baseline mortality rates across the globe.
The actual number of individuals who probably perish from this disease are somewhere between 14 and 25 million.
Most recently after the emergence event that occurred in December of 2000.
14 to 25 million people have been killed by SARS-CoV-2 is what he just said.
19.
There have been periodic sweeps of new variants of concern that have infected individuals or caused repeat infections.
Next slide.
I control that.
The first variant that emerged after the Wuhan strain was identified in December 2019 was a variant called D614G.
This emerged around the end of January of 2020, and then rapidly spread globally across the world.
It has served as the backbone for other variants of concern that have been recognized by the World Health Organization, like the alpha variant, the beta variant, the gamma variant, the delta variant, and now most recently the Omicron and the VA2 variants.
Each of these early variants from alpha to delta are characterized by mutations that enhance
the ability of the virus to bind to the human ACE2 receptor and to transmit more efficiently between humans.
So it's gotten even better?
Because I thought at the beginning of the pandemic it was already gain-of-function good at it, like orders of magnitude more than we've ever seen in nature.
And now it's still getting better at binding ACE2?
That's impressive, isn't it?
Wow.
exactly as you would expect the virus that has moved out of animal populations and is adapting.
I would have assumed that the Australian scientists would have shown us that progression as it went from good to better, since he was just on the Vajon health program for an hour and a half and we didn't talk about the current ACE2 binding affinity at all.
Omicron, however, was quite unique, which is on the right hand side of the slide.
And this virus has a huge number of amino acid changes in the spike glycoprotein.
It's about 3% different in the spike glycoprotein as compared to the original Wuhan strain.
And many of those changes have a big impact on the antigenic structure and the antigenicity of the virus that affects immune responses.
But see, you're already talking about the antigenic structure of the virus, the antigenic something of the virus.
And that's ridiculous because we already know that our immune system, when it presents these, it breaks these things down into their component antigens.
So the virus doesn't have
an antigenic signature, its proteins do, its outer coat does, its coat proteins do, and anything that our antigen-presenting cells decide to present could potentially have an antigenic component.
But the virus itself can't be said to have an antigenic component any more than a basketball can be said to have an athletic component.
It changes in the spike like a protein?
It's about 3% different in the spike glycoprotein as compared to the original Wuhan strain.
And many of those changes have a big impact on the antigenic structure, the antigenicity of the virus that affects immune responses.
Importantly, this rate of variation that has occurred with SARS-2 approaches about 1.5% per year, shown here at the bottom of the slide.
And that's equivalent or roughly equivalent to mutation-driven evolution rates for other highly evolving viruses like influenza and human noroviruses.
And so this suggests
that this virus may be undergoing a new strategy to maintain itself in the face of large amounts of human herd immunity.
These changes in the Omicron virus cause about a 15 to 40 fold reduction in the neutralization titers.
And so that has had a big impact on vaccine and pre-immune performance.
Next slide.
Next slide is a little bit complex, but this is the spike glycoprotein shown over here on the right-hand side of the slide.
The blue area is the NTD domain on the very right-hand side of the spike.
And if you look at under NTD changes,
in terms of amino acid changes that have occurred between alpha and omicron.
I don't think it should be called NTD domain because that's what he said.
I think it's N-terminal domain that's being abbreviated as NTD.
So he wasn't very specific.
He wasn't very accurate there, which is weird.
Next slide.
Next slide is a little bit complex, but this is the spike glycoprotein shown over here on the right hand side of the slide.
The blue area is the NTD domain on the very right hand side of the spike.
And if you look at under NTD changes,
In terms of the amino acid changes that have occurred between alpha and omicron, from the top to the bottom of the slide, you can see that a large number of mutations have occurred in the omicron NTD domain, which encodes neutralizing epitopes, but also can incur structural determinants that regulate, to some extent, presentation of the receptor binding domain, which is the region shown here in the blue box at the top of the slide.
The RBD, or the part that binds the human ACE2 receptor, is shown here in yellow in the figure, and dots and sequence changes that occur in it are shown in omicron.
And as you can see, the alpha variant had the first change, which was at position 501, that enhanced binding to the human ACE2 receptor, but even more importantly, it actually changed receptor recognition so that it could use ACE2 receptors for entry in other species like mice.
The beta variant had more changes that affected both antibody binding and receptor usage, but Omicron has a large number of changes at the bottom of the slide in the spike receptor binding domain that both affect receptor binding usage and immunogenicity.
Finally,
There's a cluster of mutations in the gray area of the spike ligoprotein that center in and around the furin cleaving site region that either increase the capacity of the furin site to be cleaved by this protease or not.
Some of these changes also function as a molecular switch that modulates the receptor binding domain region in yellow to an open versus a closed position.
So these are the types of changes that have occurred.
And these changes in Omicron have had a huge impact on the ability of antibodies to neutralize viruses.
So on the left side of the slide, basically this is a collaboration done with Sally Burmar and a group of people in my lab and elsewhere where young infant primates were vaccinated either with a Moderna mRNA or recombinant S2P adjuvanted vaccine that was developed at the NIH and then followed for several months.
In this case, we're looking at the neutralization titer against D614G.
This is the top panel on the right, the blue arrow.
So the higher the dilution, the more potent the serum is.
And so you can see a potent neutralizing antibody
against that original D614G variant.
The beta variant causes a three to five fold reduction.
The delta variant really is not much different antigenically from the D614G variant.
And then the Omicron variant causes a 15 to 50 fold reduction in the neutralization titer.
Just keep in mind, they're only talking about spike protein here, even though there are lots of other proteins for which your body could have immunity, build immunity, target immunity, whatever.
But we're focused exclusively on the spike protein because that's the immunogenic protein that they've been working on at EpiVax and other places to create an adjuvant function in a protein so that they could make a biologic that could function as an adjuvant.
And so these technologies have been, these ideas have been around for a long time and they've been around in the minds of people like Robert Malone and the company EpiVax and the company up in Canada that
that Palantir has invested in trying to do monoclonal antibody screening for.
It's all the same sort of scramble.
for biotechnology that can allow this exaggeration to continue, to allow this implication of fidelity to continue, even though they don't have the fidelity of understanding that they pretend they have.
None of these people are sophisticated enough in their biology to understand that.
And none of these people are sophisticated enough to understand that if this is all endogenous signaling that's being misconstrued as pathogenic,
that all of these people are doing is facilitating the study of transfection and transformation and either optimizing the immune response to or minimizing the immune response to transfection and transformation in our own cells.
and how easily the exploration of the understanding and hijacking of our own signaling via exosomes could be misconstrued as pathogenic in order to ethically justify the study of it, to justify the investing of billions of dollars in the study of it under the guise of public health rather than just, you know, using you as an experimental animal.
Blue is the protein vaccine.
Red is the mRNA-based vaccine.
The reduction in neutralization titer with Omicron on the far right-hand side of the slide is equivalent to some of the bat coronaviruses that exist, SARS-related coronaviruses that exist in nature like SHC014, which causes a similar reduction in neutralization titers.
This is at eight weeks after vaccination, 10 months later.
notice that all of the neutralization titers have dropped about tenfold.
But keep in mind that all of these people are victims of an illusion of consensus because David Baltimore and Ralph Baric and all of these people have agreed on the presupposition that viruses exist.
They just haven't been shown with the fidelity that they say they have, or they haven't been shown to be as dangerous as they have, or we disagree on the classification of them or something like that.
But nobody, nobody, not even the no virus people are willing to say and posit the idea that healthy signaling across the entire potentially eukaryotic kingdom
occurs and is governed by exosomes that all have fusion proteins on the outside with various levels of specificity for targets.
And we are barely scratching the surface of understanding them.
And there is a kind of, let's say, correlate of this signaling process in the pattern integrity of bacteria.
There is a correlate of this signaling process in the fungi that are symbiotic with roots of plants.
There is a correlate of this probably with the signaling that occurs between the bacteria of our gut and our immune system.
But we are not paying attention.
We are not investing in and understanding it in that way because we are exclusively asking questions about this, assuming that these are signals outside of our body.
These are enzymes that are exclusive to viruses.
And these are things that we have to exist in spite of.
And these are all parts of the same mythology.
These people are victims of a huge illusion of consensus that needs only a few people like Ralph Baric to be sustained.
Many individuals with very, very low titers, making them more potentially vulnerable to reinfection.
So let's take a step back now and talk about coronavirus threats that exist in nature and sort of review some of the history and try to come to some
model system to explain how these viruses move out of animal host reservoirs and move into other mammalian species.
The first example of this was with the original 2003 SARS coronavirus strain.
which is closest relative.
For which Alina Chan still has a as yet unpublished data set, which shows that the SARS-CoV-2 virus, whatever it was, sequentially didn't vary at all for the first six months of the pandemic, unlike SARS-CoV-1, which varied about between 10 and 50 amino acids every sequence they got.
very big observation that I did two bike rides about, but she just got a faculty position and a book, but they didn't have to publish that at all.
And now she works on artificial chromosomes.
Stop lying!
Identified to date is a bat, a SARS coronavirus called WIV-16.
This is about 98% identical to the SARS coronavirus strain that emerged in 2002-2003.
the current model system for how SARS coronavirus emerged, which is most heavily referenced.
I think you would be very, you're doing yourself a disservice if you don't acknowledge that there are other biologists who studied the immune system 10 and 20 years ago who proposed that the immune system would be primarily generalizing across pathogenic molecular patterns or
or damage associated molecular patterns.
So looking for combinations of molecules that are dangerous and found across bacterial species or across exosomal species or across any of these signals and then generalize across those things.
And then those same strategies could be applied to toxins, could be applied to screening stuff through your gut, the whole nine yards.
rather than the more modern idea that the pandemic biology has foisted upon our kids, which is that the immune system needs to make a new set of memories for every new thing that it ever meets in the new world all the time.
And there are novel things that can come out of viruses or come out of laboratories and bat caves.
And so I think a
It is unwise to simplify this concept, which we don't understand yet, down to garbage, because it can't be garbage.
It's definitely not garbage when it comes to the interaction between fungi and the roots that they are symbiotic with.
It's definitely not garbage when it comes to the regulation of the metabolic processes in zoonotic plankton, and not zoonotic plankton, but zooplankton in the ocean.
We already know that bacterial evolution is sort of governed by bacteriophage signaling.
So again, I would suggest it is very, if it ends up being garbage, then we'll get there eventually.
But I think that if you want to take in and acknowledge most of the biological observations that have preceded these last five years, then I think it would be very much
not in our best interest to go from not acknowledging exosomal signaling at all to then simplifying exosomal signaling down to a garbage processing mechanism rather than a natural, healthy signaling mechanism between tissues, between tissue and the immune system, between immune system cells, between the central nervous system and the peripheral.
I don't know.
Right?
Once you understand that exosomal signaling is an untapped biological idea, there is potential for exosomal signaling to play a role in almost any aspect of our physiology.
But instead, we are told that there is no exosomal signaling at all in any scenario.
and that it's all viruses.
You see, that's the crazy part.
Even AIDS, a retro viral signal supposedly transmitted between immune cells is definitely a bad guy from the outside.
And that is just not, no way.
Stop lying.
The virus in a bat infected civets and raccoon dogs in the open market where the virus replicated and evolved variants that could now affect humans efficiently and this set up a transmission cycle.
However, the truth of the matter is that WIB1, WIB16, and other bat-like SARS coronaviruses that have been identified are quite efficient at replicating in primary human airway cells from the lung.
And so these viruses could have spilled directly over into humans.
I think the most important thing to realize, Pete, is that everybody in academic biology is, to a certain extent, trusting the illusion of consensus, trusting the consensus of their mentors, trusting the consensus of the people that they meet and talk to, that some of these conclusions can be accepted as facts upon which we can base our investigations.
And so in neuroscience, I was
I was under the spell of some of these assumptions, which when they are made, you can do experiments and you can, you can say that you're getting results, but they're made, the experimental results are interpreted based on this assumption.
And if this assumption isn't true, then the interpretation of the experimental results can flip on its head.
And of course, as an academic biologist, if we're going to get to the cutting edge,
If we're going to be able to ask questions which will redefine or help to better refine our understanding of what the cutting edge is, where the border of the irreducible complexity exists and how well we can understand the details of it, those experiments are only possible if, to a certain extent, we trust our mentors and take the fast route to what we think is the edge of our understanding.
And so what you should see that as Pete and everybody else watching the show is that that potential is what makes science across generations possible and that
That honor system, that's what that is.
It's an honor system that so many of the people that are still in academia believe is true.
It's an honor system where nobody's faking their data.
No one would ever fake their data for fame, fortune, success, no way.
Everybody in academia is doing their best to just collect data and interpret it objectively and doing their best to contribute to the building of the wall.
And this illusion is ubiquitous throughout university system, throughout the academic system.
And yet the fundamental thing to realize is that if there was a national security priority to take one aspect of academia and make it into a mythological thing, or maybe multiple aspects of the academic system, and make them into mythological scholarly endeavors,
things like social justice, things like systemic racism, things like pandemic potential can be created, can be edified as real academic fields when they are based on conjecture and ideas that have no substantive support in real observations.
And that's what I think virology is.
and specifically RNA virology, specifically pandemic RNA virology.
And at the root of it is this distortion of what this signal means and how high fidelity we can probe it.
So then infected civets, and that set up the transmission cycle that maintained the virus, ultimately resolving in about 8,000 cases and 800 deaths.
What do we know about coronavirus emergence events?
Well, historically,
The human coronaviruses, the contemporary human coronaviruses that cause common colds, which are on the left side of the slide in green, the bottom part, include NL63, 2290, and OC43.
These viruses are closest relatives are from bats or from cattle and emerged anywhere from about 120 years ago to about 800 years ago in human populations.
So we really have no idea how coronaviruses evolve once they spill into human populations.
The 20th century saw a large number of animal epidemic and pandemic coronaviruses, mostly in swine and cattle and other economically important species for human populations.
And then the 21st century, yeah, the 21st century saw this accelerated movement of new bat coronaviruses that spilled into humans with SARS, of course on Delta coronavirus in 2009 in pigs.
MERS coronavirus in humans, with the camels as an intermediate.
I mean, just think about how much more complex and in-depth this presentation is than the last one, where there were four, and a couple, and four, and now there's all of these.
It's just, it's an incredible expansion of their, of the resolution of their understanding over the course of three years when no increased resolution should have occurred.
Because again, all of the resources were bent on studying this, the current novel virus.
None of our resources were being spent on studying this timeline.
And yet this timeline has become ever more high resolution as we move through the pandemic.
SARS-CoV-2 in 2019, leaving the question, what does the future hold?
So we've done a lot of work on the interface of looking at the capacity of zoonotic coronaviruses, including SARS-CoV-2 viruses, in terms of their capacity to be risk pathogens for human health.
This, on the very top right-hand side of the slide, is a phylogenetic tree of the SARS-CoV-2 family.
The clade 1a group includes SARS-CoV-2 from 2003, which is shown right here on this sort of slide.
encyclopedia of strains.
Notice that it's surrounded by other strains of sarvicoronaviruses that are derived from bats and from civets and raccoon dogs.
These strains are shown here at the top as WIV-16, WIV-1, SHCL-14.
They range anywhere from about 99 plus percent identical, like this civet strain right here, to about 90 percent identical to the 2003 SARS strain.
The SARS-2 strain represents a different branch from the SARS-CoV-2 family tree.
They're about 22% different than the original SARS strain, and over 25% different from all the others.
Now, first of all, remember that this Jedi Master is reading word for word.
Secondly, remember that this is a slide from the talk we watched from three and a half years ago, or four years ago.
Don't forget that either, four and a half years ago.
These other clade 1 strains that I just mentioned, its closest relative is a bat virus called RATG13, or pangolin, which is from pangolin coronavirus.
They range anywhere from about 96% identical to 90% identical.
And then you have the clade 2 strains, a totally different branch of the family, like HKU3.
They all have similar high-risk features, except for the clade 2 strains.
They can use the human ACE2 receptor for entry.
So although they're bat viruses, they use the human receptors just fine.
They can grow just fine in primary human airway cells.
They cause acute respiratory distress syndrome either in humans or in mice.
And they cause age-related disease gradients, just like the SARS coronavirus and SARS coronavirus 2 do in human populations.
As the amount of antigenic variation in the spike glycoprotein shown right here increases, these strains begin to escape immunotherapeutics that were targeted against the original strain of SARS.
Now, importantly, bats have been incredibly undersurveyed.
So this group of viruses probably represents less than one millionth of the kind of diversity that exists
within bats that could potentially spill within the human population.
And so many of these strains are poison.
We are underestimating the amount of danger we are in by a factor of one million, says Ralph Baric.
To emerge, and mutation-driven evolution may not be necessary to colonize new species.
Now let me give you an example of that with the pangolin coronavirus.
Now we're only gonna look at clade 1b.
These are the SARS-2 related strains that have been identified around the world.
And at the top of this tree, you see the Wuhan strains
China that were identified two different lineages in December, early January of 2019, 2020.
Closest relatives moving down the tree include RATG13 and BANL52, which are about 96 plus percent identical.
And then some other BANL strains from Laos, China, Thailand, Cambodia, then pangolin strains from China and pangolins and other strains from Japan.
So all of the closest relatives to the
COVID-19 strains that emerged in China and then went around the world are located, the closest relatives are from Southeast Asian viruses.
So this is a Southeast Asian virus that has emerged to sweep around the globe.
Don't let anybody ever tell you anything different.
This data is conclusive.
Pangolins, however, have been suggested to be a potential reservoir species.
Don't let anybody tell you different.
In studying these viruses.
And so we're going to take this GD1 strain potential, our coronavirus family.
They're not screwed up in the original SARS strain and over 25% different from all these other clay one strains that I just mentioned.
It's closest relative is a bat virus called RATG 13 or pangolin, which is from pangolin coronaviruses.
They range anywhere from about 96% identical to 90% identical.
And then you have the clay two strains, a totally different branch of the family, like HKU3.
They all have similar high-risk features, except for the clade 2 strains.
They can use the human ACE2 receptor for entry.
So although they're bad viruses, they use the human receptors just fine.
They can grow just fine in primary human airway cells.
They cause acute respiratory distress syndrome either in humans or in mice.
And they cause age-related disease gradients, just like the SARS coronavirus and SARS coronavirus 2 do in human populations.
We're almost done, don't worry.
At the amount of energy variation in a spike like a protein, I know where I want to end.
These strains begin to escape
immunotherapeutics that were targeted against the original strain of SARS.
Now importantly, bats have been incredibly undersurveyed.
So this group of viruses probably represents less than one millionth of the kind of diversity that exists within bats that could potentially spill into human populations.
And so many of these strains are poised to emerge and mutation-driven evolution may not be necessary to colonize new species.
Now let me give you an example of that with the pangolin coronavirus.
Now we're only going to look
clade 1b.
These are the SARS-2 related strains that have been identified around the world.
I'm going to go forward because I accidentally went too far back.
Relatives moving down the tree in Thailand virus that has emerged to sweep around the globe.
Don't let anybody ever tell you anything different.
This data is conclusive.
That's what I wanted to play again.
However, to sweep around the globe.
Don't let our closest relatives are from Southeast Asian viruses.
So this is a Southeast Asian virus that has emerged to sweep around the globe.
Don't let anybody ever tell you anything different.
This data is conclusive.
Pangolins, however, have been suggested to be a potential reservoir species.
So we became interested in studying these viruses, and so we're going to take this GD1 strain of pangolin virus, and we're going to recreate it in our laboratory.
We synthesize the full-length molecular clone.
that then could be used to drive RNA transcripts to recover full-length viruses.
And this is the genome of the pangolin virus.
It looks just like SARS-CoV-2.
So they made a full-length cDNA clone and then they use that to generate full-length viruses.
You see, this is transfection and transformation in cell culture and nothing more.
That's all it is.
And he's saying it out loud right there.
That's hand-waving and we recover virus.
You transfected or transformed a cell culture with the DNA that you said you just generated.
Listen.
And so we're going to take this GD1 strain of pangolin virus and we're going to recreate it in our laboratory.
We synthesize the full-length molecular clone.
The thing could be used to drive RNA transcripts to recover full-length viruses.
And this is the genome.
But when you put an RNA clone on a cell culture, we've already looked at nanopore sequencing results from that.
You get like two transcripts that even come close to being full genomes, and the rest of them are very tiny subgenomic RNAs.
So you're not recovering full genomes.
You're claiming you're covering full genomes, but you don't find them on the RNA.
This is subgenomic RNA one, two, three, four.
Look at the full genome is not even visible, but that's a huge transcript.
It's supposed to be the primary thing that infects the next cell.
Yet even here, they show you the exact same data.
Oh, I didn't have my arrow up here.
They show you the exact same data.
that they've been seeing since the 1950s and 60s and 70s and 80s since they've been looking at these self-replicating RNAs.
There is an almost indetectable level of an RNA which would qualify with the weight of a full genome.
Everything else is subgenomic RNA and it's orders of magnitude more abundance.
And so the infectious cycle that they claim is being replicated or being recapitulated by transfecting and transforming cells with an infectious clone that they call an infectious clone is just transformation and transfection of cell culture.
And then it's same exact crap happens.
They don't get high fidelity replication.
And in fact, the signal that they get is only as pretty as it is because they started with the clone.
Don't you see?
If they wouldn't start with the clone, they wouldn't even be able to get that signal.
The pangolin virus, it looks just like SARS2.
And then we made derivative viruses that either encoded GFP or nano-luciferase.
These viruses, when they replicate, they express sub-smaller messenger RNAs that encode these downstream genes.
You can see them present in the virus.
And as you incorporate larger genes into the genome, you can see the mRNAs get larger.
So they're using the appearance of a fluorescent protein that they are transfecting into these cells as an indicator that the virus is replicating, and that's not true.
What that is showing you is that the RNA to the luciferase, or the RNA to the GFP, is capable of moving between cells.
Maybe it's packaged, I don't know, it doesn't matter.
If you put enough of the pure RNA in there, come on!
If you put enough of the pure RNA in at the start, you are not doing anything natural.
You are just transfecting and transforming cell culture, that's it.
And the cardinal, fundamental bamboozlement of virology is that synthetic,
creation of these pure molecules is recapitulating whatever biology they purport to be finding in these bats in the wild.
It's that simple.
And that is the illusion that somebody like Ralph Baric, Robert Malone, Judy Mikovits, Tony Fauci, Bob Gallo, David Baltimore,
and Murray Gardner and Ruschetti and all of them are all wittingly or unwittingly sustaining.
And I am absolutely, absolutely 100% frigging convinced that some of these people that have been offered to us, forced upon us over the last four years as the default dissident leaders from the very first COVID summit in Puerto Rico or San Juan,
all the way until the very last COVID summit that happened in Romania.
These people have created the illusion of consensus about a gain-of-function virus that spread around the world starting in late 2019.
These people, along with
Tony Fauci and the TV people have gotten us to the stage where most mouth-breathing, skilled TV watchers or skilled social media users believe that, generally speaking, transfection worked well.
It's probably going to cure cancer.
They can transfect people and make them immune to shingles or protect them from
from pneumonia, because we're doing that to old people now.
And transfection was rushed during the pandemic, so some people were hurt.
We'll probably figure that out, and we'll probably punish some people.
But free-range RNA can especially pandemic if you put the right combination of fear and cleavage sites and HIV inserts in there.
So that's the part that really frustrates me a lot.
See, now here was my laptop just going away.
And I don't know why it's just going away.
But it did this to me yesterday too.
So I'm going to reboot it and then I'm going to have to figure out what's happening here.
Let me just feel it quick.
It does feel hot.
But it's not as hot as I have felt it.
I'm very curious as to why it's doing this.
I'd investigate this further.
Because it does reboot.
So these people have convinced us that whatever happened here, free-range RNA, we definitely have to be afraid of it.
And it's something that these people agree on wittingly or unwittingly, just because they're on the news doesn't mean they understand, but they definitely are going along with it because it's a national security priority.
They were probably briefed on it, that the idea that
that we had to get maximum compliance was going to require that we tell people the simplest truth they're willing to accept.
The simplest truth that they're willing to accept is that, you know, RNA can cause a pandemic and very likely a gain-of-function RNA can cause a really bad pandemic.
And this illusion of consensus is exactly...
Exactly what they created.
So now it's back up again.
I don't know what to say about my laptop.
That's a problem.
We need a new consensus, ladies and gentlemen.
We need a new consensus that transfection in healthy humans was always criminally negligent, that RNA cannot pandemic no matter what you endow it with.
But you can make a lot of RNA and you can make a lot of DNA.
And you can also murder people and lie about it.
That is also very possible and very likely.
So what I argued
And that's why I think that identifying Brett Weinstein as a traitor and a liar, specifically with regard to me and my family, with regard to me and my work, with regard to my confident
and confidential communications with him had a stage where I didn't have to waste any time on him and his wife.
I did.
And I did it because I thought he was genuinely trying to save the same future for my children and his children.
But he's not.
He's trying to put his family in a position in this new society when America and the idea of America is permanently demolished by Robert Malone and his compadres.
These people are charlatans.
They are lying to us about the fundamental truths of biology that include that intramuscular injection of any combination of substances with the intent of augmenting the immune system is dumb.
Transfection in healthy humans was always criminally negligent and RNA cannot pandemic.
Thank you very much for joining me.
Don't forget what these weaponized piles of money did to us.
It is really without reservation that I've said for the last four years that we should stop transfection in healthy humans.
I even got to say it in front of the ACIP.
I said it to Brett Weinstein in 2021 and maybe even in late 2020.
So we're talking about some serious, serious traitorous behavior.
Please, they're trying to eliminate the control group by any means necessary.
Make sure you're informing the old people in your life that these new vaccines for shingles and for pneumonia are absolutely no-goes.
If you liked what you saw, please share the restream at stream.gigaohm.bio.
And if you can, we really need some support.
We really need some new subscribers.
We need people to take a risk on a four and a half year track record of integrity and trying to tell the truth, trying to save our grandkids.
Ladies and gentlemen, gigahomebiological.com is where you can find me.
Thank you very much for coming and I'll see you again tomorrow.