Through where I think I'm at, now I'm going to give you my hypothesis in a nutshell and
then I'm going to drink a beer and probably light a fire and see if I can read some comments
before I go to bed.
My current hypothesis is this, this likely originated from a laboratory source.
Number one, laboratory leaks happen and you can look up many different articles including
a few from Lynn Klotz who will show you definitively through history how leaks have happened through
unintended infection, through waste products, lots of different ways and lots of different
places it has happened.
The second reason I believe this is true is because of the circumstantial bullseye, the
idea that this broke out in Wuhan where the research on coronavirus was happening where
the foremost groups were working on the foremost dangerous viruses and even though you want
to say and people will tell you that this was BSL Level 4, most of the coronavirus work
that is published in the literature is done in BSL Level 2 or BSL Level 3, even BSL Level
3 is not a very strict biosafety level, I work in a BSL 3 level lab with my mice.
And finally, the entangled financial interests I think are also very important to acknowledge
here the amount of money that was given away to private equity, the amount of money
that has been given away without context or identification to millions of corporations
in America and the amount of money that is being given away through the Warp Speed Act
that's allowing big pharma companies to make products that are guaranteed to be purchased
or to be supported by government funding under the pretense that we need to bring as
much of this to bear as possible.
One of the things that you have to realize here, and I hadn't made this point yet but
I know I'm glad I remembered, there is a federal law, the Defense Production Act, which allows
the government to tell companies and corporations that they need to produce certain things at
cost because it is for the benefit of all of the American people, for the benefit of
America as a whole.
This was an act that was designed to change the production of companies during World War
One or World War Two and we could easily use this to direct pharmaceutical companies to
develop specific things like, for example, produce hydrochloroquine or produce a vaccine
of a particular design or a particular type and we could limit and control the amount
of profit that was made so that nothing was, no one became rich from it.
We could do the same thing with coronavirus testing.
We could be using that act to make sure that no one is profiting from the testing, from
the antibody testing and from the PCR testing, which I'm going to do another whole talk about
that but PCR as a test is absurd right now and we know that because this test is not
specific for SARS-CoV-2 but is only specific for SARS viruses in general and that means
that we could, as I said before, be testing for the endemic version of the descendants
of the original SARS, which are almost guaranteed to have gone through at least half of our
population in the last decade and a half.
So SARS-1 and its descendants have gone endemic, that's what I was just saying.
The current PCR test is not specific for SARS-CoV-2 and that is known because it's the German
company that originally produced it, knows that they've chosen a short sequence that
they think is relevant.
It is a short sequence that just comes from one of the open reading frame one proteins.
We are being duped by a non-specific test and we would have gotten these numbers or
numbers very similar to them with or without this pandemic because we've never looked for
SARS viruses as they are spread through our population.
We've just never looked.
Nobody sampled for it until this year.
It's a huge point to make because the SARS virus originally appeared in 2003 and disappeared
in 2004 but it didn't really disappear, it just became not a problem.
Descendants of that virus of various virulence and infectivity have circulated in the time
since they didn't disappear and this test is not specific for any one of them and no one
has ever done a study about how many descendants there are, how many people are infected,
how many animals have been infected by it, etc.
So that's a pretty interesting place to be in July of 2020.
Thinking that there are descendants of the original SARS leak or leaks or zoonotic jumps
which are building up an endemic signal in the background that could then be turned
on in the flick of a switch, just kind of like Kevin McCurnan explained it in the video
interview with me and a few other people where he said you could do it with HKU1.
Just turn on the PCR and start monitoring it.
You're going to see patterns of viruses moving through the population according to him.
So if there are SARS descendants which could be used and misconstrued in that way, certainly
that was a possibility that should have been considered from the very beginning of the
pandemic and it was not.
Certainly wasn't something that Kevin McCurnan brought up during his authorship of the paper
that was let's say opposing the PCR test, opposing the PCR test by saying that some
of the primers would make primer dimers.
Never mind the whole pretense of being specific for a specific virus when the PCR test that
was designed by the German lab was using sequences that they had found in Germany, sequences
from German bats.
I mean there was a lot of other reasons to lash out against the PCR test that was designed
by Jorsten but primer dimers and this kind of thing was an odd sort of objection and
if you look back and see who was on that paper, he will see that a number of early objectors
were all roped in together.
I think we're going to be coming back to that little gathering of quote unquote dissidents
many many times in the next year or so.
And so saying that we're being duped by a nonspecific PCR test is also really not specific
enough even though right now this particular version of me was not completely queued in
to the fact that this time that there could have been as many as 150 different variants
of the test, 150 different variants of the test being utilized and being employed by maybe
hundreds if not thousands of independent labs with various levels of quality control and
certainly no oversight.
And the crazy thing is as many of those small company labs that were doing a lot of the
local testing especially in places where the testing was mandated, those are all gone.
They don't exist anymore.
Those companies took millions of dollars and they're gone.
Their owners own houses and they're gone.
And we're supposed to focus on the DNA fragments in the shot and forget about the fact that
the whole the whole theater in the beginning to make worst case scenario real was wholly
created out of out of fresh cloth.
This is not sorry to start the show like this, but this is just the way it happened to be.
I had this queued up for some reason.
So the next thing that I want to say is our lack of biological knowledge and the general
poor health of the of America, the American people is being used to create the crisis
they need to divide and conquer us to ruin.
Maybe America.
I don't know.
Crash the dollar.
I don't know.
Steel the rest of our are what limited treasury value we have left.
I don't know.
But I know for sure that they are combining our lack of biological knowledge and our general
society's lack of good health and access to health care to create a crisis to usher
in all kinds of changes that would otherwise never be necessary, and more importantly never
be possible.
Just like the Patriot acted 9-11.
Highly profitable control mechanisms based on immunity are the near term goal.
I believe this firmly now, there are too many people talking about it in the mainstream
media hinting at it.
Sound you hear is a single cicada, there are no crickets.
Highly profitable control mechanisms, I'm talking about apps that you have to have and
maybe even worse in order to cross state lines, in order to go to work, maybe in order to
go to the store, you're going to have this happen.
So there's going to be technology that needs to be distributed, there's going to be laws
that are going to be need to be passed, there's going to be all kinds of products that need
to be sold, and the whole idea is going to be to sell you on the idea that antibodies
are the only evidence of immunity, and the only way to get antibodies is to get this
vaccine, because a lot of people of course are not showing long lasting antibody levels,
so even the people who've been infected, and that's what they're hyping right now is that
you can get infected again, this is the narrative they're bringing to you so that they're going
to tell you, the only way we're going to be sure is that if everybody gets vaccinated,
and now we have billions of doses necessary, billions of doses backed by government money,
backed by government mandate, controlled by apps, distributed yearly, we are talking
about a very serious change in our healthcare system that will benefit the largest corporations
and allow them to profit, because there are no controls on that profit right now, none
at all, we have chosen to do nothing of the sort.
That's why I'm sure this hypothesis is correct, the other reason why I'm sure this hypothesis
is correct is, well I'm getting more sure that this hypothesis is correct, I don't want
to sound like non-scientific here or non-objective, is because the guy that I first really got
woken up by on the internet besides Dan of Harvard to the big house blog, is Wolfgang
Wodach, and for some reason I never searched for this guy after I saw this German video
that I had to get translated by a friend of mine, where he explained that it was likely
a SARS virus or a SARS-descended virus that has been circulating viruses that have been
circulating since the original SARS outbreak fizzled out in 2004 that we are testing for,
and he only released that video in May or in April and it was only in German, and then
I just never...
I hope you see how significant it is that Wolfgang and I have now made contact in such
a significant way.
I hope you see what kind of forward progress is about to happen, don't be distracted by
what's going on on Twitter and how people supposedly think that this story of the clones
is an open and shut case now because there's effectively no swarm.
He's been going around in circles on this idea for a very, very long time, and the reason
why he's doing that is because all of RNA virology is dependent on it and no one can
know that.
If everybody understands that, that what they speak of as virology is a gross exaggeration
of fidelity and it's a gross exaggeration of understanding, even the next strain database
and phylogeny, even the Jed said database or whatever the hell it's called, all of these
collections of genomes are presented to you as gold standard evidence of and proof
of something for which they are not proof of.
All we know for sure is that these people have managed to measure these sequences and
a lot of these people believe these sequences are real, but we don't have any reason to
believe that these sequences are somehow related to one another in a progression related to
one another in an evolutionary way.
We don't even know, no one is even talking about the possibility that these animals and
ourselves would emit coronavirus like signals from our immune system or from the outside,
from our lungs.
No one's even talking about the possibility that these signals are being produced by the
bacteria in our lungs or the bacteria in our airways, our GI tracks, wherever.
No one's talking about the possibility that there's replication of RNA or DNA being carried
by bacteriophages that's doing these signals, that's causing these signals, which really
are just signals, genetic signals that are coincident with, well, genetic signals that
are present and they're coincident with amplicons of PCR.
It's very difficult at this size scale and at this sensitivity to definitively say that,
well, this is definitely a something and we must always end up taking the word of somebody
like Kevin McCurnan.
They can't prove it to you.
He's not going to ever teach you how this stuff works.
He's always going to tell you that it's just too complicated for him to explain it
to you, but I'm definitely wrong.
When in reality, the idea that we're fighting about is really very simple and that's why
it keeps spiraling out of control behind a block where we can't really have this discussion
and why he keeps saying that we're not really, that he had this discussion a long time ago
on email or he tried to do this on his sub stack before.
I've addressed all the papers in his sub stack when they came out.
I did a show about it several times in a row, which he completely ignored.
And that's fine.
He doesn't have to watch it.
He calls my videos six hours Scooby-Doo videos.
So that's fine.
I get it.
I should write a sub stack for him.
We're going to figure this out, ladies and gentlemen.
Don't worry.
And when we figure it out the way that the ball will move forward, it will move in a very
different way with a very different direction and a very different momentum.
I assure you, I assure you, it's taken me a while to get this all straight in my head
and make sure that we can move forward confidently.
I've been trying very hard to remain true to my original idea, which was that this biology
can't be impossible to learn.
And any of the biology that underlies this phenomenon is worth learning.
And so in the case of virology, I think all of us are just going to have to peel back
our roll up our sleeves a little bit and learn some of this biology that they purport to
have a monopoly on, that they purport to understand so well that you're just going to have to
take their word for it, that they can't find any of this stuff in 2019 and before,
but they sure can find a lot of it now.
And that means that it's something going around and around and around and it couldn't
be anything else.
There are a few things in the background that we have to take and keep in mind.
And there are a few things that we haven't addressed at all.
And so it's just a real, it's a real mess right now.
And so what they would like more than anything else for us to do is to rush as fast as we
can thinking we know where we're going and thinking we know where the opening is to the
cave.
And we've got to keep remembering that we've got to keep our flashlights forward and we
just got to keep working.
It can't be distracted by the things that are going on, even if it is that you get fired
or you get laid off or you get unexplainably your position is discontinued.
And you are offered a non-disclosure agreement in exchange for $8,000.
And you're left to kind of decide did I really put my neck on the line and put on
the t-shirt and say that I was fighting for the truth and then now all of this hard work
and sacrifice was worth a non-disclosure agreement and $8,000.
I decided not to do that.
And now I'm guessing I'm at the mercy of the internet for a little while.
And we're going to try and make this work because I think actually this biology could
save our kids.
I actually think that if we can work through the literature and find truth in it, especially
pre-COVID truth, and we can find biologists that we're working toward what they thought
was the truth, I think we can find something that will be solid enough to stand on, that
we can hand down to our children as an understanding of what these people lied about, what these
people misled us about.
And I think you're going to find that the illusion goes back farther than we thought.
I think that's why so many of the interesting players in this are not like your typical
players, like people who dropped out of grad school to start working on the Human Genome
Project and then had like patents and companies and companies and ultra success.
And then their boss went to the White House and was involved in the writing of $65 billion
proposal for Warp Speed vaccines.
And now he's been involved from the very beginning with objecting to the PCR test, but not PCR
testing, and then all kinds of other random appearances for the RNA not being pure and
then the RNA code on optimizing being responsible for different G quadriplexes and then came
out later to be the double stranded DNA and the whole time this guy's been right there.
Why has he been right there when his whole life is right now pot genetics and trying
to, I don't know, I guess take over the commercial pot market by controlling genetics and virons
and screening or providing testing materials for pot growers that will eventually become
required by the government or some other scam.
I'm sorry, but this is just this game has got to end.
And these people, whether you like it or not, are not playing a small, tiny game.
This is a game for all the marbles is for our grandchildren.
That's why it seems so ridiculous.
That's why it's being fought on Twitter.
Do you think that Kevin McCurnan could have a real discussion about this and a group of
people that all kind of knew about this stuff?
Or would it would it really always have to be like him and Meryl Nast and then Andrew
Kaufman and Christine Massey.
The one time that we had a conversation a year ago, he couldn't really object to it.
As you will see in tonight's recap, he just basically spit out exactly what I'm pointing
out when everybody should be pointing out.
That by making an infectious RNA and significant quantities, you could seed a coronavirus pandemic
that was highly homogenous across many different places and maybe even would be highly stable
for a little while.
Yes, it's possible that clones transmit.
I never said that they wouldn't.
My main argument was that infectious clones and the whole principle of how they should
or theoretically work is that you can create a much more homogenous viral stock that allows
you to make a higher quantity of it.
In fact, an infinite quantity of it is really only dependent on how to investment.
If you wanted to do Jurassic Park, you could just do PCR construction of all the six or
seven strands of DNA that you're going to use to ligate together and derive your RNA
from.
I mean, this guy's the limit if the idea is to just do it right.
I'm just kind of, it's just kind of sad because this is where we're at, right?
We have to protect our children from liars.
Liars like Paul Offit, liars like Tony Fauci, liars like all of the people that work at
the top levels of these pharmaceutical companies that know better.
And we also have to protect our children from a bunch of people who don't know any better
who aren't wise enough, smart enough, or I've turned the other way.
In the military, they have caught what is called a lookaway doctrine.
You know, if you're going to waterboard people, just let me close the door and get out of
here before you start doing it.
There are a lot of people involved in this little mystery that are also involved in that
way.
They know exactly how dangerous this was.
They knew exactly how nasty this was going to get.
And they knew that if they were going to get through this, they were going to break
some eggs, but you know, make no mistake about it, ladies and gentlemen, breaking eggs
is also going to require people on Twitter that have no business being on Twitter, talking
about coronaviruses and fidelity of coronavirus replication and all this other stuff in their
spare time while they're running companies on the genetics of weed.
I mean, we are very, very, very close to exposing a group of people who some way or another
were involved in the containing of the narrative at the same time they were involved in the
perpetuating of the worst case scenario, making absolutely sure that the existence of the transmission
of a novel virus was never questioned.
And think about how strange it is that Eric Lander's former protege is the guy who was
right there from the beginning, from the PCR objection to the RNA purity objection to the
G quadriplex objections and the codon optimizing objections to the frame shifting objections
all the way up to the double stranded DNA objections and what's really weird about the
objections about the clones and about the proofreading in coronaviruses is that this
thing that they recommended really, really early, that Cina Bavari predicted that they
would use very, very early, that Rick Brighton knew that they were going to use very, very
early, that Paul Cantrell knew that they were going to use very, very early, Remdesivir
messes with the proofreading of coronavirus.
So the proofreading of coronavirus is actually pretty significant.
We need, we need to have high fidelity coronavirus replication that can be interfered with by
Remdesivir and other antivirals so that the, the subtle balance between the mutagenesis
in the quasi-species swarm and the stability of it is disrupted and you get this collapse
of genetic stability.
That's the story that they tell.
That's the story that Mark Denison tells.
That's the story that Cina Bavari told in his paper.
That's the story that Ralph Barrick has told.
And that's the story that is told when you argue that coronaviruses are very, very stable.
You're arguing for Remdesivir's mechanism of action.
Coincidence?
Yeah, maybe.
Believe what you want.
What I want is high morbidity.
I want people to complain.
So what do I do?
I go to Des Moines.
Ladies and gentlemen, the people on the screen, I have nothing against Des Moines.
I live there for four years.
I go to Des Moines.
I infect a couple of sentinel cases.
I go to Seattle.
I infect a couple of cases there.
I go to North Carolina.
I go to Wisconsin.
What I'm doing is I'm using a dispersion methodology to be able to infect sentinel cases with a highly
morbid condition.
So I think what I want to do tonight is just quickly put up for a study hall.
I've got this video queued up, a couple videos queued up on coronavirus replication, but
I just want to look at...
I just want to look at a couple things first to make sure that we still cover what we're
really covering here.
Let me escape out of this and start the new deck right away.
I probably should just go really fast through it to bring everybody up to speed, but I hope
you don't mind if I do that.
So first of all, make sure you remember that one of the big, big, big things that is obvious
to me as we move forward and we watch all these people scream and yell about how bad
Jonathan Couey is for putting people's names on there or how bad it is that Jonathan Couey
doesn't remember why somebody blocked him or whatever it is that they're crying about
now.
The one thing that you will remember and what I have been calling for more than a year now
is that all these people will ignore this slide.
You could be wrong about the clones, but right about this, and it wouldn't really matter
now would it?
And I assure you that I'm right about this.
Intramuscular injection of any combination of substances with the intent of augmenting
the immune system is dumb and transfection in healthy humans is criminally negligent.
And by having me and you and all these people on Twitter that are trying to defend me,
thank you very much, arguing about clones and whether or not the viral swarm is significantly
diverse enough to support the idea that clones are different than the regular virus.
This is all nonsense.
This is all nonsense because this is true.
And as long as they keep us occupied about whether or not J is right or wrong or whether
it's okay to believe in J, then we're not going to we're not going to talk about this
stuff.
This is my most important message.
This is the only message that I want to get to our children because if our children understand
the big picture biology that underpins this statement, who cares about clones?
Who cares how they do RNA virology and who cares if somebody with a Poch genetics company
really does understand how they do coronavirus biology or not?
Clearly he's being encouraged not to understand it because he is neglecting the very prominence
of infectious clones from the early 90s on and the almost universal praise of how the
development of infectious clones and their production has allowed the expansion of the
understanding of how viruses work.
We would have to be fools to believe that infectious clones weren't involved in this.
They are the bedrock foundation methodology of all RNA virology, especially RNA virology
around viruses that are difficult or impossible to culture for whom no infectious material
is available.
And so don't be fooled by somebody who can put up a few papers and then say a few sentences
about why that paper makes them wrong.
The time I've ever followed up on one of these papers, it doesn't really demonstrate
what he says it demonstrates except for in a very sliver kind of way, but it's not addressing
the very big pictures of what the natural phenomenon, what does the natural phenomenon
look like is exactly the phenomenon that they don't want to talk about.
They want you to believe and that's what he would like you to believe that the infectious
clone replicates the natural phenomenon and that is a hundred percent wrong.
And so they have fooled us into solving this Scooby-Doo and that's exactly what McCurnan
is on right now.
He wants you to believe that I'm supposed to have the exact explanation with all the details
about exactly why the person came into my house, what they were doing there, what they intended
to steal and why they were stealing it.
And that's not the way a crime works.
And our society, my family and yours are victims of a crime.
We don't have any obligation as victims of a crime to know all the details and have a
good explanation for everything.
And we certainly aren't under any obligation to accept the explanation of the people who
probably did it or are working with them.
But we were fooled into believing that a worst-case scenario could have happened and we were fooled
into believing that we could solve them, that we were watching people solve a mystery.
That Rand Paul and Tony Fauci were arguing because they were on two sides of this mystery.
And with this Scooby-Doo, the principle of informed consent has been ignored for the
duration of the pandemic.
Here we are trapped on our couch watching the whole thing unfold on TV.
And so we've talked about how the pandemic was created from years ago up until now with
a team of people or peoples around the world and especially in Western society that were
there specifically to coordinate and amplify the worst-case scenario.
The billions of people dead, the amyloid spike, the prion disease, the spike was killing cardiac
cells, the whole nine yards.
And the worst-case scenario was very cleverly tainted with aspects that they expected or
feared would be a result of the transfection.
They knew they were going to roll out the transfection so they knew that they could
see this worst-case scenario with the worst-case scenarios of the transfection so that it would
never really be clear to an unsuspecting and completely compliant populace that they were
confounding the effects of the virus with the effects of the shot because you were given
a viral protein and the viral protein turned out to be wicked.
The people that were co-opted very early on were briefed that this was a national security
thing and so you couldn't just talk about it.
But if you go along with our little role here then maybe you can sell a book about Ivermectin
or you can sell a book about hydroxychloroquine or you can sell a book about the lab leak.
And in the end the toxicity of the virus, spike protein has been confounded with the
toxicity of the transfection along with, of course, since we saw through this, since
we saw through this little ruse a few years ago, a couple years ago, and we stopped believing
this ruse.
One of the reasons why we stopped believing this ruse was because we realized that the
spike protein that's produced by a codon-optimized pseudo-uridine chemically altered RNA is not
going to be anywhere structurally related in epitopes to that of one by the viral sequence.
And we came to that conclusion after having Kevin McCurtain on our stream for two times.
And so if the protein in three-dimensional structure is not equivalent to the protein
that you're trying to build immunity to, chances are very good that the most damage
associated immune epitopes there on that are also different.
And so here we are, we know what the game was, we know how they did it.
We know how they did it, we know they drove these mass casualty events and coordinated
them in a way that made sure that nobody could question what actually happened.
They co-opted a pre-selective group of narrative controllers and they probably brought more
people on as the narrative went out of control as the compliance wasn't 100% with the uptake
of the transfection, but a combination of background signal and nonspecific tests.
And we don't have to figure that out for ourselves, we don't have to take everybody's
word for it.
And just because one person published a paper doesn't mean that that is the definitive
Supreme Court evidence that now a scientific fact has been established, which is often
how a lot of these rebuttal papers are presented.
If you say somebody doesn't understand that the RNA, dependent RNA polymerase has a different
replication capacity and then they cite a paper that doesn't immediately mean that
that's the end of the discussion and that's really how this has gone from the very beginning.
I think that they really thought that I was underprepared that I stumbled onto this idea
and that's why the first three or four times that we had interaction with it, it was really
pretty weak.
And the one time we had an interaction live with my Kevin McCurnan and myself, I just
kept kicking the ball back to him and at some point I just had to let him go because he
just kept saying things that made it better.
And so I think after that talk is when everything really peeled out of control and he decided
that he had to make it appear as though he was slapping me down and used that stupid
complicated strategy of his, you know, where he says, April back like six times and it
forces everybody to Google it and so they all feel like fools and they don't want to admit
that they don't understand what he's writing and then by not admitting that he's not teaching
them anything, they let him get away with it, make it look like it's a consistent and consensus
win on his part.
And he refuses to acknowledge the fact that all of this stuff happened too.
So there's actually really good reason to believe that there might not have been a real
active spread.
There's really good reason to be skeptical and that's part of what I find very funny
about the one sub stack that actually dresses JJ's hypothesis in that sub stack.
I think three times Kevin says maybe only twice that again, I'm not trying to decide
here how much of the all-cause mortality should be attributed to COVID and how much
of it should be attributed to bad ideas and man-demic.
He makes the joke man-demic in his sub stack addressed to me from earlier this year, or
maybe it's late last year, sorry, yes, it could be late 22 or early 23.
And so I don't like to be accusatory, but in my perspective, we're dealing with someone
who's behaving dishonestly.
And from the very beginning, sort of a limited hangout kind of thing, giving as much, only
as much information as to feel like he's giving a little bit, but never really bringing us
all the way to the finish line.
Are you telling me that Kevin McCurnan couldn't have imagined that there would be double-stranded
contamination from the process two that he didn't know that they were going to use
process to, that it was an option given the fact that Enovio was on BBC News with process
two right behind them?
I mean, how stupid do they think we are?
How stupid does Robert Malone think we are that he doesn't know that process one and
process two are very common differences that we knew that they made the joke on Twiv?
Vincent Rancin-Yello talked about the amazing upgrade from nanograms to kilograms.
I mean, come on, guys.
And so these things all happened and they all want you to ignore the fact that they happened
and they want you to continue to focus on a novel virus that's highly, high fidelity
and that it can go around the world and change flavors repeatedly and with patterns.
They want you to believe that passage of viruses gets you places.
They want you to believe that when you stiff stuff together it gets you places.
The worst-case scenario is that they made a lot of something and then they spread it
around.
That's the worst-case scenario.
The worst-case scenario is that they made a lot of something that was pure and also toxic
and fairly good at replicating.
That would be awful.
But it wouldn't be natural and none of the attributes of its spread would be natural
because it would have started from a state that wasn't natural, a purity that wasn't
natural and I can't understand why they insist on confounding this, ignoring this really
easy thing.
People asking me to write papers and stuff.
It's like trying to write a paper about why cars use wheels.
What does that mean?
What does that mean when Alexandros Maranos and Kevin McCurnan say write up a paper?
What does that mean?
I'm telling you and it's a biological fact that the DNA can be copied with much higher
fidelity than RNA and Kevin McCurnan even admitted it that you can make a lot of DNA
and then you can make a lot of RNA from it and if you did that you would have a lot of
genomic RNA.
It'd be a little variable but it'd be a lot higher purity than anything you could ever
achieve with any other method that we know and if you invested sufficient into the fidelity
of it, use PCR methodologies, the state of the art technology, you could get purity levels
heretofore on seed on earth.
Distribute those everywhere and the signal would be brightest day.
Not to mention the fact that you would have this all this leftover DNA that would also
provide PCR signals because PCR is only looking for a very tiny amplicon so you'd
have made tons of that amplicons too that you could distribute in sewers and in water
and DNA is much more stable.
That signal could potentially last for months and months depending on where you put it.
Cruise ships could be positive for months if you had DNA that you distributed around.
I mean come on ladies and gentlemen this is this is all obviously a joke thanks to
James Giordano.
Thanks to Kevin McCurnan, thanks to Kevin McCairn, thanks to Paul Catrell, thanks to
Rick Bright, thanks to Tony Fauci, thanks to Ralph Barrick.
You know one of the things that I think is really funny about Ralph Barrick is that actually
I think he was a good guy and I think he's being co-opted.
I want you to listen to this presentation that I think we are being set up to watch.
That's all I'm going to say.
I'm not sure if it's an authentic presentation, there are a couple times where it goes silent
for like five or six seconds and I'm not sure it's an audio glitch, it could be an erasure
and a couple times when it goes quiet they are talking about very key aspects of the
infectious cycle.
So this YouTube video was actually posted in a sub stack of Peter McCullough and this
John O'leke or something like that and so that's how I found it and so I'm watching
it for that reason but what I want you to remember is that this is in between SARS-1
and Ralph Barrick may in theory, I want you to entertain this possibility, Ralph Barrick
may still be an innocent bystander, a guy who's just part of the of coronavirus biology
and he could still be in earnest thinking that coronaviruses could be one, a biotechnology
to a pan vaccine technology and three, some kind of, I already said that, but some kind
of future genetic modification technology so as they stand, some useful, then also modified
and then also modified again I mean they were a huge potential in his mind and so I really
think it's cool to listen to a video like this, even if it's altered, even if we're
being tricked, I'm willing to bet that you're gonna hear enough of a guy who is fascinated
by what he believes he is doing and I think he is doing it and that is studying synthetic
viruses.
So viruses that they can't culture, that they couldn't really get to grow in a lab and
sustain themselves but has found another way to do it when we have these sequences
and we decide on a consensus how can we do it and to really hear somebody explaining
how they are developing this technology to assemble full coronavirus genomes, I'm confident
it's gonna help us in terms of moving forward and really breaking the veil of this whole
thing.
Well, Carolina, you're gonna tell us about the synthetic genomics of SARS.
So I also would like to thank the organizers for inviting me to talk, it's been wonderful.
Now you are gonna be disappointed with the video here.
Capture some new ideas that can be tried out on viruses.
Well, this is not very loud.
I'm gonna talk about today our basic short introduction into SARS biology.
Talk about the synthetic resurrection and reconstruction of a variety of zoonotic SARS
viruses and their applications.
Okay, so already we're talking about synthetic reconstruction and he used the word resurrection.
So resurrection would be from a sequence, from a partial sequence and it's very important
to hear that because this is part of the reason why, again, clones are not just nothing.
They're very special because the vast majority of coronaviruses cannot be easily cultured
and when they are cultured, they only really barely culture it, they call it extremely
low titer, but it's not really culturing that you can't make enough to share and it's
not culturing.
So they have a big problem.
It's not just that they don't have, they don't have them in the right cell culture
or it's not the right receptor, it's more complicated than that.
And I think it comes down to the fact that infectious particles are oftentimes replication
and competent and if you get at the heart of this, you're gonna find that that's really
where this all peters out, where the rubber meets the road is right there and that's
where they just do the hand wavy.
And that's why the no virus people had so much to stand on.
That's why I think they were so dangerous and I think that's why they were so confusing.
But are we, do you feel the pendulum swinging back now, do you feel it?
Where we were almost all the way to no virus and really exploring the possibility that
wow, did they really only put clones in like four people?
Like Sohomish County man and a couple other people and sequence those and then the rest
is all nonsense, it's possible.
But there's a whole possibility space that expands from that very tiny number of people
that were infected with clones that never went anywhere to another medium possibility,
which is that they actually did put a significant a number of and concentration of clones in
several places so that several people or many hundreds of people would be infected with
a very pure infectious RNA.
And I think over the next few days, as we explore these papers together, you're going
to find a preponderance of evidence as I have, which indicate that these RNAs all by themselves
do some pretty cool stuff.
And as far as most virology papers are concerned, these are better than or more reliable than viruses.
And what they do and how they do it is more reliable and you're going to figure out that
that's because of the purity of the RNA, the purity of genomic RNA that gets into each cell
is several orders of magnitude higher than the amount of genomic DNA that gets into a cell
during passage.
And that's what's really extraordinary here. That's really what's extraordinary here.
And therapeutic and vaccine design.
I'll also touch on codons, the optimization as a way to attenuate SARS pathogenesis,
but I certainly haven't gone to the depth of studies that Eckerd's group has done.
And then I'll talk about rewiring SARS-Coronavirus transcription circuits as a way universal strategy
to attenuate viral pathogenesis.
So this is a schematic diagram of the SARS-Coronavirus particle.
It's about 100 nanometers from diameter.
It contains a helical nucleic acid inside.
It contains a single-stranded plus polarity RNA genome.
This nucleic acid structure is surrounded by a lipid bilayer.
It contains several viral glycoprotein spikes.
The important ones for today's talk include the M glycoprotein and the E protein,
which are shown right here.
These proteins are absolutely essential for maturation and release
and the production of virus particles.
So keep that in mind.
The second viral protein of interest for today's talk is the escolycoprotein gene
that's shown right here, which gives the virus its unique occurrence in the electron microscope.
It's the viral passion protein that binds to the receptor to mediate,
docking, and entry into the cell.
It regulates tissue tropism, species specificity.
It contains a large number of important neutralizing epitopes,
and it's the principal component of protective immunity.
Now, if you tear this virus particle apart and look at the viral genomic positive-stranded RNA,
it's about 30,000 base pairs in length.
It's the largest plus polarity RNA genomes in nature.
The first 20,000 base pairs are shown to encode the replicase proteins.
So the job it is to replicate the genome, replicate the genome,
and express sub-genomic messenger RNA that encode these downstream open reading frames.
Here's the first blank space.
Now, these downstream morphs encode the structural genes like the SEM and
nucleocapsid protein that I just mentioned that were present in the virion
in a variety of accessory morphs.
To get these expressed in cells, you find a nested set of sub-genomic messenger RNA.
They're ranged from the three prime end of the genome so that all the sequences in the smallest
message are in the next largest message and so on and so forth.
This organization allows different open reading frames to be placed at the five prime ends of
different messenger RNAs so they can be efficiently translated and expressed in cells.
Now, the trans...
Here, again, is another dropout.
I don't know.
How 70 nucleotides shown here are these little blue boxes.
That is derived from the five prime end of the genome.
So these are discontinuous stretches of RNA that are joined going transcription.
And these little red box elements right here are absolutely essential
for mediating the joining of these two sequences.
This will become very important later on in the talk.
So keep the...
Okay, so what he's explaining here just to kind of to bring you up to speak.
You can't really see it here and I apologize.
I told you it was going to be a bad... the graphics are bad.
It's weird. This was uploaded last year.
I can't find another copy of it.
There's those two things that were edited out there or blanked out in the beginning there.
I can't tell but it sure feels like there was an erasure there.
And he's talking about these TRSs which are translation regulatory sequences.
They are small sequences that are repeated throughout the genome.
And it's not very clear to me upon reading the genome...
or sorry, the literature exactly how these transcriptional regulatory elements
interact with one another.
But it feels like, if I can give you my best impression, it feels like that these TRS segments
are repeated because the RNA molecule has a three-dimensional interaction with itself
and makes it not so that this part gets looped over to this part.
And so then the RNA-dependent RNA polymerase can make a very short RNA that goes bloke
and then it goes right to here.
And it goes bloke and then it goes right to here.
And so every time it gets to a translational regulatory element,
there's the potential for this part of the five prime end to be looped in over here.
And so then the RNA-dependent RNA polymerase that's translating it can
to make this sub-genomic RNA.
And that's probably completely wrong.
But I do know that the translation regulatory elements are all the same.
And it is from these spots in the genome that the recombination is most likely to occur.
And one of the ways, and Ralph Berwick will explain it in this talk later,
that they thought to make an attenuated virus that could not
de-attenuate by recombining with other viruses in the wild
was to artificially change the translation regulatory segments of the artificial genome
so that this virus, when co-infecting a cell, would have translation regulatory elements that
were incompatible with the genomes that would be present in the wild.
And therefore they could not rearrange their genome to acquire genes from wild coronaviruses.
So what he's explaining here is an aspect of the coronavirus genome that if you take their
word for it, as I'm doing right now, is part of the regulatory mechanism by which the
entire signal genome actually gets translated into these sub-genomic RNAs that we've been talking
a lot about and that we understand are in abundance of several orders of magnitude more
abundance than the full genome, whenever they try to find the total RNA in any of these preparations.
I hope that helped a little bit, especially because you can't see Jack in this sort of blurry thing.
But we are listening to the great RB, so it's pretty fun.
The concept of TRS elements, a little red box element, is being essential for regulation of
messenger RNA synthesis. Now, let's talk about synthetic genomics in the context of a platform
to control emerging infectious diseases. If you think about emerging viruses, they have tremendous
potential to cause high morbidity and mortality. They have tremendous potential to cause high
morbidity and high mortality, meaning that there are small examples of this happening. But again,
it's the pandemic potential is different. I'm sure that if you had enough clone of a clone
of an RNA like this and you put it in somebody's lungs, yeah, or squirted it in some,
an animal's nasal passages, you'd have some problems. If you put that RNA in a cell culture and then
passage it a few times, you're going to have a lot of RNA in every cell. It's all going to be
the same. It's all going to do its viral thing. It's all going to package a bunch of stuff up.
You're going to have a huge concentration of highly homogenous RNA particles, as far as we can tell,
viral particles, exosomes, whatever, that you would not have if you just started with a sample from
the bat and then started passageing it and tried to make a lot. And that's the point.
Let's let it keep playing here. Maybe I should just quick, just let me give you this one thing here.
I had this queued up and then I just, I just realized we were going way, I was going way off
balance here. But here's a mini review from a virology in 1994, infectious transcripts,
CDNA clones of RNA viruses. Recombinant DNA technology makes it possible to analyze and modify
genomes at the molecular level and thus gain deeper insight into their organization and expression.
Oops, sorry. In this, in this respect, viruses because of the small size of their genome are
particularly amenable to such investigations. In spite of this, the study of molecular biology of
non-retroviral RNA viruses has long been hampered by the fact that these viruses do not encompass a
DNA intermediate step in their replication cycle. Therefore, since to date, the extremely varied
and powerful molecular biology techniques aimed at modifying nucleic acids have been directed
essentially at DNA substrate, new molecular tools had to be developed. The possibility of
obtaining infectious clones as CDNAs or as in vitro transcribed RNA copies, which is what an RNA
infectious clone is. Corresponding to the genomes of RNA viruses has greatly enhanced the
potential of investigations. Indeed, they can facilitate studies of viruses that are present
only in low titers in infected cells or whose isolation is problematic. Interesting. That's from
1994. Let's go to 2019 from Cina Bavari and Alison Totura, a former postdoc of Ralph Barrick.
Section 2, 2.1, reverse genetic systems. Advances in the study of highly pathogenic coronaviruses and
potential pan-coronavirus drug tech candidates partially depends on the technology to genetically
manipulate coronaviruses to probe mechanisms of viral pathogenesis and antiviral drug activity.
Reverse genetic systems synthetically generate viruses from known viral sequences. In situations
who wear clinical isolates of infectious material unavailable and due to restrictions for collecting
patient samples, shipping infectious materials, availability of containment laboratories,
reverse genetic systems, provide the essential research materials for studies on viral pathogenesis
in model development. Prior to the SARS pandemic, robust reverse genetic systems to manipulate the
genomes of Scarsco V2s, sorry, of coronaviruses had already been developed by systematic assembly
of cDNA consents to full-length infectious clones, allowing precise and genetic targeted
manipulation of viral genes. More importantly, to me, infectious clones allow the creation of
near homogenous viral stocks where the traditional viral stocks are prepared by
amplification of infectious material in cell culture. Infectious materials, that's the stuff
they take from bats, that's the stuff they take from sick people. Over many passages, strategies
to build reverse genetic systems were rapidly applied to both SARS and MERS within the first
year of identifying these viruses. In addition to reconstructing epidemic,
epidemic strains of SARS-CoV-2 with reverse genetic systems allow targeting of mutations
to specific viral genes and assembly of these virus when infectious material is not available.
So they've seen pretty significant for RNA virology in general, but for some reason or another, a guy who
was at the White House when he was what, 25 or something like that? I don't know,
how old was he when he was at the White House for the first time and probably because of his dad,
maybe, I don't know, but and then his, he drops out of grad school, goes to work for Eric Lander,
Eric Lander's in the Biden White House, running stuff for the mRNA, and this guy's involved from
the very beginning from the PCR shot all the way through all the objections that were ever made
about the transfection and titrating them one by one and we're supposed to believe that
clones are just like everything else. It's no big deal. Clones don't do anything. Clones are
chemtrails stupid. It's pretty phenomenal, really, if you think about it. And severe economic
hardship, good examples are HIV, the 1918 flu, far as coronavirus, H5N1,
chicken and guinea virus, probably most recently. Now it's clear that zoonotic introductions are
increasing and a large number of these viruses have large reservoir pools of animal strains
like SARS and H5 that are maintained as sort of heterogeneous swarms of pools of viruses
of which someone may actually emerge in the future to cause epidemic disease in humans.
This raises a conundrum in terms of how do you protect the public health against the future
occurrence that is hard to predict. I wonder how we would differentiate between a pathogen in bats
that doesn't make bats sick. How would we differentiate that from a immune signal?
Like let's say that the bats physiology is to emit coronaviruses. Let's say that a lot of
mammals emit self replicating RNA packaged in a lipoprotein coat. Just just imagine that for a
second. Is that crazy? Is that a crazy idea? Are we crazy? Are we a little crazy to assume
that these RNA molecules coated in a lipid dental, a lipid protein, a lipoprotein coat,
aren't we a little? Isn't it a little weird to assume that these guys are just all independent
actors that are out of the control of the bats, out of the influence of the bats,
out of the hands of the, despite the bats best effort, these coronaviruses are thriving inside
of the bat population. Why does it have to be like that?
Is it, is it really like that? Are we sure it's like that?
Are we sure that Simeon virus 40 was really a virus that the monkeys body really wanted to get
rid of but couldn't get rid of? Are we assuming that the pangolans have coronaviruses that they
don't want that they're not supposed to have but they're just there because despite their best
efforts, that's a huge assumption, isn't it? As opposed to it being like a signal or an offgassing
or a noise, I like a signal. I like the idea of it being a signal.
I don't like the idea so much of it being a pathogen anymore.
But I definitely like the idea that Ralph Barrick thinks it's a signal and thinks that what he's
working on is important and what he's working on is something that's worth understanding and that
he's made a major breakthrough by figuring out how to make these full genomes and start there.
I think it's possible. I think your your sliver of understanding, your sliver of specialty could
be so great that you could get so fired up about making machine guns that you just don't realize
that, wow, I made really, I mean this machine gun is pretty amazing and I'm proud of all the the
the ingenious ideas I put into it but I'm a little disappointed with what it did to them all.
That's possible. It's totally possible.
You know, I was a clock maker but then I got into guns and I just figured out this thing and it
was super cool and and then somebody took it to a high school but you could still have your you
know if you were really hyper focused on something if you really were interested in making something
cool out of coronavirus is because somebody said that something cool could be made out of
coronaviruses and you're a clever guy maybe that's who Robert over there that's who Ralph
Berwick is. That's why he's trying to attenuate them. That's why he's trying to find combinations
of monoclonal antibodies that will neutralize all of them.
That's why he's trying to change their translation regulatory sequences so that they can't recombine
with with natural viruses and that they can be permanently attenuated. These are all laudable
pursuits if viruses are real and and if they are potentially a biotechnology that could be harnessed
for good. A endogenous signal that could be that could be used and harnessed as a as a tool.
Why not? Sounds great. I think Ralph Berwick might be innocent. I think we might be led to believe
that in this little Scooby-Doo this is the guy we're supposed to unmask. This is the bad guy right
here. Look at him. I don't think so. How do you develop drugs and therapeutic against an unknown
from this heterogeneous swarm of variant strain that will actually work against the unknown that
will emerge in the future? How do you target your scarce resources? We think platform technologies
like synthetic biology, phylogenomics, structure modeling, high-throughput sequencing really will
provide a platform and our goal is to use SARS coronavirus and its large pool of zoonotic viruses
as a model to develop rapid response platforms to protect against this broader heterogeneous
pool of variants. We also would like to develop strategies that would attenuate all family members
so that you could rapidly develop vaccines for the public overall public health.
And so that's funny because he's talking about rapidly developing vaccines. I wonder
anywhere in this talk he's going to project a time frame. Is he going to say five years?
Because if he says two years that would be very interesting, wouldn't it? If he says
five years or he says one year anything that he says about development time will be interesting
in 2007. This is going to be cool. Keep your ears open. Now a lot of beautiful work in Malek's
lab as well as other labs here in China worked out the basic molecular epidemiology of the SARS
coronavirus. The virus originated most likely in bat. It probably jumped into civets or humans
and in that context set up a transmission cycle between civets and ratoon dogs and marketplaces
and humans who frequented those marketplaces. Over time it's selected for strains that were
more efficient at infecting human cells and recognizing the human ACE2 receptor for doctor
human entry leading to the 2002-2003 epidemic which caused about 8,000 cases and 800 deaths.
Now I want you to keep 8,000 cases and 800 deaths in mind as the
as a certain quantity of clone. Let's call that one clone unit and so if you release one clone
unit in a place in China and it can cover 8,000 trackable or suspected cases and 800 deaths
with a few sequences. So let's just call that a single clone unit as 8,000 cases and 800 people
dead so that we can think about what we would do if we had two or three clone units, if we had
10 clone units released in four places. How many cases would that be? How far would it go?
How much molecular change would occur per unit time in that scenario? I want you to start
thinking about the possibility that that's what actually was done. The first time single clone
unit this time maybe five clone units and the difference is that these five clone units were
all so clones right they're the same so instead of having a SARS outbreak originate from a apartment
building in China and ultimately end up somewhere in Toronto of all places which was probably part
of an exercise again because they were elevated as people who knew what they were talking about
at the beginning of this one and so with more clone units you could just have a bigger brighter
signal that would be as homogenous as you wanted it to be and so interestingly enough when we were
having this argument before Kevin McCurnan and I he brought up the idea that there should be some
purity in the thing which I find curious and I just want to throw that up there for people who
are listening and watching so this was from earlier this year something you know the things that he
says that I ignore this is from a slide that I made for that I think it was in the in the last week
of April the first week of May ask yourself why he's making six hour scooby-doo videos instead
of downloading data from NCBI and trying to find a signal for his hypothesis in real data
if the clones offer some advantage to Dr. Evil surely there is evidence of reduced mutation rates
to prove this now interestingly I didn't want to make a big deal about this I went really fast
through it because I'm a little scared it's going to disappear I'm a little scared that somebody's
going to make an excuse for it to disappear but this is the paper from Alina Chan in May of 2020
Alina Chan with the book Alina Chan that works at the Broad Institute that Eric Lander is the head
of at MIT Eric Lander the former boss of Kevin McCurnan at the Human Genome Project ladies and
gentlemen the one that worked at the White House for Biden yeah him now runs the Broad
Institute or still runs the Broad Institute at MIT where Alina Chan works Alina Chan submitted
this paper this pre-print to bio archive on May in 2020 and here she has nucleosides nucleotide
substitutions in the genome of SARS-1 versus nucleotide substances substitutions in this genome
of SARS-CoV-2 and lo and behold what is this it looks like there is evidence of reduced mutation
rates at the beginning of the pandemic relative to the beginning of the pandemic of SARS
hugely reduced mutation rates publicized and observed by none other than Alina Chan who was
incidentally has never published this paper officially under peer review
and instead accepted a position at the Broad Institute as a staff scientist and sold a book
about the lab leak it's a pretty interestingly tiny circle of monkeys considering the fact
that Kevin McCurnan just recently said that I gave him the George Webb treatment like I mean
have we are really running out of characters here is it really that many people aren't backstage
anymore or what like when we when we spike this football ladies and gentlemen it's going to be
quite a spike okay it's going to be quite a spike let's go back to some more traditional virology
with the Great Ralph Barrack if you do phylogenetic analysis of the isolates that were sequenced
you find they fall into two broad categories these this line indicates the strains underneath
that line were identified during the epidemic and you have early phase isolates primarily of
January 2003 after a variety of super spreading events you had middle phase isolates shown here
by this group of isolates and then following infected physicians who came to Hong Kong and
resulted in a super spreading event that some transmitted the virus to the rest of the world
these were considered late phase isolates now if anything is suited to a super spreader event
it is somebody who is infected with an infectious clone because all their cells will have been
infected with a genomic RNA that was identical which means when they start making this swarm
of of slightly altered viral genomes and they make this huge collection of sub genomic RNAs
the collection of proteins that they produce will be much more homogenous than anything
that would have been generated from a typical cultured virus if you could culture it but you
can't you see you see what's magical about this you see how beautiful this is
and so Ralph knows that he's making something that's super cool Ralph knows that he's making
something that is not natural but he's arguing that not only can we make something super pure
but if we find a way to alter it so that it's not dangerous so that it's useful to us we can make
huge quantities of that useful new synthetic virus from Ralph Barrack's perspective he is on
the verge of tapping into a biotechnology that has almost limitless possibilities
once he can figure out a way to attenuate them so that they replicate in a way that we want them
to that they have no toxic parts to them that the most toxic parts of their replication process
are minimized then potentially we would have the ultimate transfection tool the ultimate gene
therapy tool the ultimate personalized medicine tool that's what he sees here that's what Ralph
Barrack is chasing he's chasing a universal vaccine a universal transfection tool a universal gene
therapy that's what he's teaching chasing here and he wants to use this diverse set of coronaviruses
in the wild that's present and sustaining in the wild in these populations has a basis for understanding
them if this biology is it checks out it's a very noble effort in my humble opinion it's not the
Scooby-Doo bad guy we're looking for it's just not the vast pool of heterogeneous zoonotic strains
however reside up here most of these were in fact none of these were ever actually successfully
cultured they actually exist as sequence signatures in silico so one of the immediate goals that we
became interested in during the outbreak was to develop a platform of viruses that captured the
heterogeneous that exists within the family of viruses and to do that we identified sort of
representative strains for example middle phase early phase isolate or bony we had in the lab
middle phase isolate with cohk w1 kzo2 with early phase isolate animal isolates like it's from sivets
fc 16 and hc fc 6103 a raccoon dog isolate which is shown down here the sporadic 2004 human case
and a couple of other viruses sequences were identified as good candidates that would capture
all the diversity that had been identified within the sequence pool this shows the sequence that's
the sequence variation within the spike like a protein if it's a blue box amino acid that's an
animal associated residue early phase changes are shown here in yellow middle phase changes
shown in orange and late phase changes shown in red in addition in 2004 there are a variety
of other animal strains of sporadic human cases were identified that had additional variations
shown here in white and it's interesting as much i i hope that everybody was paying attention right
what i put up here before you were paying attention right um this paper is actually
this paper this paper right here
broad spectrum coronavirus antiviral drug discovery by allicin totura and cena bivari
written in 2019 allicin totura was a postdoc of ralph veric
so she's at us amrit
you don't think she knows how to make infectious clones
you don't think everybody that went through ralph veric's lab knows how to make infectious
clones are you kidding me where did these people go off to they're not working at starbucks or
something like that you think
this paper is not accidental that it talks about a virus getting out of china and needing to use
remdesivir as an antiviral for it it's not for nothing that we're defending the proof reading
ability of exo x one gene or or our exo and gene uh the the ribonuclea we're not we're not
defending these these things for nothing they're all related all these people all their nonsense
it's all related don't you remember the the the domain program run by ditra
run by robert malone who supposedly made an x-ray crystallography computer model
of the three cl protease of the virus and then interface that computer model with all known
pharmaceuticals with a volunteer team of researchers in a matter of weeks to identify
femotidine and remdesivir as two usefully useful antivirals
and cena bivari knew about it a year before that
and ralph veric and mark dennison knew about it a few years before that
for zika or for for Ebola for whatever else they were trying it on
because they're all RNA viruses right
don't you see the pattern here there is a mythology that has been laid down there is a
mythology that is being defended
this paper got in bobbie's book this paper that is in bobbie's book and actually actually
right uh uh robert malone sold bobbie's book today on his sub stack which is pretty badass i like
that a lot maybe that was part of the deal if you get that you stop that kooie from talking about
me on his stream i'll i'll sell bobbie's book on my sub stack maybe that's what it is
it's a pretty simple deal right you know robert malone's got a million subscribers if he tweets
out a book probably a hundred thousand people buy it or ten thousand people buy it
he better sub stack the book he wrote a wrote a review on the back cover
i'd say buy a copy i'd say buy a copy and we'll meet and i'll autograph it for you
um there's some bad stuff in there there's some good stuff in there it's probably the best
document of all the nonsense people said
the person who showed me this paper the person who showed me this paper his Mark
Housatonic Mark Kulacz it wasn't shown to me by by Kevin McCairn it wasn't shown to be by
Paul Cottrell it wasn't shown to me by George Webb wasn't shown to me by Kevin McKernan or Stephanie
Sinev or Steve Kirsch or Robert Malone the only person that's ever mentioned this paper to me
ever shown it to me ever found it and said holy crap dude did you read this
this is Mark Kulacz
i just can't stress to you how all of these things line up in a way that that can't be
discounted anymore all of these people all of their behavior line up in a way that cannot
be discounted anymore even if we find out that there's a huge coronavirus background that
coronaviruses can transmit for months even if we find out that clones can transmit for months
the ultimate conclusion is is that we have been lied to by a group of medlers that sustained
a worst-case scenario sustained a confusion and uncertainty and a doubt that allowed the world
to be transfected and only after the world was transfected that these people do it about face
and pretend like they always knew and the list of these people is long but it doesn't include
Ralph Baric the list of people who lied to us about the worst-case scenario at the beginning
of the pandemic only to pivot after our kids had lost two years of school after our kids have
been traumatized with masks after we had been locked down for a year and a half that's not Ralph Barrick
case you can't tell i'm trying to get Ralph Baric to come and interview on Gigaohm
Biological wouldn't that be badass much of the variation actually falls within residues or regions
that neutralizing epitopes were identified and in fact although the number of residues that are
changed aren't that great you can actually reduce neutralization titers by about 20 fold
with some of these variants now importantly Farzan's group showed that the two key changes
during the epidemic where this life seemed to asparaging change at 4.79 and Assyrian 3
change at 4.87 that drove animal adaptation to human strain and so keep that in mind so
without access to this pool of strains we decided to synthesize basically a portfolio of
spike like a protein genes of about 4k each and then use a molecular clone for the
urbani epidemic strain that we had built in the lab basically replacing the urbani spike
one at a time with these various spike like a protein from different phases of the epidemic
now all of these viruses were viable except for the sc-16 variant this actually can't recognize
the humanase receptor so it didn't grow until we made mouth cells that consistently expressed
the civetase to receptor and once we did that this virus to grow well before we had those cells
since Farzan had identified this 4.79 changes the key residues so be careful there now they
just admitted that they use mouth cells which have been genetically altered to express the
civetase receptor now i can't stress enough we had this paper come out that everybody's been
yelling about it i'm probably gonna have to do a show about it in the next couple days again
about this paper that um you know i should do that video tomorrow that's what i'm gonna do
tomorrow i'm gonna do i found this video with mccernan and um christine uh parks christina parks
and um John Beaudoin and i've i've been meeting to do John Beaudoin um on HighWire and so I should
do John Beaudoin on HighWire this week and then I'll do this this multiple person stream that
happened a few days a few a week ago or so with McKernan and parks and Beaudoin that'll be good
that's two good good study halls for this week um so what he's talking about here now is making a
number of different clones where he's swapping the spike out um this is of course supposed to get
us really excited about making chimeric viruses but here again he's gonna make clones of all these
things so if there's a danger the danger is is that he's making clones if he wasn't making clones he
couldn't even study these things the regular virus of these things is not attainable won't grow
and even if you could grow it the titers would be so low it would be almost unsequitable
that's the problem with these guys right and so don't let the the nonsense fool you
infectious clones are the bedrock methodology of RNA virology change especially build a recombinant
virus with that change and that virus could be cultured uh interestingly enough two of these
the gz-o-2 and the uh hcse-61 of three viruses actually caused lethal infection in aged animals
they produced an ARDS like disease saw SARS caused ARDS in humans or predominantly in age
populations uh that's acute respiratory distress syndrome it's a clinically devastating end stage
lung disease with about a 50 mortality rate so these are actually some of the first real good
animal models for SARS infection and so remember what I said the other day again you have to
take everything with a huge grain of salt if it's an animal model especially a genetically modified
one then the expression of the protein that the virus interacts with could be so over or so
inappropriate or any other number of of wrong that when exposed to these exosome collections
these animals produce a really robust immune response or a really robust infection because
these signals go everywhere so if you believe the biology that they need a receptor and that
the receptor has to be somewhere and if the receptor isn't there then the virus can't hurt you
if you believe this then these animal models are also very scary because you could imagine
a scenario whereby genetically altering the animal you create an animal that is hyper
susceptible to this manipulation hyper susceptible to the exposure to these signals
so if you believe viruses work the way that these people say they do and that they need receptors
and then you alter the expression of those receptors or even worse you homogenize them
across the whole animal then their susceptibility to exposure to these things could be very different
and that that could be great if you're writing grant applications that need an animal model that's
very repeatable and very robust and so don't underestimate the stuff that we talked about with
with Wolfgang Wodock keeps coming up here where you have academic biologists that are essentially
academy-gicians they've been they become so good at doing experiments that are fundable
asking questions that are fundable that they have stopped asking useful questions that they have
stopped asking questions that actually move the ball forward but they're now asking sort of circular
questions they don't want to make any progress they want to make the illusion of motion right
and so in this scenario i don't think that's what what Ralph barracks doing at all i think he's
actually making forward progress there are these RNA signals which have been very difficult to study
in the wild because they're almost unculturable there's no infectious material available it's so
rare and if you take this infectious material and try to culture it you often get very low to
no tighter so infectious clone overcomes that Ralph barrack is a genius now um these viruses
replicate of the human epidemic strains replicate efficiently in human airway epithelial cultures
these are cultures that are derived from cells lining the trachea of transplant patients you can
actually culture them on liquid air interfaces and they take on the architecture of the human airway
stars coronavirus all the epidemic strains actually like to infect ciliated cells and these epidemic
strains replicate very efficiently the animal strains however do not and this is just some
fluorescent microscope images showing the cilia of the ciliated cells with an expression of the
sars nucleic acid protein from an epidemic strain on the ciliated cells and the zoonotic
strains se 16 in this and hdse 6103 and replicate however if you passage these viruses on human
airway cells and culture you can actually rapidly select out variants that can replicate efficiently
in human airways those viruses actually do not contain the mutations that would be had been
predicted by mike farson as being which were clearly responsible for the 2002-2003 epidemic
rather we saw changes um at positions 442 and 472 and 479 and so this is an interesting
presentation of the data where it seems like this single trial of putting a clone on a epithelial
cell culture a differentiated epithelial cell culture and then seeing sequence changes in the
consensus sequence he seems to talk about it like okay so we put the car on the road and it drove
down the road and then that's how it works and so if we did it again that's what would happen
and i don't think that that's really how virology works i think if he did this again he would get
different results here it might be a similar kind of selection process by which non-infectious
particles versus infectious particles are selected and and can be seen in in in subsequent passages
or detected in subsequent passages but that selection process is purely based on function
then it's not going to be based on fitness nothing is is fitness unless it's number of copies right
so then we're talking about a whole different thing and we're really only doing a selection
process we're taking the whole supernatant here there's there's no like you know
race to see who can make more copies of themselves we're not selecting based on fidelity or anything
like that in fact we have the argument that there has to be mutation rate otherwise there would be
a collapse so it's interesting um that's it's that's it mediated the cross species transmission
event so in reality we've done this a couple of times there's actually several pathways by which
the zoonautics are it could actually adapt and recognize the humanase receptor what's interesting
is that the epidemic strains actually efficiently use both the humanase receptor and the civetase
receptor when we in vitro select for human adapted strains on human airway culture
they actually lose the ability to recognize the civic receptor so what this data suggests
actually is that ours had existed in a transmission cycle between humans and civets actually probably
for several several years prior to the 2002-2003 epidemic allowing the virus to
regain the capacity to recognize both receptors okay so those were the easy ones to do
oh with an application um so now that we had a large panel of our of uh variant viruses we could
use those for therapeutic testing over vaccines in this case i'm going to show you an example of
about 30 human monoclonal antibodies that were derived by Antonio Lanzavecchia if you take those
30 monoclonals and test their ability to neutralize all the strains that we've made in the laboratory
you find some that only neutralize urbani some that neutralize all human strains some that neutralize
some civets but not all the animal strain but you do end up with four antibodies that neutralize
all strains we have in our portfolio including the ones that were in vitro adapted on human
airway culture importantly if you select for escape using these antibodies these antibodies
select for changes in different locations of the receptor binding domain
and in fact three of them actually don't overlap yes 109 the 230 and the 227
don't overlap and so these represent good therapeutic cocktails that would capture most of the
diversity that exists in SARS therapeutic cocktail what an interesting story we can tell there so
there's a guy by the name of plumber who used to work on AIDS in Canada who died at the beginning
of the pandemic he had a postdoc I think she was Chinese and she had a three antibody cocktail
called Z map that was trialed against remdesivir and was actually being trialed against remdesivir
probably at us amrit right before the pandemic and then it was shut down
so the trial comparing remdesivir with Z map was stopped this is all Kevin sorry this is all
marcoolax work here that I'm reciting from memory so we have an AIDS expert dying I think he fell
on the sidewalk or something crazy like that and we have this spy Chinese lady who supposedly
took some samples back to China and so she's a spy she she got put away but actually she was
like on the cover of magazines and stuff is being the star of of of biology one year for Z map it's
really cool because that was a three antibody cocktail this is also another proposed three
antibody cocktail as a as a pan by an antiviral that's pretty that's pretty cool I I'm starting
to see Ralph Barrett as a good guy it's weird and probably work in potential patients that would
be infected during future epidemics and these also actually protect young and aged animals from
lethal infection that was a paper published by Barry Rock in a couple papers now the civet
and the raccoon dog strains were the easy ones the true reservoir for SARS is within bat population
so if you look at a phylogenetic tree the human strains are shown here in red the civet strains
raccoon dog strains are shown in purple but the real variation is within the bat strain
um the reservoir it's thought that these were probably the reservoir for the
emergence of the virus now these are about 80 to 90 percent identical to SARS they can't be
cultured and they exist to sequence signature signatures in silico there's also extensive
variation see they can't be cultured they exist as sequence signatures in silico well that just
means they're stored on a computer they're keyboard viruses and so clones are really really important
because you can take a virus that you've only detected in the wild as a sequence and create
large quantities of that RNA and electropyrated into cells and get those cells to run it through
their ribosomes and package it the only thing you can't do sometimes is passage it
but the cells can be made to take the RNA up they can be it can be electropyrated in
you can use lip effectamine to get it in and then those cells will read the RNA and those
proteins will produce and the sub genomic RNAs will be produced and everything will be packaged
up and then you'll get this this effect this is cool because this is really underscoring
that downplaying the clones is just it's absurd it's absurd it is a bedrock methodology of RNA
virology through the replicase and elsewhere in the genome so when we decided we were going to
synthetically resurrect the entire virus now before we started it's important to note this is a
the cryoem reconstruction of the SARS glycoprotein spike notice that there are three receptor binding
domains shown here in with bubbles that actually engage the ACE2 receptor if you look at the sequence
the receptor binding domain shown here in yellow there's a large amount of sequence variation
especially within the contact interface residues that engage the human ACE receptor
and in fact there's only four of 13 contact interface residues that are retained in these
fat strains but we don't actually think it's going to use the human ACE receptor to get into cells
in fact we think we're going to have a tough time culturing the virus now it's important to note
that the SARS RBD that is was identified has been proposed by a couple of groups that it may have
been introduced by recombination processes from unknown strains that haven't yet been identified
and that that led to the initial cross-species transmission events now to get back to the
issue of in silico sequences they actually represent hypothetical viruses most synthetic viruses that
have been resurrected to this point actually we knew that the sequence was infectious in this case
we actually don't know which of the sequences in GenBank were infectious if any so to do that
with an error rate in GenBank ranging from about one to five hundred to one to ten thousand depending
on the sequence we had to do extensive bioinformatic analysis to identify what we thought was the likely
consensus sequence well that sounds like that sequencing is a lot more hairy than i thought it was
I just thought sequences were sequences you get one it just kind of spits it out
beep beep beep beep beep beep beep beep beep beep beep beep beep beep beep beep beep beep beep
then you just kind of read it off right now we're getting back to the Vincent Rancin yellow
explanation of consensus sequence the the more traditional Vincent Rancin yellow will say that
the consensus sequence might not even actually exist but Kevin McCurnan says that there are 15
million SARS-CoV-2 genomes on on gents said they're all real they're all independent they all come
from different people so they have to be real what's Ralph Barrick talking about here then
I see a battleship size incongruency between pre-COVID virology and post-COVID virology
I really do I really think we're on to something here I think with a couple weeks of work
this is going to be over and we're going to be able to you know incorporate all of these
various factions into a common explanation for why a lot of people were mistaken
why a lot of people were fooled why you could be taken all the way by no virus why you could
be taken all the way by lab leak why you could be taken all the way by my market zoneosis and
why you could be taken all the way by by any of these other in-betweens including
including iatrogenic murder
but in the end there's only one explanation that fits all of them that lets the most people on
earth be right and I think that's why everybody's so angry because the explanation that we are being
fooled into believing it's Ralph Barrick and Tony Fauci and eco-health alliance
instead of understanding that this technology was actually available available it was available
to us Amrit
probably for a couple decades right ever since they first did it with the polio virus
we have to wake up and apologize to our kids sooner or later we might as well do it now
none of the strains that we actually saw we thought was completely correct some of them had
deletions in the sequence of the five prime ends that we had to make some educated guess
the basic approach that we build coronavirus is using our molecular clone is shown here
with the SARS clone shown in blue is the clone is broken into six five kv about five kv thesis
each piece is flanked by bagel one restriction endonucleate sites these are class two S restriction
enzymes that recognize a palindromic sequence and so this is asymmetric and this is almost
certainly one of the enzymes that was mentioned in the foyer request that was recently released
and so the release of this enzyme or related enzymes as a list in an email or a supplementary
document or something like that is now being misconstrued as evidence that the diffuse proposal
is real and that they were making clones and that they were spraying them into bad caves and they
put fear and cleavage sites at the joint between S1 and S2 yada yada yada so most likely that's
why we're being fed this video is so that we get to this point right here and we see how clones
are assembled and now i'm sure he's about to tell us that this right here represents a S2 S1 S2
clone junction there so that they can substitute the S1 from other coronavirus is right in there
let's listen this allows since these ends are asymmetric they actually will not concatomerize
like classic sticky ends left by restriction enzymes but rather they become directional
so if you end clone A with a bagel site that leaves one three nucleotide overhags and the
five prime end of the B fragment with the complementary three nucleotide overhags they
totally get it directly you change different bagel sites at each piece it's midnight
assemble up into 30k B chromosomes like tinker toys like tinker toys like tinker toys
batching home that we made that's actually a good way to date somebody like do you know
what tinker toys man i had tinker toys you know i had lots of them like a lot of them i had a
lot of tinker toys i think i had like three of the cylindrical containers i could go down
with tinker toys hey by the way it's uh past midnight so technically speaking i just turned
52 years old yeah 52 52 years old how's that for old using blue heron and biobasic basically
is interchangeable with the urbanic clone the only real difference was that we broke the F
fragment into two pieces so that we could play with the receptor binding domain easily if this
thing didn't turn out to be infectious and in fact we made this clone we built the fool on cDNA we
drove transcripts electroprated that in the cells and we can see evidence of replication by
the synthesis of sub-genomic messenger RNA but we couldn't culture the virus and we couldn't pass
it from cell to cell ah we couldn't culture the virus we couldn't passage it from cell to cell so
they could see that the RNA was being sorted into sub-genomic RNAs but they couldn't passage it from
cell to cell does that mean it was not getting packaged or does that mean that it wasn't binding
in the next passage i think it wasn't binding in the next passage is the right explanation
which means that you could make virus from these clones you just have to have a receptive cell type
on the other end that's going to do it so they transfected listen carefully they transfected
this clone into that cell culture and it packaged virus for them you know it packaged virus because
it made the sub-genomic RNAs those were translated into the many many many copies of the proteins
and all this stuff happened it's just that when they took the supernatant off of that cell culture
and tried to put it on the next cell culture it didn't propagate and that has to do with the spike
protein receptor binding domain compatibility with the cell culture that you're using according to
their methodology explanation so let's listen to that again because i want you to hear what he did
he electroporated it into a cell culture but couldn't get it to jump from cell culture to cell
culture which is what culturing is what passaging is clearly there was RNA the cell and we could
clone we built the full-on cDNA we drove transcripts electroprated that in the cell and we can see
evidence of replication by the synthesis of sub-genomic messenger RNA but we couldn't
culture the virus and we couldn't pass it from cell to cell sub-genomic electroprated that and in fact
we made this clone we built the full-on cDNA we drove transcripts electroprated that in the cell
and we can see evidence of replication by the synthesis of sub-genomic messenger RNA
but we couldn't culture the virus and we couldn't pass it from cell to cell so clearly there was
probably a defect in entry to solve that problem we use literature data that has suggested that
RBD domains of coronaviruses may be interchangeable between species so we took the human
the urbani epidemic receptor-bonding domain that's 210 amino acids and went
and dropped that into the bat genome backbone producing a chimera with the receptor-bonding domain
driven from the epidemic strains now when we built that clone drove transcripts and electroprated
that in the cells we got a virus that could replicate quite efficiently this is just some
growth curve data showing I think the black box is the urbani wild type and the white circles are
open open symbols are the bat viruses you can see they replicate exactly as good as the urbani
epidemic strain at low and high multiplicities of infection they recognize the human ACE2 receptor
and dbt cells at low and high multiplicity infections and grow just like the epidemic strains
and they also retain the ability to use the CIVID ACE2 receptor just like the epidemic strains
low and high multiplicity they also are capable of infecting human airway epithelial cultures
and targeting ciliated cells just like the epidemic strain and they grow to similar titer
now if you make aniseera just against the bat spike like a protein
and use that aniseera to target the SARS wild type virus it will not neutralize that virus
so clearly aniseera and vaccines derived against epidemic strains are not going to protect against
the bat strains to use that same sera against the RBD chimeric virus you can neutralize it
indicating that there are neutralizing episodes that resist that exist outside the RBDs and if
you take the human monoclonal to target the epidemic strain RBDs you can neutralize these
virus with quite efficient so one thing that I think we all need to learn is exactly what neutralized
means in this context because I kind of was under the naive operation or operating under the naive
assumption that that neutralized means to bind to the receptor binding domains so that the receptor
binding domain is not able to interact with the receptor and therefore you don't get
infection so I thought that's what neutralizing was but I think neutralizing has more to do with
like precipitation and if you get enough antibodies stuck onto you then you come out of out of solution
and I'm wondering if it's something like this too like uh aggregation or something like that
that causes neutralization and precipitation so I need to learn that a little bit better because
I do know that that people like Mark Bailey and and uh Steven Lanka have been working on trying to
understand what it is that virologists are meaning with that and I do think that that is something
that we should be masters of here as well so I apologize for that so in summary um certainly
synthetic genomics and reverse genetics this can be a platform to recover uncultivatable
zoonotic precursors can be used to synthesize this is actually the largest synthetic virus
to date it's going to be a short record but it is a record um and you can use it now to identify
a broad spectrum antiviral from the vaccine clearly the RBDs are interchangeable uh this is with an
89 percent amino acid identity within the spike it's the minimal domain required to host shift
coronaviruses what is the phylogenetic limits to RBD interchange we actually don't know
clearly the human monoclonals and vaccines targeting the SARS RBD would provide protective
immunity against natural isolates that emerge that's not my sound the overall process is in
future or unfortunately by deliberate design so now I want to move to the next part of the
talk which is synthetic the optimization scheme to attenuate SARS coronavirus pathogenesis
this is the maturation pathway okay so after as he explains the maturation pathway I want you to
imagine that we're trying to solve the puzzle of the infectious cycle as well and then I also
want you to listen carefully to the amount of effort time thought and ideas that are going into
the attenuation of coronaviruses and a general strategy to attenuate all coronaviruses specifically
in the context of recombination and so he's keenly aware that there's a problem with the
oral poliovirus vaccine that when you give the oral poliovirus vaccine it can mix with other
polioviruses in the gut of people and then become active polio again and he's at least
theoretically aware of the possibility that should you make a de attenuated coronavirus like say
take out some genes then it would be very easy for that clone that you're using as an attenuated
virus to attain that gene to acquire that gene from a co-infection and so what he's going to explain
to you is how these translational regulatory sequences can be altered in such a way to prevent
recombination with wild type viruses that's his strategy I think it's a pretty cool idea
it suggests that these self-replicating RNAs are are some kind of a real biological phenomenon
and it suggests that making infectious clones of them is a really handy way of exploring the
variation within them that is otherwise un-intractable by laboratory means so here we go again I
apologize that this is such a fuzzy thing but I will try to help you follow along way for how
far it gets out of the cell the nuclei caps is the line underneath an intermediate compartment
in the ruffiardology with a M glycoprotein and the E-protein are expressed and then these the M
and the E-protein actually drive the assembly of virion which then mature in the Golgi and then
are released in the cell and secretory vesicles which fuse the last membrane. Now if you knock out
E-protein expression this pathway is still viable but you reduce virus yields by about two logs
and if you knock out the M glycoprotein expression or M and E together you don't make any virus
so M protein will stop without the M protein nothing happens the E-protein will still
get some viral production I wonder what they mean by that I guess it's just detectable RNA in the
supernatant. So our approach to de-optimize SARS
coronavirus the SARS coronavirus genome and to attenuate pathogenesis focused primarily on the
E and the M glycoprotein genes of about 350 amino acids in total. The strategy we used was to
progressively increase the number of de-optimized codons so we started with serine to produce a
D-serve virus serine-loosing R gene to produce the SLR de-optimized strain or a five-set DSLR
VA strain basically the idea is you create a real stat where you're increasing the number of
de-optimized residues and turning down expression of critical proteins needed for release.
So that's an interesting strategy right he's changing the codons
not changing the codons like to different different amino acids but he's changing the amino acid
codons so that they're not as they're not what they were in the virus which he assumes is optimized
which I think is a pretty cool thing because the the assumption for the mRNA
transfection is that the viral codon selection the the actual codons used by the virus are not
important and in fact we can change them to whatever we want so that we get more protein
and we can even chemically alter the RNA with M1 pseudo-uridine alteration so that's fine
we don't care about that either even though here Ralph Barrick is saying that just by changing
these synonymous codons for one or two or five amino acids he can progressively attenuate
viral production he can hamper viral production he can handicap the virus just by changing its
codons this is pretty antithetical to the idea that Moderna can just change those codons and
it doesn't matter at all right that's that's pretty impressive this is just a cartoon to show
amino acid sequence and the wild type virus sequence here so like in the three set at the
searing residue which was optimal in the case of SARS we just change it to the most
rare codon if you look at the statistics here in general in the wild type E and M gene they're
about 39 codons that are de-optimized in the one set this increased to 52 the three set 94 and the
five set 134 so they're only de-optimizing the codons of the M or the E protein which is even more of a
subtle modification think about that so look at the ct ctb values that Eckerd just talked about
by these values here so these are very minimally
on the negative side of the codon pair usage we also made random controls where we scrambled
the codon usage much like Eckerd did retaining the wild type genome organization lightless and we
made three set in the five set this is we made these in a mouse adapted background so they would
be pathogenic in mice mouse adapted growth is shown here black the blue lines show the searing
de-optimized viruses which also reach high titers by about 24 hours post-infection if you look at
the three set mutants however you see about a log log and a half reduction as compared to wild
type the three set randomized virus and the five set randomized virus in this case i'm showing
two different plaques and the five set randomized viruses through just about like wild type so just
like Eckerd had reported if you randomized the sequence it really has very little impact on
replication but the optimization does affect final yield now in contrast to what Eckerd talked
about we actually deoptimized in the middle of the downstream ores which would potentially affect
critical sequences that would affect RNA synthesis we're very careful not to knock out any known
sequences regulatory sequences that make messenger RNA however both the searing and the SLR mu knocked
out messenger RNA six expression which you can see right here these actually were the messages
the genes the messages that encode the gene so this is supposed to be a northern blot where
the darkness is supposed to show you RNA so this isn't a very clean blot there's an awful lot of
what is this i mean holy balls you're not getting a clear signal here certainly i mean
i don't know what i see here but that's not what i would expect to see um he's looking for sub-genomic
RNAs i guess so this would be the full genome up here i don't know that that's what i would assume
um it's two hours and i don't think he's going to say very much i'm just going to leave it go but i'm
going to say very much i'm just going to leave it go but i might put it on a little faster and i
got to get to bed holy cow it's my birthday today tomorrow so we deoptimized so we actually found
some evidence of long-range RNA RNA interactions that are regulatory elements that we're trying to
decipher the five set the optimized trains showed no cpe in culture if you develop primaries to the
five prime end of the genome and the leader sequence and a primer down here in the message six
that encodes work six you can actually identify leader containing transcripts which are signatures
of the messenger RNAs that are made during infected cells in these cultures you can see evidence of
message seven i'm sorry message six five four and three this is a day one post-transfection
even by day ten you can still see these transcripts infected cells and they continue at that level
with about five passages at five-day intervals but you actually never can actually develop
a virus you can never plaque a virus you can never actually show a virus is there producing cpe
so that's interesting so now he's looking at how the RNA signal develops over days of passage
and he he shows how the robustness disappears i think that's kind of cool
um i don't see a control here though i don't see how the RNA sustains over in days when it's
not attenuated that would be a nice control to have here right um anyway i think this is where
he's going to end it he's probably just going to close he had deoptimization he's going to show
these three different ways that they did it and the sites that they changed and then he shows
pathogenesis of these things in the mice he made a mouse adapted version of it for aged mice um
it's an it's an it's an oh these are all papers that we've looked at before they're all relevant for
the clone discussion because the clone discussion puts us in um the context of the pandemic and
trying to explain what's happening here i want to just leave you with the slide that i put up
earlier um with regard to alina chan um and kevin mccurnan's objection that uh maybe there should be
some some so ask yourself why he's making six-hour scooby-doo videos instead of downloading data
from ncbi and find a signal for his hypothesis in real data if the clones offer some advantage
for dr evil surely there is evidence of reduced mutation rates to prove this and i would humbly
submit that actually alina chan and employee of the broad institute for whom your uh old boss is
now the director for quite some time um has data from the beginning of the pandemic that seems to
show a much lower mutation rate in the sars 2 sequences than those found during a similar time
frame in the sars pandemic which might be the reduced mutation rate you were looking for um
we have a long ways to go we got a lot of stuff to talk about but i'm not really worried the reason
why i'm not worried is because people have lose in their minds and when people lose their minds
it usually means that you're right over the target have never seen so many people lose their
mind at once and i've never seen so many people do it that weren't doing it together before
um people are coming together and retweeting and talking to one another and patting each other
on the back that heretofore have never really interacted in that way before and that's pretty
special not only that but it's brought together a few of these dream team members and uh i think
the spontaneous sort of confluence of efforts are going to become obvious what everybody's
arguing about is we all got to come together because because because i'm making exactly the
opposite argument i don't need to come together with anybody because if we are fighting for the
same things then our our efforts will buy necessity and buy natural
by natural order where they will they will become a confluence of effort toward the same goals
my goal is to have our children realize that the vaccine schedule in america is a criminal
enterprise my goal is to have our children realize that virology especially RNA virology
is wholly dependent on cloning technology and in fact a pandemic could not have occurred in
the way that they said it is no matter how much they insist that the sequences are here and not
there or that they're real or they're not they are lying about the fidelity and that's all that i
can say and and all this this insistence is not good enough they need to start teaching because
that's what we're doing that's what we've been doing for three and a half years no one else is doing it
just us just here and so if you like what we're doing you like what we've done
please support our work go to get your own biological and subscribe share the work if you can
we are gaining momentum tomorrow is my birthday but i will be on i'm going to try and be on as
often as literally as often as possible i don't know if it's going to be every day or not
um but i really am targeting every day but i also have other things that i'm trying to get
regular with including the sub stack i don't think i'm going to make a sub stack and transcript of
this one but i want to do it for a lot of them and so i don't know if you've noticed it or not but
there is a sub stack now the sub stack has videos that are on vimeo um those videos i've added
uh i've added subtitles to and so that makes them also kind of um better to watch you can also
share them a little bit better the sub stack maybe is a better way to share them because people can
scan the the the transcript as well and so wolf gang wodocks interview is up there um my presentation
to the uk doctors is up there um and uh i'm just going to keep trying to do it every time i get a
stream that i think is good enough or is worthy of it um we're going to do a sub stack on it i
don't think i'm going to do this one because tomorrow i'm going to try and do if all goes well
i'm going to try and do a pretty decent show tomorrow um but it's a birthday and i've got two
basketball games so i don't know there's going to be a show and it's don't know if it's going to be
slam-bam crazy show or if it's just going to be an average show like this one was but anyway
we've got the momentum going again or at least i got it going tonight and so hopefully i can get
some sleep and uh get it going tomorrow again and uh we'll get this this pace up to speed thank you
very much for joining me and i will definitely see you again tomorrow
i have no responsibility for the current pandemic