Ladies and gentlemen, welcome back once again to the Rounding the Earth podcast.
Rounding the Earth is a multimedia education project based on the popular newsletter series
published on Substack written by applied statistician and educator Matthew Crawford.
Topics of discussion range from critical analysis of conventional wisdom to Bitcoin and everything
in between, in particular the ongoing plandemonium, so called.
Our goal is a careful examination of important topics and perspectives shaping the world
that too few people talk about.
Subscribe to Rounding the Earth on Locals, Substack and Rumble to join a burgeoning research
community and to help us unflatten the earth.
Shout out to all of our BitChute viewers.
My name is Liam Sturgis.
I am a musician, music producer and writer slash editor coming at you live from the beautiful
Vancouver, British Columbia, Canada, and I will be your host for today.
And now please allow me to introduce the author of Rounding the Earth and my cohost for the
podcast, Matthew Crawford.
Good afternoon, Matthew.
Good afternoon.
Have you, you've never been to Vancouver?
I have.
Well, no, no, no.
Um, okay.
So I'm actually technically not sure.
It was a while.
I have not.
Um, I went to, um, uh, Tillicum Village is the closest I've been.
Do you know where that is?
I think I'm saying that right.
That this is like, this is way back in high school.
Uh, I was in Seattle.
Okay.
And I know that, um, we went to this like island, um, that I guess is still, you know,
Washington, but, uh, technically I've only actually crossed into Canada once.
And that was, that was actually way back in middle school.
Um, like just, uh, Windsor, like across from Detroit.
Yeah.
The other side of Canada.
So that's the only time you've ever actually been in Canada.
Let's see.
Unfortunately, unfortunately.
And so I've been close several times.
I've been in upstate New York near the Niagara area and I've been in, uh, in the state of
Washington.
Um, uh, so no, I have not been to Vancouver.
Well you're welcome anytime and this came up because, uh, we have, uh, uh, one of our
lovely guests for today who, well, I don't want to give away too many details, but let's
just say we were talking about Vancouver and let's get her thoughts on my beautiful hometown
and others, uh, allow us to introduce our guest, Jessica Rose.
How are you Jess?
Yes, I am beautiful.
Yes, you are.
Um, now I don't want to give away details of your recent trip, but, uh, what are your
thoughts on that?
So we can talk about it.
Well, so you were in Vancouver.
Give me all of your best compliments about my lovely city.
See, the thing is I've been there many times and it never made the impression that it made
on me this time.
So it's probably more that I've changed since last being there, but I found myself really
aligned with it, um, which is nice.
I mean, it's always nice to find alignment when you travel.
Um, I was, I was just stricken mostly by how much you could walk and, and where you could
walk anywhere, which, uh, like I can go to the dangerous areas, but, um, like East Hastings
or whatever, but like I, I didn't feel restricted in my wandering, which I really appreciate.
Um, lots of green spaces, um, huge trees like ancient trees, which I really love, um, in
Stanley Park.
And I didn't see any mountain stuff.
Well, I mean, I did see, but I didn't experience the mountains this time.
Um, nice people, uh, lots of variety, um, in what you can, um, I suppose experience
in food.
Oh yeah.
Well, well, yeah, but it was very expensive.
I was shocked by how much food has risen in cost, um, in BC at least, cause that's, that's
where I was.
Um, eight bucks for a loaf of bread, for example.
I mean, I just, I was literally blown away by that every time I asked, uh, you know,
for my, my price or whatever, for the thing I wanted to buy, I was literally just like
in goth mode.
Like what, what, you know, how, how are people living, you know, day to day who have families
and stuff.
But, um, anyway, the good stuff, uh, it's beautiful.
It's spring.
So the weather was, it was just, I don't know if it was because I was there, but it was
just spectacular the whole time I was there.
Like it was, it was warmer in, on the mainland than it was on the island.
Cause I was also on the island on Vancouver Island, but, um, yeah, it was, I was surprised
it was only three days.
So I probably just had some kind of honeymoon experience.
You know what I mean?
It's like, but I mean, it was, I liked it.
It was, it was a nice time.
Well, I'm really happy you got to come back.
Cause for those who don't know, Jessica is Canadian, been living in Israel for, uh, for
how many years now?
Uh, I don't know forever.
Long enough that one forgets.
Um, and you tell it like, just, just broadly, you, you went to other parts of Canada as
well.
Give us just the Coles notes of the rest of your trip.
Um, Victoria was nice.
Uh, it was changed though, from the last time I've seen it because of the COVID shit.
Um, just kind of more rep oppressed, more homelessness, uh, more, I don't know how to
describe it.
It was something in the people that you felt when you walked by them.
And it's always kind of been there in Victoria, like Victoria is kind of a weird population
of like people who go there because they want to be homeless because it's warm and old people.
So there's kind of like a non communication there anyway, amongst, you know, the community,
but it seems enhanced somehow.
It might've just been me because I'm, you know, I'm like a tourist or whatever, but,
um, it's also the capital of the province.
It's like our Washington DC or our Ottawa, you know?
So I think there's a lot of stuck up types.
There's a lot of government people who live there.
That might be it.
No, you're absolutely right.
Yeah.
No, there was a lot of stick up or I noticed that too.
Um, but yeah, it was beautiful as well.
I mean, it's, uh, lots of flowers, natural beauty, um, enormous amounts of wealth, which
was, um, crazy.
I mean, there's no two homes that look anything alike.
I mean, this, this is a more to do with the architecture, but it was, yeah, it was, it
struck me how everybody had a unique home with land.
It's not something that you experience in many parts of the world anymore.
Um, and I went to Pender Island, which is one of the smaller islands that you were probably
close to Matthew.
Um, and that was lovely.
Um, you know, small community, everybody knows each other type thing.
Um, but yeah, I just, I tried to experience as much of the nature as I could.
Um, and, and I found plenty.
So yeah, I was, it was a hectic time.
It was quick, but it was, it was nice.
Um, I was pleasantly surprised because I thought there was going to be a lot more, um, stuff
that would make me want to throw things.
Yeah.
Come at the tail end of that and hopefully not the calm, you know, in between storms.
Uh, well, I'm glad you had a good time.
And as you suggest, next time you come, we're going to get our drink on drink referring
to tea, of course we're going to, in fact, we should, we should do high tea.
There's a bunch of high places here where we can just pretend we're royalty.
Now let's talk that.
And this looks nice.
What is this?
Oh, I just looked up Vancouver trees.
Just to see if I can see some pictures.
What's that?
It looks like Stanley park.
There are some massive cedars there.
I mean, you could make an entire ship out of one of these trees.
Not, not that I want to cut any trees down.
No way.
Wow.
Look at that.
Where's that?
Oh, let's see.
Oh, Capilano suspension bridge.
So that is on the North shore.
That is, I wouldn't walk there, but it's so close to where I live.
Um, and yeah, you can go over a big, uh, uh, a big, well, a very tall bridge that freaks
people out, um, over a waterfall that you don't want to fall into.
Uh, but it's just so beautiful.
Okay.
Well, if the world goes mad max, let's just take that area over and build a tree house
and well, they're already built.
That's the best part.
Um, well, this is awesome.
Um, now today, so we've got Jessica with us now and it looks as though we've got Jumi
coming in a little bit later and I think JJ is still coming in a bit later as well.
So, um, do you guys want to officially get started with our second monthly, awfully interesting
science journal club?
Yeah, might as well.
I was actually, I thought I was, um, uh, throwing a paper in that would be kind of like, um,
you know, one that we would tack on or, or if we had extra time or something like that,
because, um, you know, here we are with so many scientists who, I mean, there's so many
papers that have to be read constantly.
Right.
Um, so, you know, I figured there was going to be something that was going to be very
sort of timely and upfront.
I was going to throw this one in as an example of, uh, of the science that looks sort of
Orwellian upfront.
Um, and we do have Jumi now.
Hey, okay.
Jumi, welcome.
Hey, how are you, Jumi?
Good.
Well, we're doing a little bit slower introduction than usual.
We haven't even gotten started with the first paper because, uh, Jessica has been telling
us about all the awesomeness of Vancouver and, and of course Liam's, uh, Liam's eating
that up.
So I am, um, Jumi, uh, uh, how are you doing?
How have you been since we last spoke?
I'm doing well.
Very well.
Excellent.
Um, what, what's new in your world of science and other exciting things and orthodontist
appointments?
Yeah, I came from an orthodontist appointment.
I had invisalign and straightened out my teeth and everything.
Um, now yeah, same old, just, uh, write my sub stack, you know?
Um, yeah, it's kind of funny how some people, um, are interested in certain types of articles
and sometimes I don't want to write those articles, but I can see what people are interested
in is a little different sometimes than what I want to write, you know, interesting.
Like what?
Um, I think sometimes I want to like write about things having to do with like general
science and like, you know, like, um, sometimes like what, like there was this paper, it was
like a sociology paper and it seemed like from what they found, like large fields of
science, um, sometimes people will just hone in on like the top few papers and they'll
ignore the rest, you know, which is kind of interesting, right?
Um, but maybe it was the way I wrote it.
I don't, I don't know if anyone read that article, but anyway, it's fine.
And people want to read about like vaccine injuries too.
I get it.
So that's my audience, I think.
So you're finding yourself, uh, aimed in the direction of what your audience wants to hear.
I think, and we've had other, like JJ has been, um, making some really good points about
that lately.
That maybe that phenomenon of if you have something that I suppose in your instance,
we're talking about the audience seems to want to hear something.
So there's pressure to then write about that.
Um, do you, Jessica and Matthew as prolific substackers yourself, do you relate to this?
You guys were nodding emphatically.
Well, I mean, I, I, ultimately I got into substack because I had all this writing that
I was already doing on like, you know, the chloroquine wars, the early treatment medicines
initially and then, and then also, um, uh, when Monica Hughes called me and said, um,
yeah, you need to start taking a look at the vaccine statistics in early 2021 after I'd
been already writing for a year about the early treatment medicines.
Um, so, so in a sense I kind of ran toward that, but I, you know, if I hadn't, I could
certainly see that, uh, that's what people, you know, want to be talking about and hearing
about because they're trying to make sense of it because there isn't a lot of sense in
a lot of what's gone on.
So, um, and, and, and I think people are, people are, uh, terrified and rightfully so
of the amount of change that's going on in the world.
And so if people can find a way to shuffle the deck, uh, I don't know, in a natural way,
then maybe they can create an orderly amount of disorder in the world again or something
like that.
Right.
Like, like people, people want, um, people want to push the clock back to, um, when it
was that it didn't seem like controlled horror.
Yes.
People want, uh, those, those who can be honest and understand science to be writing about
it, uh, right now.
So I, yeah, uh, it doesn't shock me at all that, that Jimmy would get pressure or we,
not pressure, but like, you know, um, interest encouragement from an audience to, to be,
you know, doing those things.
And she writes, uh, unique articles, uh, you know, in so far as, you know, pandemic science
is concerned.
So, um, you know, Jimmy being sort of outside of the pressure of, uh, the mainstream academia,
um, means that, uh, she is, she has been able to be, you know, a more free voice and has
put enough care into, you know, writing articles that people didn't want to see.
So yeah, I can see why people appreciate it.
Jessica, do you find the same, uh, the same phenomenon in your work?
Um, not as much.
Absolutely.
I, I read a lot.
If I had the time, I'd read all of the comments, but sometimes the hundreds and, um, my readers,
I swear, like, um, Substack is so wonderful for its ability to, to bring together really,
really interesting and smart people.
Like my, my readers are so cool.
Um, they give me feedback on, on, on things that I write about that make me feel like
I didn't even understand what I was saying when I wrote it, but they do, which is really
interesting because it was through the process of reading what I wrote that they understood
something.
You know what I mean?
So it's like this interesting feedback and I wrote one lately.
Um, it's the first one I've written in like two and a half weeks.
Um, it was my, my, uh, my answer to I can define a woman, you know, cause there's a
lot of these people out there these days who can't seem to define, uh, what a woman is
when asked.
Um, so I thought enough.
So I wrote a set.
So apparently that's funny.
You say that because I said I can define a woman and it's not because I'm a biologist.
That's actually the title.
So yeah, I got so much positive feedback from this and a lot of people said, this is my
favorite piece of writing that you've churned out.
Like I mean, okay, maybe they like it more because it's not some jargon about immunology,
but uh, yeah, I find, um, a lot of the articles that I write on the fly that I don't think
about, it's just like something I need to get out of my head are the ones that people
respond to the most.
And so if anything is requested, it's, it's more of those personal stories.
Cause I agree with what everybody, you know, you guys are saying, I think that people are
really looking to have some, someone to relate to because if everything's crazy, it's like,
what the hell did I just see on Twitter or what did I just hear in the news or what did
just happen in my kid's school?
Like, I feel like I'm in loopy land.
So it's, it's, it's very grounding.
Um, reading a lot of the, the sub stackers is his work.
So I'm happy that, uh, that I can be one of those, um, grounds for people, uh, cause it
really helps me too.
Cause it's like, you know, I, I learn a lot when I write these things, like what a woman
is anyway.
Yeah.
I just came back and we're defining what a woman is, which is fascinating.
Well, there's a new paper out on it.
Yeah.
Not a paper.
Well, I'm curious what Matthew's definition of a woman is.
I hate to put you on the spot like this.
I know it's controversial.
Come on.
It's someone who identifies.
Now for the, for what is potentially the actual answer to that question, um, reminder in the
description, no matter where you're watching, I have put these sub stack links for do me
for Jessica and for JJ.
So don't hesitate to go and get caught up if you haven't yet, if somehow you haven't
yet subscribed, um, you guys should do that.
Um, so let's use this opportunity to, um, jump in.
Is there, Oh, very nice.
So yes, I think all four of us have cats somewhere in our background.
Mine are currently hiding behind my green screen.
They are.
Oh, there's a, um, so let's use this opportunity.
Let's jump in now, Matthew, you've got a paper pull up.
Do you want to, what, what, what is this?
What are we going to look at here?
Okay.
Um, this is a paper.
This was interesting.
Uh, it's one that I came across, uh, during the pandemic in 2021, um, because Eric Topol
had tweeted it out and it was, um, it was about whether, um, well, I guess, I guess,
uh, we could, uh, take a look at the abstract here, but it's, it's about selection pressure.
And um, and the interesting thing about the paper to me, well, it's about selection pressure
on SARS-CoV-2, right.
And like emerging variants.
Um, and well, you know, let's take a look at the paper.
Um, it's going to involve sort of a unique statistic, um, called Tajima's D. So before
we actually, um, get into reading the paper, I was going to ask, um, if, uh, either Jessica
or Jumi has like a common sense explanation for Tajima's D because, um, it was something
that, uh, like for me, my familiarity was actually only what my wife had mentioned in
passing conversations before.
So I actually had to look up Tajima's D and learn a little bit about it in order to read
the paper.
Um, and, and that's the way, you know, uh, statistics goes sometimes, right?
Like you have this, this metric that gets used in a field.
Um, and if you're not familiar with it, you just look it up, you'll learn a little bit
about it.
And, uh, and so, yeah, what, what is there, is there Jessica or Jumi, are you, are either
of you familiar enough with Tajima's D to, uh, to give it some sort of like a, a common
sense explanation?
I am not.
Sorry.
Okay.
Well, I'm going to do my best having looked it up in fact, and maybe I'll just, um, I'll
pull up a Wikipedia article.
Now I do before you answer, JJ is in the background and he might have, he might have an answer
to that question.
I don't want to bring him in while he's in mid he's, he's eating something.
So I don't want to be that guy who, who jumps him in without permission, but this, if he
has an, okay, I'm going to bring him in.
I'm going to bring him in.
Sorry.
I was eating, I was eating my oatmeal.
Was it Tajima's oatmeal?
No.
Why don't you take a shot at explaining it first and then if, if I can't augment it,
then I won't.
Okay.
Um, well, so they're, they're it within micro revolution, you've got like a genetic strand
and you've got two different things going on with mutation.
Statistically, one of them would be, um, mutation rate and one of them would be mutation frequency.
And mutation frequency is just how often one of these, um, you know, like 30,000 for, for
Sarge Cove two, you know, we'll just say at 30,000 nucleotide sequence of any sort.
And these individual nucleotides, uh, have these single nucleotide polymorphisms.
That's how most of it occurs.
Right.
So like, you know, a little change here, change there, you know, an A, a T, a C, a G, whatever,
um, and they happen all over the strand at random intervals.
And uh, and so those are single nucleotide polymorphisms snips.
Your mutation frequency would be how often one of those blips occurs.
One of those snips snips occurs.
So there's mutation frequency and then there's, and you know, you could describe that as,
as some amount, you know, some number of snips over some period of time.
Um, and it doesn't necessarily have to be snips.
You can have insertions and deletions, but most of it's snips.
Um, but then there's, there's mutation rate, which is actually how far, um, that sequence
drifts from its original position, right?
You have this original state and it's sort of hard to imagine what drift is because in
essence you've got this like 30,000 dimension, yeah, 30,000 Taurus dimension, you know,
um, model of, of what that nucleotide sequence is.
But um, you know, if, if you've got like a cluster of genomes and then it, it sort of
moves in it, you know, outward in a direction, I kind of, I kind of try to imagine it as
Conway's game of life and, uh, and thinking about, oh gosh, maybe I should, uh, I should
restart this.
Um, thinking about what would happen if you started sort of, you know, evolutionary progression,
but then let's see, what am I able to do?
But then you have like some sort of, um, something in the mix that pushes the, what would be
the natural evolution in one direction, right?
Um, so the changes are pushed.
So this line that I'm drawing is, is, is perhaps an evolutionary pressure.
And you can see that the original guy, it's so small, the original, you know, thing was
like right in here, right, but all the changes are happening, you know, further to the right
in the screen mostly, because that's where I'm, I don't know, putting pressure on the
screen.
I don't know if I, if I said that in a way that's sort of understandable or not, but
you wind up with not just the mutation frequency, but the mutation rate would be, um, a measure
of how fast ultimately those two things happen in combination.
And Taj Mahdi specifically, let's see, um, and I'll have to go back and read exactly
how it's computed again.
Um, but specifically it is an interplay between mutation frequency and mutation rate, uh,
like a ratio between these things.
So how, how close am I, JJ?
Um, well, as I understand it, you're not too far off.
It gets more, I was going to see if I could find a paper that would help us do this.
Cause it's, I'm still, I'm still getting a grasp on, on how this stuff all manifests.
But the, the gist of it is all the, another thing that you should have in the, in your
model in your head is the idea that when changes are made that are silent nucleotide polymorphisms,
that doesn't mean that nothing has changed.
So, um, there was a science paper in 2011 that had a cover on it where the zipper on
its mouth of a lady and the cartoon was a zipper on the mouth that was being opened
because this science article was trying to talk about something that geneticists didn't
want to talk about, which is that a lot of the genetic disorders that we have in humans
are actually defined by polymorphisms, which don't change the amino acid.
They're silent mutations and these silent mutations for whatever reason, change the
tertiary structure of the protein or how it's regulated or how it gets us for related or
how it gets guy class.
We don't know, but the end result is, is that the redundancy of this code, which they are
using to describe whether or not the, the virus is changing in response to vaccination,
um, is something that they, they understand how it occurs and they understand the mechanism
by which it occurs.
And the basis for which it occurs is something that they're not acknowledging.
I'm kind of, because of the fact that, that the silent mutations are not silent.
So they label this as, as synonymous or non-synonymous mutations.
And they're trying to give you the idea that synonymous mutations don't do anything.
And non-synonymous stations do, but in reality there's evolutionary pressure on both of those
changes because it's likely that the synonymous change is not synonymous except for that.
It doesn't change the amino acid, but it likely has some, some impact on the tertiary structure
of the protein or how it is post translationally modulate modulated or how the mRNA is pre
translationally modulated or post translationally regulated.
And that's how all of these silent mutations result in genetic diseases.
And it's also how they are oversimplifying the signal to try and describe whether the
viruses is changing in response to the, the vaccination or not, because in reality we
expect to see these changes in a certain ratio.
And that certain ratio seems to be independent of the preservation of the protein in the
spike, but with other proteins, and this is getting too deep, maybe, but other proteins
are more functionally constrained so that even single nucleotide polymorphisms result
in loss of function.
So you can imagine a perfectly constructed enzyme is also dependent on the exact sequence
that's there because if you change a silent mutation will result in a slight folding,
which will result in a loss of efficiency of that enzyme.
It's very likely that the RNA dependent RNA polymerase and its associated proteins are
all highly constrained.
That's why they're very homologous across all these coronaviruses, whereas the spike
protein isn't.
And what they find in this paper is that there are very many parts of the spike protein that
are almost doesn't matter what they change to.
And so if you vaccinate people to that protein, there's lots of room for it to change and
avoid this memory, whereas all these other proteins don't have that space within which
to maneuver because they're already so functionally constrained.
And so they're trying to tell a story that this is a signal of evolution when in reality
they're not being very precise about what these changes mean and don't mean and make
very simple about how synonymous means one thing and non-synonymous means another.
It's much worse than that.
There are a bunch of questions I would want to ask, but I feel like we would wind up going
down the virus-like particle rabbit hole.
And I want to steer us toward the actual purpose of today, which is to take a look at a scientific
paper and see what it is that we can do.
And so the audience can watch what happens when several people together pick apart a
paper.
And I may even go out and find Eric Topol's tweet because it's actually, it's kind of
funny.
I'd like to hear what he said.
Well, I think he had no idea what the paper said, which reads even though abstracted or
even reads contradictory to me, right?
I mean, I contradict themselves in the abstract as far as I can tell.
Okay.
So let's take a look at the paper.
And that was my interpretation was that the authors stated something that was very, very
different from what their actual data showed.
Yeah.
They say in the abstract that full vaccination against COVID-19 with other mitigation strategies
is critical to suppress emergent mutations, but then their data shows that the fully vaccinated
people are producing the mutations.
It's extraordinary.
Right.
Okay.
So yeah.
So let's see, what is their statement taken together?
Our data suggests that vaccination plays an important role in the purifying selection
force of SARS-CoV-2 Delta variants.
Purifying selection force is with you, young Skywalker.
So any other thoughts on this?
Has everybody read the paper?
I skimmed it.
I have not, sorry.
Okay.
But it's very confusing.
I have the same impression from having skimmed it.
Jumi has to clean the chalkboards when we're done then.
Okay, because this is going to be a little harder than usual because there's more probably
math that's new math to the average reader.
This is not as easy to read as a lot of biology papers, but you know, so here's the abstract
to say our data suggests that vaccination plays an important role in the purifying
selection force.
Oh my gosh.
I forgot that part.
I don't know.
I skimmed it very much.
You all skipped it.
If you all skimmed it, if you didn't see the first sentence in the introduction and start
laughing COVID-19 vaccination resistance has become a major challenge to prevent global
SARS-CoV-2 transmission.
Can I write off the back?
And then the introduction says legally required vaccination against various infectious diseases
and essential to public health policy in many countries.
Damn.
Yeah.
Okay.
See, I was going to point out the word resistance has multiple meanings, neither of which is
it's not clear which one it is.
Right.
Talking about supposed emerging variants because of the immune pressure.
So there's perhaps a resistance there, but no, they quite clearly because of later in
the introduction mean I don't want your shot that qualifies as resistance vaccine resistance.
Yikes.
Yeah.
I've actually wondered multiple times or many times during the pandemic if there is an attempt
at lying without lying going on in many places, signaling information anyway.
So introduction legally required vaccination against infectious disease is essential to
public health policy in many countries.
Okay.
So let's see, where do we get to?
Where we get to the point here?
Get blathering till we get down here.
Is there a correlation between mutation frequency and vaccination?
Okay.
And so as I said, there's mutation frequency and there's mutation rate.
Frequency is just, you know, that's how often things are changing along that strand.
That's how often you have the snips.
So let's see, to explore this question, we analyze the correlation between the rates
of full vaccination and the point mutation frequency.
So they look at data, you know, collected from 20 different countries from these genomes.
And this assumes that all of this, this assumes that all this data is collected with high
fidelity.
But you know, that's a question left for another time.
They're taking in data.
And so they find that mutation frequency is logarithmically reduced as the full vaccination
rate increased in most countries.
And does that make sense?
You know, intuitively, does that make sense?
Yeah, the purifying selection.
Yeah, it makes sense to me.
If you're sort of cutting off, you know, if you think of the potential genomes as this,
you know, 30,000 dimension space, right?
A selection pressure is something that takes away some of the domain of that space.
So you know, you wouldn't really have snips into that space that there's pressure to avoid.
So you would think that you would have reduced mutation frequency.
So that part makes sense to me intuitively.
And I would have said so if I were writing this paper, I would say I would expect this
to occur, you know, just on a pure mathematical basis, if all the space were open, not that
it is, but if or, you know, even if a subset of the space is open, and you cut off some
other subset within that, then you have, you know, less domain for this thing to get into,
you know, for genetic sequences to be, to emerge into, right?
So okay, so that makes sense to me.
So to our knowledge, this is the first evidence suggesting that vaccinations could successfully
suppress viral mutations.
Okay.
So I mean, we have an expectation, and we're seeing the expectation happen in real time
since the spike protein is the target of the vaccination program.
We further examined mutations of Delta variant spike gene.
Likewise, we found that the mutation frequency of the spike gene is also logarithmically
reduced as the full vaccination rate increased.
So they're, they are looking at, at, you know, percent fully vaccinated versus the mutation
frequencies that are found.
And take a look at the picture that they get pictures.
So you can see the more vaccinated people are, the less mutation frequency there is.
Okay.
So but then Tajem is D brings in mutation rate.
And you know, what do you guys think the mutation, you know, what should the pressure do to mutation
rate, not just the frequency?
Should the rate be also suppressed?
No, I mean, it's going to go up.
It should go up.
Should it?
You're cutting out a subset of space for this thing to move into.
If they're looking at mutation rate in the spike, and then you, you make antibodies to
the spike, it's, I, I don't know, it's, it's tricky because I don't think that that mechanism
is really influencing too much.
But I think you're right.
I think frequency goes down and rate goes up.
That's my intuition.
Why does the frequency go up?
The frequency goes down because it is constrained.
You have a space that you can't move into.
You have sort of immediate rejections of certain single nucleotide polymorphisms.
Okay.
Yeah, that was the earlier thing.
Sorry.
Yeah.
And then rate would go up because you would, you would see the viral swarm being sort of
pushed out of, you know, where you've got territory on one side for, you know, perhaps
that is being cut off.
And so it has to, it has to mutate in, in, in a direction that, that, you know, gradually
pushes it away from the territory that's cut off.
I think we're oversimplifying the fact that making immunity to the spike is going to necessarily
benefit and reduce the space that they can move into because there's lots of ways that
off-target antibodies can assist infection.
So then you would, you would not have that selective pressure.
So we have to take that into account as well.
That if the antibodies are not helping you fight the infection, but are enabling it through
FC receptor infection of immune cells, like a lot of people think, then a mutation frequency
would go down also because the, because the vaccine is actually not putting pressure on
the spike, but making it more likely that you're going to make antibodies that help,
help the spike.
And so if in that scenario, if the, if the majority of the antibodies that you make are
not specific for a neutralizing site, but are, are essentially neutral or, or bad for
you, then you would also find the mutation frequency would decrease in the vaccinated
people because they're not putting any pressure on the virus by, by making these off-target
antibodies to it.
You can explain it two ways.
Yeah.
So I guess, um, the, the vaccine is only specific to like 13 ish percent of the sequence and
there could be other interactions to the rest of the sequence.
That even, yeah, even, even the, yeah, that's the whole basis of, of, of antibody dependent
enhancement that the antibodies bind to the protein, but the protein can still every do
everything that it normally does.
But now with an antibody bound to it, it has a receptor for macrophages.
So the, the virus is still infectious.
It might even be stabilized in a highly infectious form because the antibodies stuck to it.
But then now you also have an immune receptor present.
And so it makes it, it increases its tissue specific or increases its infectiousness with
the presence of the antibody.
Um, that's, that's how Dengue fever works.
And a lot of other, these, the antibody dependent enhancement is because the antibodies bind
to the glycoprotein, but do not neutralize it.
And so then you just have added infectiousness for the macrophages that take it in.
That would not normally take it in.
You see, that's the tricky part.
So I can see why the mutation frequency would go down in those, but I think it's, it's,
to me it's 50 50.
You could say that the vaccine, if it makes good enough spike protein, which you and I
both know it doesn't, but if it did make good enough spike protein, you might imagine that
it produces specific pressure on the spike protein, but it's much more likely that it
doesn't put pressure on the spike because it makes crappy antibodies, which are neutral
or bad for you.
And then that's the reason why the mutation frequency goes down.
That's my guess is I've, I've really become convinced that this idea of enriching the
virus is a way of, of pretending that the transfection worked because I don't think
it did.
Yeah.
And as you guys know, I have, I have believed for two full years that, that the vaccines
did not work.
That's been my belief for two full years.
When I looked at the national data going back, I was looking at the our world and data set.
There's a positive correlation between vaccination rates and COVID-19 rates and mortality among
nations around the world.
And that's what I found all the way back in March of 2021 and kept up with that for like
eight months.
So anyhow, moving forward with this paper.
So we have some intuition.
We also have the possibility that the data isn't even real.
You know, it's very possible that, that SARS-CoV-2 sequences were sort of, you know, modeled
and put into the database.
I'm bringing that out as, as, as a hypothesis that I thought is more and more realistic
the more that I've learned.
But let's just, let's move on with the paper and sort of see what it is that they come
up with.
I don't know how much of the technical detail we need to discuss here, but you know, I'll
let you guys tell me, you know, when to stop here as we kind of scroll down and, and, and,
you know, look at what's going on in the paper here.
And we see there's some discussion of synonymous mutations or silent mutations.
And JJ, I do want to have a conversation with you separate at some point about, about synonymous
and non-synonymous mutations and virus-like particles, because I've actually wondered
if, if, you know, if Omicron was engineered, like I suspect it was, then the reason for
the high percentage of synonymous mutations might be to make it continue to fit a specific
virus-like particle.
If that makes sense.
Do you hear what I'm saying?
Oh, yeah, I'm just writing it down.
Interesting.
Have to think about that one for a little while.
Yeah, I don't know how well a virus-like particle fits, you know, any particular viral strand.
So I wasn't sure if, if there was some sort of like attempt to make it continue to fit
by specific.
Why, why are you just curious?
Why do you, I thought you were just as convinced that maybe Omicron was always there.
What is tipping the balance for you right now?
That was one of my hypotheses, which is that Omicron was in the background.
But the more that I've thought about viral swarms and the more that I've read, I like
the survival of the flattest principle, which is that I don't think that the viral swarm
is like, you know, these very far apart clusters so much as I think that it's, that it looks
more like the Milky Way galaxy, you know, with a dense core and, and, you know, less
and less material sort of in a related way around that core.
So there is the possibility, like, I still think about the possibility that, that.
What do you have in that core?
I know it's in my core, but I wonder what you have in that core.
Things that are closer to each other, you know.
I think if you want to model it correctly in your imagination, you have to think about
genes that are closest to each other, because that's the swarm illusion is that RNA viruses
have this beautiful assortment of proteins that they use to attack us when we're in reality,
they have this set of proteins and almost all of them are incredibly conserved.
That's why they've always used pan coronavirus primers to find them because these proteins
are all homologous.
It's the spike protein that defines individual variants because it's the most varied protein.
But I think they're, they're pulling the wool over our eyes on that one.
And every time you find a spike protein, you get to claim a new strain.
Every time you find a spike protein, you get to claim a new virus.
And they've been doing that for way too long.
When in reality, our immune system focuses on that center of the Milky Way, the genes
that don't change.
You know, it's funny to have a paper like this that claims to be looking at all of this
genetic variants when the testing that was going on after each variant emergence, they
were determining a variant not by specific sequence, but by S gene target failure.
Yep.
Meaning, meaning that we're going to call it whatever the new variant is simply because
it doesn't match the last spike protein.
And here you have this paper that seems to be taking granular detail from 20 different
countries, which contradicts the idea that we would need to use S gene target failure
to identify.
But maybe, maybe somebody could say, well, that's just a matter of slowness of production
of the tests.
So I'll take that on good faith for the moment.
I'll, you know, I don't, I don't know if that's a cartoon version or not, right?
I don't know if that's, if that's a Scooby Doo as you put it.
So you know, continuing with the paper.
So you know, we've got, they did, they did do it, give them credit though.
They did do it for the full genome and for the viral spike gene alone.
I don't really see how they're displaying it yet, but table one seems to be both full
genome and spiral spike gene, but I don't see how they divide that.
So now we have this non-synonymous to synonymous ratio.
Yeah.
And the more fully vaccinated, the more we have non-synonymous mutations as opposed to
synonymous mutations, which, which fits the idea of the vaccination providing selection
pressure, because now you have mutations that are, you know, that lead, that make the amino
acids functionally different.
If you know, it forces them to be functionally different.
They look more different in order to avoid the, the antibodies.
And if you go back to, um, Trevor Bedford's talk at the, um, Fred Hutch Institute in 2021
or two, where he's talking about this non-synonymous synonymous ratio in the spike protein or rather
in any viral gene, he states very clearly that it is extremely rare to find this ratio
higher than one in any flu gene.
And the ratio at the spike, um, and his papers was at some point over one and a half, like
they show it here for Israel.
So, um, it's extraordinary because the virologists have decades of data that show that none of
these genes change at this pace.
So something is going on.
The question is, are they just revealing a background and, and pretending it's changing
or is the background really changing?
And they're just emphasizing a change that doesn't matter.
I think that's probably what it is.
And was this curve sculpted, right?
If there was a, if these are bio warfare agents that are being released, then you would expect
someone to have modeled information like this sort of along the way and decide where to
release it according to where they were going to sort of force vaccination rates.
So, but you know, that's the conspiracy theory conversation.
It's a real, it's a realistic conversation, but let's go ahead and, um, and just sort
of take, take this on good faith for the moment.
So, um, you know, we can see more synonymous mutations, um, as a proportion, the more people
are fully vaccinated and that makes intuitive sense.
Okay.
So what is their conclusion from this?
Well, let's see, let's, let's read this here.
It's a neutrality test, I guess.
Yeah.
Um, synonymous versus non-synonymous.
Non-synonymous means you're going to be changing the, the, uh, physical structure of the protein
formed by a greater amount.
Yeah, that's correct.
I mean, I just, you have to remember that the spike protein has a lot of freedom to
do that in some, some regions of it.
There's a functionally constrained portions are the portion that's that hinge out and
that are hydrophobic for, for membrane fusion.
Um, sorry.
Oh, my cats just, I didn't know if you were making a comment on the paper or not.
No cat cat comment.
I mean, sometimes I don't report.
Yeah, sometimes I'm just like, you know, you, you are such a good statistic.
You're such a good statistic to the cat.
Nevermind.
I, I, I, I, I find it interesting that they don't give the non-synonymous to synonymous
ratio, um, for the full genome.
They only give it for the spike gene.
Um, and they only give it during the time that vaccination is being rolled out.
Right.
I'm not sure if I should have seen it like before, you know, is it, is it like stable
and then it started to change after the vaccination rate?
Yep.
I really think it's interesting.
It's an interesting paper because they don't get what they want and they spin it as though
they did.
Um, okay.
So, okay.
I, I agree with you.
Tell it, tell, tell us, tell us what they want and what they got.
Well, what they wanted to find was evidence that the vaccination limited the changes that
they would observe.
And the, the two ways that they show it are one, they look at a mutation frequency, which
is calculated by a very interesting computation, which is somewhat dependent on the very dependent
on the fidelity of the sequencing that they did, knowing that they're just telling you
up here that they got sequences from all these people that had full coverage of the genome
without really explaining adequately what that really means to them and how much, you
know, how much faith they have in the consensus genome that was reported because each of these
sequences that they're going to use as a basis for whether or not there was a mutation is
a consensus sequence.
So you know, there you're assuming that their average sequence and the polymorphisms that
they claim to find are not errors, which they definitely could be depending on the depth
of coverage.
And then they're looking at full genomes from Australia, France, Germany, Indonesia, India,
Ireland.
They were all collected from the global initiative on sharing all influenza data, the just said
database and the mutation frequency is calculated by the total number of instances of polymorphisms
detected within the genome. And then they divide by a factor of the nucleotide length
in the genome and the sequence, the number of sequences that they find this in. So that's
also difficult for most people to understand. But when they do the sequencing, they get
repeated copies of a amplicon. And then when they line them up, the number of times that
the amplicons agree at a particular nucleotide gives them some idea of how likely it is that
that nucleotide is actually conserved across most of those particles. And depending on
the nucleotide they look at, they could get a very high probability or a very low probability
of that nucleotide being right. And they don't seem to make any effort to distinguish between
single nucleotide polymorphisms that are real and ones that might not be. And they just
classify them as synonymous or non-synonymous, again, ignoring the fact that protein folding
is dependent on these silent mutations where the amino acid isn't changed, but still results
in a different form of the protein. And then if you do change the amino acid, of course,
you do change the protein even more. And then what they do is they show you that the mutation
frequency calculated in this manner is lower in the places where the vaccination occurred.
And then they parade that as evidence that the vaccine is doing something useful, which
is lowering the mutation frequency. However, we would point out, of course, that bad mutations
in very few number could still ultimately be disastrous. And so the number of mutations
that occur is not necessarily the best readout for whether or not the vaccine is stopping
the mutations or limiting the evolution of the virus. And looking at non-synonymous to
synonymous changes, we find that the vaccinated people appear to be propagating amino acid
differences in the spike protein that non-vaccinated populations do not propagate. So where the
mutation rate may have gone down, the possibility of dangerous mutations appears not to have
gone down and maybe even is higher in those people that are vaccinated because they have
the more consequential non-synonymous changes being present. Wow, that was too much words,
too many words.
They say in the final paragraph that we need to suppress the generation of deadly mutations.
So yeah, it seems again, there's a bit of a contradiction in there. I just wonder like
how much of this would have happened in the absence of the injectable products. Like I'd
like to see that side by each plot.
Right. It's why I wanted to see something like all of these statistics presented prior
to vaccination.
You need that because otherwise it's like, oh yeah, look what we found because of the
injections.
Right. Yeah. Did you know we're-
Because of the injections. Yay.
And so by hiding that, could they be hiding something like the fact that these variants
were actually pre-engineered in the lab?
Or just already just they found all the variants in the background and arranged them in such
a way so that they knew what they needed to release to tell the story.
That's possible. I just don't believe that all the variants were together in one cloud.
That was something that I considered and I guess I'll still consider it, but I'm less
likely to think that they're all there in the swarm than I was before, particularly
Omicron. Maybe the regular variants were. Maybe I was explaining Milky Way with a dense
core. Maybe it is that you have Wuhan strain here and Delta here and Alpha and Beta and
whatever. Maybe some of those early strains were near enough each other to be part of
the same core. But Omicron is so far away evolutionarily. It's like a 10 year evolutionary
distance according to these mutation rates, sorry, mutation frequencies.
In this fight. Frequencies or rates. I mean, the rate is
contained in the frequency, right? You can't have a rate higher than a certain amount.
You can't have a rate higher than the frequency. I still think we've got a we can't just give
them the spike protein as their basis and their their solid handled in the sense of
you can't let these evolutionary people sell the spike protein is the thing we should watch
if all the other proteins are not changing, then our immune system is not being challenged.
I can't stress enough how Omicron is different in the spike. It's not different in the XON
gene. It's not different in any of the non structural proteins 1 through 14. It's different
in the spike and that means very little to our immune system. It really does. Unless
we're focused only on the antibodies that bind to that protein, then it then it matters,
I guess. I want to I want to hear what thoughts this
is bringing up in Jumi and Jessica because I know part of where JJ is coming from because
I've been watching I watched your last video where this or two videos ago where this came
up specifically and I know you emphasized how Matthew was writing about the Omicron
hypothesis at a certain time and how compared to how in particular Brett Weinstein has been
talking about it. And so I understand a bit of the recent context why this is sort of
an important reconciliation of ideas. But I want to hear what Jumi what is coming to
your mind for myself and the audience who are following along mostly but need perhaps
a little bit of a bridge of of what we're talking about here. What is this talk about
Omicron as it relates to the paper or more generally what are your thoughts right now?
I don't know what to believe when it comes to Omicron. But I haven't looked that deeply
especially at comparing sequences. But I'll say that there was a paper that Matthew I
think we chatted about this a little bit on signal that paper with the prison the prison
inmates and it just seemed like Omicron wasn't as infectious as we thought. You know and
this was like a you know like in prison cells like people should be like you know giving
each other infections up to right. So that was one thing. But another is just related
to what this paper is talking about is I don't have so much to say about the paper but more
like what could be the mechanism behind how the vaccine might possibly be influencing
like the virus like this. Like there's animal studies right where it seems like sometimes
occasionally it looks like it lowers the amount of virus in the upper lungs but usually not
the lower lungs you know. So like let's say that we make antibodies in the and then there's
antibodies in the blood right from the vaccine there has to be some way for it to get into
the lungs. And I know of a mechanism in the lower lungs where like when there's inflammation
sometimes like when you get an infection you can get some of the stuff in the plasma going
like crossing into the lungs you know. But I don't know if that happens in the upper
lungs. So like what's going on. I mostly just have questions like I'm very confused about
all of this honestly. It's very good point that you mentioned about the prison study.
I have I have not reconciled the claim that Omicron was discovered in you know South Africa
or Botswana and like within like 17 days had visited like every discotheque in Europe.
I just I have not I have not found that very believable at all. If that were the case then
I think that the original Wuhan strain would have you know covered the earth in much more
rapid time than it did probably even before we would have known it was out there. Right.
You know our art is something that changes by context. You know you go to a slum in India
and the are for a coronavirus can be 200. It can just sweep through the population just
you know boom like wildfire. The idea that Omicron you know was several times more infectious
or something like that. It just doesn't jive with with a lot of things that we've seen.
It does jive with how quickly that wave occurred in early 2022. But but I think that there's
some sort of shenanigans there. But I'm going to this is something I didn't know where this
was in the paper when I originally read the paper. There's another graph that that was
really important to me. And and maybe maybe it was in the appendix or something. But anyway
one way or another I put it in an article that I wrote a year and a half ago ish. And
this is it right here. And so we've got you know these Taj Mahdi you know computations
down here. And you know we can see you know UK and India we have Taj Mahdi being pushed
very negative after vaccine rollout. And then later we have Australia being pushed very
negative though. That's I don't know. Australia is sort of a weird thing because everything
happened differently there. But here's the thing. When Taj Mahdi goes more negative that's
when you have a that's when you have a recent selective sweep as it's called. That you have
a bottleneck that is constraining you know where the virus can be in that sort of Milky
Way galaxy formation. You're cutting out some territory and therefore shifts away from from
where it is. You've got the blackout or whatever. And so you have you know immediately higher
rate of evolution. But you should have some sort of re equilibrium some sort of new equal
equilibrium that it reaches for stability. So you should see it go negative but then
come back up. And and we you know right here we just see the selective bottleneck pressure
and it's sustained. You know it should come back up to positive but we don't have that
in this paper or they cut us off to not see any further progression. Whereas I think the
more interesting thing would be you know both the time before and the time after we're seeing
this. And you know given given what this I would I would have thought I would have thought
that like a follow up paper to this would actually be the more interesting paper. And
there was no follow up to it was there. This wasn't even this didn't get past preprint
am I right. Is it still not past preprint. They have data from flu that they could they
could use to show us what a baseline looks like here. It's it's all very it's very all
very sketchy just from the language that they choose to open their abstract in their introduction.
It's clearly a biased paper. Now I don't want to jump to the end if there's more to go through
with the paper itself. But I do think there's some interesting questions then if we explore
the premise that this is biased presumably there's a reason why. So what we did last
time was we went and did what everyone should do and looked at the funding and the conflict
of interest disclosures. Is now a good time to move into that realm or is there anything
else we want to cover before we go a little more meta. Oh it's not very interesting paper.
There's no there's no fun and no conflicts apparently. Now I want to challenge us to
think one step further. Is this where we stop or is there still useful information to glean
that you would think would appear in those funding and conflict of interest areas. Spoiler
alert the answer is yes. OK. What did you find. So let me see where it is. So if you
look at yeah the the author affiliations tell me what you're seeing there. Agriculture biotechnology
laboratory so these are biotech. So there's a specific company mentioned. Oxygen oxygen.
I can cut it a bit of time. Do you mind if I share my screen. Go ahead. So I thought
that was interesting. You know just finding that company. It doesn't mean that it is a
funding source that should have been included. It doesn't mean that it's a conflict of interest
per se. But I do think it is still probably good information to have because as of now
it is the only information we have about who these people are and maybe why they would
have put together such a paper. So this is oxygen. It is an agricultural biotechnology
laboratory. They apply novel biocontrol solutions to human agricultural and environmental disease
to reduce the chemical loading of our soils and waterways. And I. So here's here's a
brief overview of their thing and just top right here I believe I guess this may refer
to maybe there were more studies they published on covid but I think this is in reference
in part to the preprint we just looked at. And I'm I'm not entirely sure how I guess
I guess the rest of their pipeline has involved work with viruses so it's not totally out
of the blue but they're developing stuff. So this is a commercial company. They do have
products that it seems to me they would benefit from somehow publishing the research the way
they did in order to advance their the development of whatever it is they're doing. They're an
agricultural biotech company and the the co-founder and and chief scientific officer yay spent
sixteen years at Johns Hopkins. Yes he did. Yes he did. And you know where he was before
that well Cornell but that before that he was a medical commander in the Taiwanese army.
So just interesting. So I I'm not totally sure. I don't I don't know what product this
would be in reference to. It sounds like they've got private investors so it's nowhere near
as obvious as last time where you've got all conflict of interest with Pfizer or they're
developing a nasal vaccine or whatever. But I think I think that the minor takeaway lesson
I would put in here is the information on funding conflict of interest who these people
are isn't necessarily limited. You don't want to stop at the blank disclosures or the blank
you know conflict of interest. Absolutely. Absolutely. I didn't get any feeling though
that we were you know I don't think the paper itself is necessarily where there's misleading
going on. But you know talking about Baltimore biotech what would you assume Baltimore biotech
would be associated with. I mean yeah they say agriculture right. But you know what what's
in Baltimore military. Well yeah you're real close to Annapolis right. That's the US Navy
and of course we know that the US Navy has been the branch of the military that has been
used as a major arm of you know like bioterrorism defense type stuff. Operation Sea Spray and
subsequent operations that that very likely took place according to congressional testimony.
So you know this is somebody who may have been brought to the US from the Taiwanese
army who had a proclivity toward toward this type of stuff and stationed at you know first
at at Johns Hopkins and later you know Bill helping build this company. So that that is
interesting. That is interesting. So we should be viewing this from a lens of possible you
know bio warfare operations. So just as an anecdote you know the guy that I was working
for at the University of Pittsburgh was an active nuclear submarine captain semi-retired
and you know with full clearance and everything he graduated top of his class in his engineering
class. He was not an idiot but he was definitely in the Navy and definitely still had all the
clearances that you would expect from somebody who was a captain. And he threw me out with
with great prejudice while he was wearing two masks. Whether or not his Navy had anything
to do with that but he was definitely a Navy guy and he didn't do anything for me in respecting
other Navy guys. That's for sure. I hope he's in a novelty. So guys there was a suggestion
in the chat on another paper that was being held up. What was the exact quote? Let's see.
Held up in pro-vax camp as C it creates T cell memory too. Now I'm under no illusions
we have time to do a full critique but I wanted to bring it up and see if this is something
you guys have seen and maybe there are some initial perspectives that we can offer. Let
me just pull this up here. You guys have time for it? I mean we you know this was a long
discussion on one paper so we could call it a day here but you know I'm happy to keep
going if you guys are. I don't know how much time you guys carved out for this. I'm all
right let's do it. Right. Yes and to be clear I'm not asking us to do the same amount of
time we just did on this but I figured it'd be good to give just a brief a brief take
a look at. So are you guys familiar with this paper? It looks like it just came out just
under a month ago. Theoromers reveal robust T cell responses to the Pfizer BioNTech vaccine
and attenuated peripheral CD8. How do you say that? CD8 plus? Yeah or positive probably.
Okay CD8 positive T cell responses post SARS-CoV-2 infection. That's a lot. Are you guys familiar
with this already or is this brand new to you as well? I haven't seen the paper but
it it makes sense in the title. Yeah new to me I have not been reading as many. What is
a spheromer? That's the only thing I don't know I assume it's like. I don't know what
it means. I can guess but never heard of it. Some technique that they used oh yeah it says
it's in it. That's what I kind of thought some kind of technique to isolate the T cells.
Very interesting okay. Yeah I also have not read it so just to do what I always do I'm
going to start at the the disclosures part because that usually well what do you recommend
in terms of order of how people would look at a paper like this? How do you guys approach
it? Do you do what I just did and you jump right to the bottom? Do you because I think
the interesting part here is showing people each everybody's process right? So if someone
like me is going through and starting to read something like this something we're not familiar
with what's the first thing you guys recommend people do? Read the abstract. Read the abstract?
Yeah and use the abstract to parse the title because the title is one of the most carefully
you know of language in the whole paper. If they chose the word may they really meant
the word may and if they chose required they really meant the word required and then you
got to decide whether or not they're allowed to use that word or not. That's really that's
the strategy I have. So what are they saying they're certain about? What are they speculating
about in the title? Says reveals robust T cell response. So their technique whatever
spheromers is is revealing a robust T cell response to the vaccine and an attenuated
peripheral CD8 T cell response post COVID infection. So there's two things we should expect to
see in their data robust T cell responses after the vaccine and an attenuated response
in the CD8 positive T cells post infection and so now the trick is are they really going
to prove that to you or not? I think if I remember correctly and this is just with a
disclaimer because I it's been a while I know when you glance at this but it was it was
post infection people who had been infected and then they looked at the response after
vaccination so I think they're comparing people but all were vaccinated but comparing people
who had been infected before and people who hadn't. Right. Yeah. And they're looking at
CD8 only or T cell broad and then they hone in on CD8 for the peripheral pool because
they found something. They put MHC molecules on little spheromers and then they suck up
the T cells with them. That's funny. Okay so help me out here. So the way that this
outlining I was expecting something that says abstract and I was going to go there but I
see we got a graphical abstract which is not what I was expecting and then we have a summary
which is also not what I was expecting. So when when you're saying let's look at the
abstract what would that refer to how do we translate that to this. Well graphical abstracts
are awesome. I find them when they're done right they're really descriptive of all the
important things that happened in the paper. So that's that's always a good if it's good.
I mean it's not always good but and the summaries you know it's it's basically the abstract.
It's the same thing. So I'd go for both of these. The only thing about the graphical
abstract is that you know you you have to have a background in everything that they're
talking about to put everything into context. Right. It can be difficult to interpret.
It definitely looks pretty. Yeah. They have they have fake people there. That's nice.
Are we are we to guess from this that the COVID-19 patients are also vaccinated because
it looks like a continuum. Yeah that's what we said. Oh wait right. Where is that in the
graphical abstract it looks like the COVID-19 patients are taken from the unexposed subjects
that received the Pfizer vaccine. Is that not the case. And then they also have recovered
patients receiving the Pfizer. So these people are cheating all the time. Oh wait wasn't
this also the one where the the some of the COVID-19 patients were like in some trial
or something. Didn't Amanda point that out. You know I'm talking about. Yes I think so.
Right. They were in some trial for some like treatment and COVID treatment. Right. And
then they use the same people for this. Yes. Yeah. Some of them some of the COVID patients.
It was so weird. It was like here's something on a left field. If you made that sphere and
then sprayed it on people it seems to me that would be really nasty because it would activate
it would bind to all T cells. Right. It's like a MHC multimer. It's like a universal
display or of antigen presenting cell. And I don't know which MHC if it's if it's really
the HLA subtypes then they're really that could be an incredibly dangerous thing to
have a powder of. Yikes. Maybe I'm completely crazy but I think that would that would make
your if you if you had that in your body your T cells would go bananas. That's why they
can pull T cells out with it. And furthermore it looks like I don't think that using that
spherom or you're going to pull out SARS specific T cells but it does say that they're doing
that. I wonder if the the peptide is the spike that could be the peptide MHC multiple. I
wonder what that is. I got to read that. OK. Well let me read this link. I'd like this
link. Yeah. Yeah. I put it in the private. OK. I got it. OK. Yeah. I'm going to switch
over to the summary now and maybe this is and we can we can sort of wrap up after this
but maybe this answers some questions that were not answered in that graphical summary
T cells are a critical component of the response to SARS covid 2 but their kinetics after infection
and vaccination are insufficiently understood using spherom peptide MHC multimer reagents.
We analyzed healthy subjects receiving two doses of the Pfizer BioNTech BNT 162 B2 vaccine.
Vaccination resulted in robust spike specific T cell responses for the dominant CD4 positive
HLA dash DRB1. This is crazy. I don't know how to read this thing. What does that refer
to. So human leukocyte antigen is the same thing as an MHC molecule usually say MHC molecule
or major histocompatibility complex in animals say HLA in humans but they're the same thing.
OK cool. And CD8 plus T cell epitopes antigen specific CD4 plus and CD8 plus T cell responses
were asynchronous with the peak CD4 plus T cell responses occurring one week post the
second vaccination boost. Now that's confusing because I thought that was the primary series
and not a booster anyway whereas CD8 plus T cells peak two weeks later these peripheral
T cell responses were elevated compared with COVID 19 patients. We also found that previous
SARS COVID 2 infection resulted in decreased CD8 plus T cell activation and expansion suggesting
that previous infection can influence the T cell response to vaccination. So isn't that
saying don't get the shot if you've had COVID. I think that's a pretty good short through
the corner way to say it indeed which I think a lot of people have already kind of known
it. It does seem to suggest that. Yeah this part of the discussion has been happening
for for 20 months now. Yeah the T cell immunity from post infection seems to be better than
than from post vaccination. And so the premise of this coming into the discussion was that
apparently it's being held up in the Provax camp as see it creates T cell memory too.
So I'd like to hear from you know from each of you does is that what this seems to show
without on a first glance keeping in mind we we have not done a full deep dive. What's
your impression just based on the little bit we've looked at it. What of the paper. Yeah.
Well it's funded by Gates so I don't care what it says. Seriously that's I went to the
you know that's the next step for me like look at the funders and then if it's not conflicted
then I'm more interested in reading about the methods to find out like exactly how these
spheromers work for example. But yeah I don't know it's like. I would piggyback on that.
I would piggyback on what she said that you can look at this methodology and what I found
with my brief select brief reading is that they can't really differentiate what kind
of CD4 positive cells they are so they don't know if they're pulling down a what ratio
of regulatory T cells to non regulatory T cells they're pulling down and whether or
not there there's a couple different kinds of CD4 positive activated T cells and not
all of them do the same thing and they're just pulling them all out and the same to
a lesser extent there are fewer differences between the the the pool of CD8 positive cells
that they would find and so it to me the trick is to know what proportion of these helper
cells are regulatory T cells because that'll determine how how the crescendo and decrescendo
of the immune system play out and so if they're not differentiating between those those populations
then they can't really be sure if there's a parallel and so you can say yeah they're
activating T cells but if they're activating only active T cells and not regulatory T cells
then there won't be a transition to memory cells in anybody that's vaccinated whereas
after infection you still have the whole complement and so you get a regulatory change that sends
some T cells into apoptosis and others into a memory state but you need that ratio to
be correct and I don't think they can measure that with these spheroids no they didn't measure
as far as I can see in the methods there's also something interesting in the limitations
like if you go down limitations in this study those are also really important to read yeah
our study has limitations in that we measure peripheral T cell responses and differential
tissue location of immune cells after mRNA vaccination starts between infection can contribute
to the differences observed between the cohorts so what does that mean peripheral T cell so
if they I think and I have to look at the study a little bit more carefully but I think
they only looked at blood samples right but what you find in the blood is different from
what might be going to your lungs like homing like T cells homing to the lungs which is
what you would probably want if you got a lung infection you know absolutely right in
your lungs you'd have less in your blood yeah this has been a common theme of a lot of the
vaccination studies is that is that they look in the blood and not at the not at this you
know surface layer between us and where respiratory viruses are are infecting us right it's this
is part of the illusion that they seem to be intent on and it may be that that that
there is that there is something going on that you might measure you know in the blood
and think oh well that's good that shows that it's working but if it's not working at at
that surface you know level then you're not actually preventing infection so it's like
okay so maybe you don't prevent infection but then there's some fight happening in a
part of the body where it doesn't even matter and yeah is that the fight that you want are
are you changing the grounds of the fight to the cardiovascular system and could this
be part of why it is we see so many cardiovascular problems and various for instance well that's
nuts Jessica thank you for pointing out the funding section because not only is it gates
it's also my my nemesis is the wrong word my point of interest over the last couple
months open philanthropy that's of course a effective altruism giant the dustin moskowitz
facebook mafia yeah that's that's ftx taking money from the crypto space and pulling into
the pandemic space which is um that true well open philanthropy yeah open philanthropy is
is sort of one of the the big like the biggest actually probably leaders in the effective
altruism space and they're of course behind uh funding virtually everything related to
the covert response including the tabletop exercises and all the sci-fi stuff yeah and
there is something very very weird that needs further investigation and and i wish i could
have spent even more time on it than i did but when i had my dinner in austin one of
the people who came to that dinner admitted to me having funded one of the mrna vaccines
secretly using bitcoin and you know then seeing all of this space yeah the guy's name is brian
bishop and he is um uh you know he's in the transhumanist community he's in the diy transhumanist
community meaning like you know let's do experiments on ourselves and see what we can accomplish
and figure out and he was uh you know putting together a company for designer babies at
some point and kind of got pushed out of certain circles as a result but um you know then and
i have no idea whether or not he has further connections to the ftx people but interestingly
uh he does have connections or at least told me he did know some of the people from like
the paypal mafia and uh also some of the people from the um the media group that created the
global covid summit yeah round table media right yeah he's friends with um with multiple
of the principal or the the uh the board members of round table media so like that that was
uh that was a little bit you know weird to find out and i have no idea you know necessarily
what all of these connections are but you know we have connections literally between
you know we have connections on both sides with cryptocurrency funding both sides of
the pandemic debates liam put that link up would you that i just sent to you and scroll
through it this is the reporter nih.gov site and the one niad grant that was reported there
the niad grant that was reported in that paper stems from 2006 to 2022 it is continuous but
it's shared between several different pis and it starts in 2006 at stanford or three
with ann arvin with protective mechanisms against pandemic respiratory virus and it's
continuous funded grant by the niad for literally 20 years it's exactly actually 20 years and
you can see how the the pi changes as the the grant moves through stanford but it stays
with the same cardinal driving number i don't know for sure what that means but i do think
it means a different kind of priority funding in the sense that they didn't have to reapply
from scratch every year even though it's a wide variety of pis that get listed as the
project leader it's extraordinary there is no one there's no one in neurobiology that
has a track record with a single grant application that has been renewed so many times in a row
nobody just understanding the the timeline here yeah it starts in 2003 and it gets renewed
annually but 2008 and 2009 is when it kicks way into high gear and it never stops as you
say oh yeah those are all collaborators now i see why those other names are there now
i get it i see wow that's really extraordinary well again just to be clear stanford was one
of the two competing arms of the human genome project right you've got the washington university
side which sort of became more famous just because they they won the race by like three
weeks or something like that right i mean it was it was literally like a neck and neck
race to map the human genome but the the other side of that was the stanford side where was
kevin in that mccurnin um so you know mit had stuff going on um within i mean mit was
you know obviously one of the centers where a lot of genetic research has been done but
like the primary sort of competition to map the human genome once the very first time
was washu stanford okay i see well this has been uh fascinating i think we should aim
to wrap up now um i really appreciate how much insight you guys have been able to bring
i think the thing that i like about doing these shows is it is about showing the process
and um i think there are a lot of people um who are you know scientists of their own caliber
who are tuning in and a few people have said you know i'm a i'm a stem student and this
fascinating but then there are a lot of people like me who are sort of passed more the conspiracy
theory type videos you know it's very interesting but at a certain point you really want to
get into the nitty gritty of what how how the world actually works and this is it this
is going in and trying to piece those pieces together um and it's not that any given paper
we're going to pick will answer all the questions but the act of going through the process the
practice of it i think will help refine skills that can be applied then to just critical
thought in the future but also how to read other papers um so i appreciate it very much
uh thank you and and another piece of that is uh the fact of the matter is as a group
we are better reading these papers than we are as individuals um and and it's going to
be different from paper to paper uh you know different people are going to have different
strengths and be able to pull different pieces out uh jumi mentioned something um which i
i didn't actually read this paper prior but my wife had read it and made some comments
on how the cohorts were sort of you know selected in an interesting way uh and and may not be
sort of true cohorts for the for the kind of comparison that the paper claims to be
making right and and different people um you know with their different levels of experience
and different things that they look at coming together and having a conversation are more
likely to um you know look at all the the proper corners of what's been done better
than any one person reading a paper so this is this is how a lot happens you know with
scientific discussion especially when when several people come together outside of the
lab where it happened we are not specialists at what what goes on in that lab only the
people in that lab are specialists in what goes on in that lab and so it takes time and
it takes you know um a lot of points of view jumi are you doing any cooking shows you really
look like you have a kitchen that's ready for a cooking show so if you want to like
you know do a mise en place while we're doing this next time
like a multitasking journal club it's very it looks like a very cozy kitchen jumi and
emu emu is the cat by the way for anybody who doesn't know i um okay guys well i want
to remind everybody that the sub stacks and or websites of all three of our fantastic
guests and friends here today are in the description of all of the platforms wherever you might
be watching this so please if you haven't yet go and visit and subscribe to all three
of them um i want to go around and and make sure we have a chance to plug anything else
you guys might be working on or anything i might have forgotten jessica what do you have
going on in the next couple of weeks oh my god um well catching up um but i'm doing something
really important for my my our country um i'm going to be providing testimony for the
national citizens inquiry i believe it's called um yeah dr laura brayden presented i think
it was today or recently and i after i finished listening to her testimony i was like well
i don't need to speak anymore she was she was she was incredibly good yeah she yeah
um she's a good friend uh through all of this i mean as good as you can be with someone
without meeting them in person yet but she's she's she's hardcore like canadian beauty
and uh yeah she did a fantastic job so it's not a plug for me it's a plug for the inquiry
and for her testimony like listen to um hers mine's gonna be coming up sometime between
the 13th and the 15th it's gonna be uh live streamed some at some canadian hour in winnipeg
oh yeah there's my name yeah expert on the fair data for some reason they wrote expert
and big letters so and by the way oh bears or something so i watched uh dr laura brayden
who's who's the immunologist near the top of this list um yeah that's one of the uh
she is excellent um she really was she did a bang up job man yeah i i put i think i posted
the video in um in our locals group um but i you know i would encourage like people who
haven't seen it like google that uh she she's excellent yep yeah she really are all these
here is going to be recorded yeah yeah so they're all live streamed and they're all
uh as far as i know they're made into clips uh after the fact and so the website is national
citizens inquiry dot ca i'll put that in the respective chats right now um this is a uh
a um this is a next step in a series of events that have happened one of which i was very
happy to have been a part of called a citizens hearing um and it's going on across canada
both in person and online and i'm hoping i might be myself testifying briefly in front
of the vancouver one um no confirmation there yet that's a cool symbol it's got a person
embedded in a maple leaf that's dope but it's also doesn't it look kind of like the classic
like niaid antibody yeah it does it does got all the things you need isn't that fun i just
want to see if i can pull this up um but yeah so we'll make sure the link uh to that is
uh available to everybody oh oh did everyone catch that i think there's you oh yeah this
was a anyway that's my little claim to fame but i actually have nothing to do with the
nci full disclosure okay so that's wonderful um jumi what do you got going on in uh in the
next couple weeks and is there anything else that i have failed to plug no i think you
already mentioned it my sub stack wonderful okay that's it that's all you're gonna say
okay um the weather's getting better i'm gonna get on a motorcycle soon and teach immunology
from a motorcycle for fun but other than that i'm just doing the same thing i always do
um i'm waiting for jessica to do some um from the surfboard clips where we hear about immunology
and see the wave or something like that but you know they have gopro you know you can
do that you could oh i do do that that's my profile picture for my twitter account i took
that photo myself of me nose writing it's really hard um but we haven't had waves in
ages we have something coming up but the the weather modifiers modifiers here are really
like so they only make waves on the weekends so my theory is that the weather weather modifiers
are surfers because they have to work during the week and so they make the waves happen
when they can surf i'm not kidding it's only on the weekend i swear to god and then i don't
want to surf because there's too many people oh you should get a login for harp because
then you could change that if you wanted okay you were just nearby it's just north of here
it's just just due north into alaska yeah um anyway um jj how about you my friend you've
had a you you did two weekends in a row presenting to uh medical doctors for covet ethics fantastic
presentations um anything else you got going on uh apart from the motorcycle yeah sure
i'll tell you i'm gonna do a star trek um series on youtube and i'm probably gonna premiere
it in the next couple days what does that mean a star trek series i've heard you say
it a few times um i think it's best if i just leave it but i have uh i have a plan to be
um on youtube regularly as a as a star trek i don't know what else to tell you and then
that's what i'm gonna do i'm excited about ears what's that he's got ears i got ears
and everything i'm ready for it it's gonna be funny and also biological that's the whole
point i want to get on youtube again without worrying about getting bounced and so i think
i've got an idea well uh i think i said it to you uh last time you're on say hi to youtube
for us i will i will um all right guys well last but not least make sure you join us over
at roundingtheearth.locals.com where we have been having a fantastic discussion uh this
entire time and there we are um uh and yeah it's a great place to come um either as a
free member where you can just stay up to date on everything we're doing in this wonderful
feed here or you can sign up to support the show um for as little as five dollars a month
and get access to our weekly locals exclusive supporters only live streams where we had
a listening party for uh an album that i had worked on at the beginning of the pandemic
in march 2020 and it just wound up being a music sharing session and it was a lot of
fun uh so if you want to hang out with us and do that kind of thing and uh talk about
stuff that is is better among a closer circle of compadres roundingtheearth.locals.com um
and we're gonna have a new show soon for subscribers uh we've got we've got our regular wednesday
night discussions but um we're gonna start doing one that's gonna be more general topics
uh like the universe education and everything well there's gonna be a lot of educational
content um uh you know discussions of education philosophically and everything else but i'll
just go ahead and leave it at that for now okay well thank you guys maybe i can throw
out one more thing next week maybe we can think about our next time we can think about
doing there's like three papers now that have shown these ig4 antibodies and what they're
doing maybe we can find like two or three of those and kind of cover them all together
at once that's one idea just to throw out there it's on the dub land yeah if you guys
want to send those out in our email chain we can do that okay sorry okay ladies and
gentlemen thank you so much for watching and we will see you uh well actually i'll be back
i mentioned this to matthew it's all announced here for the first time i'm going to be back
tomorrow with our friend christin elizabeth to talk about her uh fantastic article that's
just come out which a whole lot has happened since she posted it someone got arrested related
to the the rise above movement and the azof battalion it's getting nuts out here yeah
i'm really curious about this um i i have felt like um like things that were going on
in this supposed like white nationalist movement uh were were you know planned or seeded or
something like that because uh you look at all the statistics the survey statistics and
um you know all the measures of racism in the u.s were going down down down down down
for decades and then all of a sudden were beset with new stories and imageries about
these new groups popping up and it feels pretty artificial and so uh i'm curious as to hear
more you know she and i have talked a little bit but uh i want to hear some more well there's
your teaser for tomorrow uh lots to catch up on and um i hope everybody comes and joins
us for that thank you again so much any final words matthew before i let you go no good
show thank you good show okay guys thank you again and um i uh i appreciate every single
one of you who's been participating on everywhere you've been participating on rumble there's
been robust discussion on locals um and uh we had more viewers on rockfin i think than
we've ever had um so thank you all so much and we will see you tomorrow
you