I think we're going to have a
Go for 16 minutes next.
He's going on French, British, Italian, Japanese television.
People everywhere are starting to listen to him.
It's embarrassing.
He had the exact location laid out on a map.
Then he, like, hid the map in the cigar store Indian for safekeeping.
Too bad. We could have been partners.
Now, instead of being rich, he's in jail.
Hey, like what happened to Scooby?
There he is.
Scooby, put down for that gopher hole.
Scooby-loom!
One of those apples better be for me.
No.
Good evening, ladies and gentlemen.
This is Gigo, biological, high-resistance, low-noise, information free, brought to you by biologists.
This is the 28th of September, 2023, and I've got some immunology for you tonight.
Unfortunately, the immunology is going to be brought to you by a man with a limited spectrum of views
and may be part of this group of people that has been controlling our limited spectrum of debate for a long time.
The protocols were murdered, gain of function, is a mythology.
The Scooby-Doo is real and the players are only committed to lies.
That's all it requires, ladies and gentlemen.
That's all this requires.
I'm really telling you, it's all requires is a spectacular commitment to lies.
Good evening, ladies and gentlemen.
This is Gigo, biological, high-resistance, low-noise, information brief, brought to you by biologists.
It's the 28th of September, 2023, and we've got a long way to go.
And a lot of biology still to learn, thanks to the people on the scroll at the top of the screen
for supporting me over these last many months and years.
It is without them that we would not have this.
I don't even know if that was grammatically correct or not, but anyway, thanks to them, we're still here.
And yeah, we're going to keep on going.
We're trying to avoid the new world order that's goofed on this hat here.
The idea that viruses come out of bad caves.
I'm kind of done with that, and I think you should be too.
One of the best ways out of that is to not take the bait on social media or on television.
If you can turn the TV off permanently, that would be great.
Because they have, through a long series of dramatic entrances and exits, of dramatic
release and releases and fortuitous whistleblowers, we have this fundamental change in how we think about our biology
and that fundamental change in how we think about our biology has allowed them to cause havoc
in our healthcare system, which otherwise wouldn't have happened.
Essentially, through fear, uncertainty and doubt, a bunch of people were killed with bad protocols.
And a bunch more people were roped in as collateral damage because they tested positive
or even were suspected of and didn't test positive.
There was so much financial incentive to declare COVID deaths that it's likely that most or all of them
were completely nonsense.
And so it is this sort of essential mythology that has been perpetuated by all of these people
that I'm identifying as this spectrum of debate, which has been curated by people everywhere
from Joe Rogan and Brett Weinstein all the way up to Tony Fauci and Francis Collins.
And so I think this debate has basically been controlled, number one, around the idea that
this gain of function stuff is real and that it's an impending danger.
And the better we get at making genetic material and the cheaper genetic material becomes,
the more dangerous this gain of function stuff is.
Now, the interesting part about this twist in their mythology is it's not the RNA sequence that matters.
It's the quantity.
And if you have enough of it, you can make a pandemic.
And there is no doubt of that.
But the idea that you can make a special combination of RNA sentences or letters that can result in a virus
which has the capability of doing something that all other viruses don't have the capability of doing,
which is spreading from person to person to person to person to person to person
was extremely high fidelity in waves of variance over many years.
This is just never before in the history of mankind and with any precedence has occurred.
And now you might think, oh, no, wait, there was that 1918 thing.
Yeah, there was that 1918 thing.
Has no bearing on what happened here.
No, no, even comparison except for the hysteria of a mythology spreading around the world
can possibly happen in the different places where that mythology lands.
And without a doubt, their idea has always been to use this mythology to coerce a surrender of our rights to privileges.
And this inversion is going to continue with the mythology of public health and a mythology of the shared planet and climate change.
And you can see very clearly how a religion or a language or a culture or a music was never going to unite the earth.
It didn't matter how good the king of pop was and how many albums he sold.
He wasn't going to be able to bring the world together.
Bono and Michael Jackson was never with it together couldn't bring the world together.
But the fear of a gain of function virus being made in somebody's garage.
That'll bring that'll bring the world together.
The fear of five years from now, the earth being on fire.
Now that that'll bring the people together.
And that's what this debate has been all about.
I gotta put it in the hell.
That's what this debate has been all about for so long and it's been very frustrating because it has been curated by people who you expected not to be curating things.
You thought that people were really speaking of their own accord and really trying to find their way around in the cave.
And these people weren't trying to find their way around at all.
They already knew where they were and they had already agreed to try and keep you there.
That's really the trick.
And so we're trying to track down who are the people who laid down this worst case scenario narrative.
Who are the people who aren't talking about PCR or masking or lockdown or the spread or lack of spread.
The death certificate fraud.
The protocol frauds with the do not resuscitate orders.
The ventilation for money.
The protocol for money like remdesivir and medazalam in the UK.
And the early treatments and the lack thereof and the stereo around the idea that we were not being honest about these early treatment alternatives.
All of this stuff has virtually disappeared from the narrative for most of the leaders and people speaking in the front lines of this debate.
And this should be very frightening because this in effect does not account for the fraud and the lies.
And instead the accounting is done by people who are willing to attribute most of the damage to the virus and some of the damage to the mistakes that were made.
And that completely removes the lying from the the equation.
And this list of lies where is it over here over here over here over there this list of lies needs to be acknowledged.
And that's what this whole people experiment you know thing has been all about trying to figure out how to do this.
That's what we've been trying to do with this picture.
Let's try and figure out which of these people has been genuine and which of these people has not.
And I think we've got a good way to figure this out now because we can more succinctly codify what it is we're trying to describe to them what it is we object to.
Number one to be very succinct.
Transfection is not immunization.
The second thing is to say that intramuscular injection of any combination of substances with the intent of augmenting the immune system is dumb.
And that might sound a little bit brash but I think at this stage we are sophisticated enough with our biology that we can say that.
And more importantly I think we can make a very good argument for it.
Especially especially I mean especially with regard to a respiratory virus.
So we've been looking at these people.
And tonight I would like to look at a very special person.
The other night I was allowed to plug a few people I'm going to plug those same people tonight again.
Number one is the work of Jessica Hockett.
I think she's really done a steadfast job with keeping people focused on the bullseye and not being distracted by other things and looking for other manifestations of that bullseye around the United States and she's been very successful.
I think Nick Hudson is very very consistent in his pursuit of the truth.
You're going to be able to find videos where he's saying some weird things or some funny things because he's not a biologist and so sometimes he might say things that don't really make logical sense from a biological's perspective.
But if you talk to Nick and you explain it to him he's going to correct himself.
And his main insight that has really caught fire on the internet until was I guess the fire was put out artificially was him saying that if they ever come to you with global problems that require global solutions then you know that that's baloney.
And I think that's a very good starting point it's a very good litmus test are they telling me that this is a global problem.
Yes, are they telling me that they have a global solution. Yes, then we probably shouldn't listen.
And Denny Rancor I just saw him present today to a private zoom meeting and again it's a it's such a large body of data and a body of work that that paper when you download it it's a little frustrating because it's so big but
the gist of it is is that there are are pretty detectable signals in every country where we have semi reliable or objective data.
And these signals are correlated with the rollout of the countermeasures and specifically the MRNA shots although there's probably a signal associated with the the adenovirus DNA shots as well.
And so we've been investigating talking about thinking about reflecting on the behavior of some of these people because it turns out they seem to be more connected than we thought.
And an interesting player for tonight is going to be here funded boss a guy who worked at Solve I believe with Robert Malone on the flu vaccine in 2007 and 2008.
I'm going to listen to his opening lecture in an immune, immune biology course which he's going to teach at the IPAC University, which was founded and is headed by James Alliance Weiler PhD from originally I think he was working in Pittsburgh at the start of the pandemic but now lives in Michigan.
Sorry about that.
So as you know I've known and thought about here funded most for a very long time.
He actually yelled at me one time in a zoom meeting. I believe this was in 2021 and I asked him to speak to the possibility of previously educated T cells from previous exposures to coronavirus and he yelled at me yelled at the group
and said that he's tired of these questions about T cells. There's no evidence for any T cell memory associated with SARS-CoV-2.
So he's pretty insistent about that.
Let me see if we can.
Oh wow that worked a little smoother than I thought it would.
I think we're just going to play this.
I'm going to get that mousey mouse. There he is.
So let's see what happens. I'm not going to speed it up but I'm probably not going to interrupt that much wink wink.
Okay, so yeah the first slide is of course what it is all about the immune biology of natural and immune escape pandemics and epidemics.
So let me tell you first of all, very very important.
What is very often misunderstood or not understood at all with regard to pandemics and epidemics is the immunology.
So there is a lot of people who are interested in following the virus, the evolution of the virus and how it evolves over time and talking very generally not only with regard to the current COVID-19.
I'm going to interrupt very much but I'm probably going to interrupt a lot.
It's crazy, you know he came out at the end of 2021, 2020.
So he's been on the scene a long time.
He's had a lot of opportunity to teach us about how the immune system and he's done it.
He's given a lot of half hour and hour lectures. He's put out a lot of publications.
And we've looked at them and we've talked about them.
We're going to see something very extraordinary here tonight I think and I've got a strategy problem and I'm going to surprise you within a few minutes.
But not that many people are interested in following how the new response is evolving.
And to me that is very, very strange because as you know the higher mammalian species have what we call an adaptive immune system.
These are basically the B and the T cells.
And so that means that this type of immunity can adapt to several different situations.
So, however, nobody is asking the question how does the immune response adapt to when the virus is evolving.
We hear many, many things about mutations and the evolution of the virus, but we don't hear a lot of reasoning about the evolution of the adaptive immune system and how that adaptive immune system is then again.
Let's say exerting a certain pressure on the virus so that the virus evolves.
So, first of all, in this course, I will highlight and focus on a few definitions, but definitions I tell you that are so important that are absolutely key to understand how pandemics and epidemics are evolving.
And that hopefully I hope will give you many, many answers to questions that have been remained unanswered or that were very unclear and led to a lot of confusion.
So, the definitions, it's about definitions of immune selection pressure.
It's about what is an acute self-limiting infection. So, for example, SARS-CoV-2, but also influenza, but also other coronaviruses and also, for example, other viruses like enteroviruses, parvoviruses or causing acute self-limiting infections.
Then the key notion that is very, very important with regard to pandemics is, of course, herd immunity. How do we define this and how does it evolve and how do we find out whether or not we have herd immunity.
And then there is also, of course, the definition of what is an endemic infection, what is an emissivity, what is a pandemic infection, what is pandemicity and an epidemic.
So, I'm sure you have heard about all these different notions, but maybe not always understood how they are best defined and what they mean exactly.
So, a very important thing also notion to bear in mind is when it comes to evolution of microorganisms, it is important to understand that the Darwin, of course, never said that it is the strongest and the most intelligent of the species that is going to survive.
But according to Darwin's origin of species, it is the species, the one that is best able to adapt to the environment and to adjust to the changing environment in which it finds itself.
That is the species that is going to be survived. And I'm already emphasizing this right from the beginning, because what we are dealing with, especially currently with the current pandemic, when we vaccinate many, many people at the same time, is that the virus finds itself into an environment that is pretty hostile
in terms of immune responses that vaccinated people are mounting. And so viruses that can add that to that immune response, elicited or induced by the vaccines, they have a better chance to survive.
Viruses that are, for example, intrinsically very infectious, but have poor capability to adapt to immune responses in the population. So that is very important to bear in mind.
So then what is immune selection pressure? Well, immune selection pressure refers to the process by which the immune system exerts a selective force on, you know, microorganisms, pathogenic agents in general.
And this elective force enables the pathogen, for example, a virus to adapt to the host immune response. I'm always very often saying it's a host style immune response, because it is causing for the virus, an undesirable creating, generating an undesirable environment.
So this elective pressure enables the pathogen to adapt to this immune response, and thereby shapes the genetic diversity of the pathogen. It can broaden this genetic diversity. It can also narrow it.
And I will explain in a second how this works. This is just an overall definition.
So changes in this immune selection pressure, I was already saying the immune response of the population can also evolve, the adaptive immune response can evolve, and these changes will derive the evolutionary dynamics of the virus, because the virus is going to try to adapt to that in your response.
And such changes in immune selection pressure, we will see in one of the next courses can occur in your refocusing. So in this pandemic, we had events of the new refocusing.
I will not elaborate on this during this course, but in one of the next courses.
And to understand really the evolutionary dynamics of the virus and of the pandemic, for example, of the current pandemic, is absolutely fundamental to understand what immune selection pressure really is, and how it is generated.
And in the next slide, I will expand a little bit on this.
So how does immune selection pressure work?
Well, very easily, I hope everyone will understand that the more viruses replicate or the better viruses replicate, the more they produce viral mutants.
So, viral mutants are produced when viruses replicate and it depends on the type of virus.
For example, RNA viruses, they are pretty prone to mutations, even though they have what we call a polymerase proofreading function.
It's pretty funny that he mentions that I'm almost sure that him mentioning that polymerase proofreading function is a sign.
I know this is going to sound crazy, but I think it's a sign of coordination with other people because there's really no reason for him to mention that it doesn't really matter.
And the proofreading function of the polymerase still leaves it at about one error every 10,000 basis.
So I just want to take a side note here to kind of explain the swarm a little bit better than I have in the past, because I want you to understand the real wickedness of this live, because I'm only going to go on things that I've learned from reading pages and pages.
I mean, I'm no Charles Rixi. I haven't read 4,000 papers in the last three months, but I have tried to read as much as I possibly can, while also being a decent father and a decent husband and doing some streams.
And in that reading, I have come across this general trend, which I think best describes the way that this works, and so I want to share that with you now.
If you think as simply as possible and think about a viral genome being released into a cell, and if this is the viral genome in the green line here, the RNA dependent RNA polymerase is going to copy the RNA from one end to the other.
And because of the nature of RNA, there is a beginning and an end, and the RNA polymerase can only copy from that will beginning end and go down to the other end.
Now, keeping in mind that there is a high propensity for the RNA dependent RNA polymerase to jump off of the strand that it is copy and either find another strand to begin on or to float around until it hits the beginning again.
They're not really sure how to describe this, but nevertheless, the odds of it getting on a strand and completing it are not one, but less than one.
In addition to that, for every roughly 10,000 bases, and it could be worse, you know, but let's give them the numbers that they publish, for every 10,000 bases, there's going to be an error.
So if we try to distill this down to a funny cartoon, we could say that this single RNA dependent RNA polymerase protein was already successfully made by the translating of this genomic RNA into a poly protein, that poly protein got cut up reliably,
and then it assembled into the RNA dependent RNA polymerase, and now we're about to copy the genome for the first time.
So I've already given the virologist like half of their infection cartoon, because the virus got in.
It opened its genome, its genome was faithfully translated, that translated poly protein was then chopped up in a way that left it functional and folded correctly and assembled correctly, and now it's copying the RNA.
Let's just say that works.
Because it makes an error every 10,000 bases, the first copy of the genome will have three errors in it because the genome of a coronavirus is roughly 30,000 bases long.
So we'll have another genome over here, but it'll have three errors in it, which we will label A, B, and C.
Now the RNA dependent RNA polymerase has gone all the way down to the end over here in order to make this second strand, and so now the RNA polymerase is going to float back around and choose one of these two to copy again.
Now let's just say for lucks sake that it chooses the original genome again, and it makes another copy of it.
And that second copy also has three errors in it.
So those three errors are encoded there.
Now the RNA polymerase went all the way down to the end, and it made that copy, and so now it's going to come back down again, and oops jump down here and it made this one.
But that one's also got three errors in it.
But not those three errors, and additional three errors.
Now the RNA polymerase is going to come down float over here and it's going to pick one of these three and copy four and copy it again.
And I hope you're starting to get a strong enough imagination after having come here for evening after evening to realize that as this process continues, the likelihood of the RNA dependent RNA polymerase of choosing the original strand goes lower and lower and lower
and the odds of it choosing a strand with up to six, or even nine point mutations goes higher and higher and higher.
And when the virologists talk in numbers, they're talking about millions of viruses being produced so at what stage does this mathematics end up being that the original virus sequence doesn't mean jack.
Are you starting to understand what's happening here with the regard to the coronavirus quasi species swarm or really as,
as Vincent Ranciello said it's really just a mutant swarm but this old term quasi species swarm is what he still uses.
I mean that's not a very difficult explanation.
And it's not something that is impossible for you to understand right because the RNA dependent RNA polymerase comes around and copies this one this time.
And this one had a D and an E and an F and now it's going to also have a J and a K and an L.
And so now the RNA dependent polymerase is going to come around again. It's going to come down and up it got the original one again.
With three errors L, M, N, and O. Now the RNA polymer is going to come back around again. Oh, it landed on this one.
A, G, B, H, C, I, and then M, I know P.
Q, I'm running out of ink. See is it just too bad.
P Q and R.
And so as this system continues, as the replication of the viral genome continues, the mutant swarm, the quasi species swarm is defined exactly like this.
It's not a bad cartoon. This is the real thing right here. It's no more tricky than this.
And if you understand this, then you realize why even the consensus genome sequence doesn't mean jack.
And it is from this mutant swarm that the virus evolves.
And from this mutant swarm that it often crashes.
And it is from this mutant swarm that they told you that, you know, uniform sequences, clouds of Delta, then Epsilon and then Edra and Omicron swept around the world, country after country after country taking over.
As if somehow this process is a pattern generator that could make such a phenomenon.
Think about how preposterous that is.
Now keep in mind, these mutations are occurring across a giant genome.
So the changes are very consistent across the genome in the sense of, you know, they're tiny little changes among 30,000 bases.
But this process from person to person from infection to infection doesn't result in a directional movement, which parallels one another in each.
If I get a virus, I'm not going to produce the same delta that my wife does, even though we're married and have lived together for 20 years.
Because our immune systems are based on our genetic background and that random assortment of things and random responses to previous viruses, random memories from previous exposures that is unique for each of our histories that ultimately is
how our immune response will be to a particular novel signal.
So the idea that somehow or another, the virus will end up having the same sequence going around the world in different countries.
It is just the most absurd cartoon story ever.
And that's why the people who know it's a cartoon story are happy to go along with it because if you don't get it, wow, we don't have to worry about you figuring anything out.
Because this is available.
Anybody could have drawn this for you.
Anybody could have explained the basics of the swarm and the basics of the randomness.
Geert Vanden Bossche could explain this right now.
And explain why as this goes on, and this randomness happens, remember that for every one of these that makes it to the end, what was it again?
600,000 make it only to the E protein.
600,000 only make it to the end of the N protein.
Another 400,000 only make it to the end of the S protein.
And so only 11 of every 500,000 make it to the end of the whole molecule.
And all of them have the same error rate.
Try to start engaging your imagination as much as you can because it's your best tool for learning this biology, for letting this iteration go on in your imagination.
If you can close your eyes and do that, that's a huge bonus because you can really start to see how ridiculous this is.
If you're a programmer, you could write a basic program that would do this and you could start to get a feeling for what that swarm really is.
They could teach us this if they wanted to.
A polymerase is basically an enzyme that these viruses have and that enables them to correct some errors that are made in the DNA replication.
So the virus replicates, it needs to replicate its DNA.
And sometimes there are small errors so that they don't make an accurate or an exact duplicate of the original form.
And then to correct this, they have a polymerase proofreading function.
So an enzyme that can correct this, but despite this enzyme, you still will find it doesn't work at 100% viral mutants.
And of course, the more the virus replicates or the better, the quicker the facets replicates, the more viral mutants you will have.
So that is one thing. On the other hand, we all know that when a host is confronted with a foreign agent, for example, a pathogen virus, then there will be an immune response.
And the immune response of the host will target specific antigenic motifs on the circulating virus.
So there are certain antigenic domains on the virus that will easily elicit the new responses.
So the immune response of the host will then target those motifs and makes the virus, in fact, vulnerable and can destroy the virus, can neutralize it, for example.
But this progeny virus will, of course, also comprise mutants that have genetic variations of the targeted entities.
So if the antigenic motifs that are now targeted by the new response, if they change in certain mutants, for example, then these mutants can, of course, escape to this immune response.
So the antigenic variation that we, antigenic variations that we find in mutants and genetic variations of the targeted motifs, they can escape from the new response that was previously mounted by the host.
For example, this could be, this is the case, for example, in the coronavirus with influenza, with a number of other viruses, the primary new response that is targeting the pathogen is based on antibodies.
So ABS is the abbreviation for antibodies.
So antibodies against the circulating pathogen, if the target motifs are responsible for eliciting neutralizing, for example, anti-spank antibodies, then, of course, immune escape variants that can evade this neutralizing antibodies, just by chance, because they have incorporated some antigenic variations that enable them to escape
these neutralizing antibodies that have been elicited.
Well, those immune escape variants will have a competitive advantage.
They will be selected.
So now it's important to realize that that is not sufficient to generate immune selection pressure, because imagine if this phenomenon only happens in a limited amount of people,
then it will have no effect, because the virus need to be transmitted from one host to the other.
If, for example, 5% of the host population is putting, so to say, the virus under pressure and derive selection of some mutants, that is not sufficient to really make this mutant dominant in the population, because it will be transmitted, for example,
to other people who have no antibodies who are not going to put this selection pressure on the virus.
And therefore, this effect of immune selection will be completely abolished.
However, if this immune selection pressure occurs in a sufficiently large proportion of the population, then it will provide the selected, for example, more infectious immune escape variant
with a fitness advantage, not just in the one or two or, you know, percent of the population that, for example, is mounting these antibodies.
But at the level of the entire population, for example, or at the level of the majority of the population, if the majority of the population is indeed mounting such antibody responses.
For example, in the case if we do mass vaccination, we all of a sudden within a few months provide like 40, 50, 60, 70% of the population with antibodies.
Then, of course, the virus passes on from one individual to the other.
It will very regularly encounter the selection pressure, and it is this selection pressure that will give the virus an overall, an overall fitness advantage in the population.
Of course, it's more likely to survive and reproduce, and this will eventually enable this variant to replace other circulating viral lineages and become the dominant strain.
So that is important to understand immune selection pressure requires in fact that the majority of the population is able to exert such pressure.
The virus passes on from one individual to the other that a particular mutant that can overcome the activity of these antibodies has a fitness advantage in the majority of the population.
So we are 14 minutes into an intro lecture on the immunobiology of pandemics.
And as far as I can tell, so far, I'm not counting exactly, but this is what I had marked on the other page.
He has said virus, I stopped counting at 16, and that was on the third slide.
And now that he's starting to talk about the immune response and immune selective pressure.
He has talked exclusively about antibodies and neutralizing antibodies with the abbreviation and ABS or, yeah, neutralizing antibodies.
So it's not a very sophisticated immunology lecture because it's not going to teach you how immunology works.
It's not going to teach you how the quasi species swarm actually evolves and why Omicron going in can't be Omicron coming out.
And so therefore, Omicron coming into Pittsburgh can't be Omicron leaving Pittsburgh for Cleveland. That's not how it works.
It doesn't work like that.
And we're not even talking yet about the vast majority of these RNAs that end up being translated are sub genomic RNAs.
The vast majority of the viral particles that get produced are non-infectious.
We're not talking about any of these details yet.
And we're already way off course with antibodies, antibodies, antibodies, antibodies.
He already said antibodies to the spike protein because his whole stick in this course is going to be 12 lectures about how the mRNA vaccinations to the spike protein have pushed the virus around.
And they're going to make it more infectious or more virulent.
And this giant assumption that goes along with this lecture is that the mRNA vaccines can't hurt anyone.
And in fact, they augment the immune system to such a perfect degree that we can affect the specific evolution of a specific protein on a specific virus.
Think about how spectacular that is.
That is the 15 minutes in. That's already the summary of what this is all about.
That the antibodies produced by an mRNA vaccination and sufficient quantities put in sufficient arms as the capability of changing a global phenomenon in a specific direction based on a single protein of 31.
And we can see that pressure on that one protein across the whole globe.
Holy man, that's an amazing story.
I think it's a gamma delta omic wrong.
Some people are saying, yeah, this this variance existed already before the mass vaccination, et cetera, completely true.
But what what what was unique is that after mass vaccination, for example, this variant started to dominate in the population. And that was pretty exceptional.
So that's an interesting thing to say is that mean that he's really absorbing my story and our story that these variants were in the background all along.
And that now we're bringing them out of the background essentially by sequencing for them by adjusting the primers, adjusting the primers so that they find different things. Can you imagine?
Trying to target, trying to target sequences that are made up of this kind of randomization with primers?
And which ones you pull out would of this huge swarm of millions of sequences with this kind of error generation?
What sequences you pull out would depend on what primers you use?
And in order to amplify the entire genome of a coronavirus, you need to have 99 primer sets.
99 pairs of primers, 99 across the whole thing.
99 pairs of primers are in the average sequencing reaction.
And so if you subtly change those primers, then out of this swarm, you just draw different mutants.
Out of this background signal, you just draw different sequences. Don't you see it, my friends?
Nobody's checking this. Nobody's doing this.
Everybody takes for granted that this is being done above board, that nobody would ever screw around with this.
And they're counting on us not to see this. They're counting on us not to understand this.
Those variants were definitely in the background all along.
They were a random low level noise all around the earth for millennia.
And I have no doubt that every once in a while there are local amplifications of these RNA signals.
I don't know why or how or where they come from.
But you can be damn sure that they cannot pandemic like they have described on television.
Like he is describing now, there is no way in heck.
Propagation, dominant propagation of this variance does not necessarily result from immune selection pressure.
It is true that dominant propagation of more infectious variants may result from immune selection pressure at the population level.
That is what I just explained. However, even in the absence of immune selection pressure, there can also be spontaneous mutations that randomly occur.
And they may just by chance involve a number of variations of antigenic domains that are responsible for a higher level of intrinsic viral infectiousness.
That means that even in the absence of any immune pressure, a virus can become or muted can be more infectious.
And that more infectious virus will have of course an advantage towards other circulating viruses because it's more infectious and it could also become dominant.
However, and that is where we are saying the more the virus delivery.
If you have trouble understanding and picture the count from Sesame Street and then you can understand them easier. That's what I do.
For example, at the higher its level of infectivity, the more likely variants that exhibit a higher level of infectivity are going to emerge and dominate.
Antigenic motifs that confer a higher level of intrinsic viral infectivity.
So, even if immune selection pressure, for example on viral infectiousness vanish, that is what we are seeing right now in the pandemic.
The variants that are circulating right now, they are all very difficult to neutralize.
That means that they are largely resistant to the neutralization.
So, there is no fitness advantage of one of these circulating strains towards another because they all have in the context of the predominant antibodies in the population.
They have all a similar, I would say a similar advantage of being difficult to neutralize. So, if that is the case, if you cannot distinguish.
I mean, the whole immune response is neutralizing antibodies.
I mean, think about the level of sophistication that we are talking about here and the level of insulting that this really should be seen as.
This is not somebody who is trying to bring everybody up to speed to understand why natural immunity is something to be respected.
This is someone who is trying to explain to you why taking the vaccination was a mistake.
We should have only given it to old people or something. I don't know what he is going to say.
But if he wanted to teach immunology, he would have started in a different place.
If he was trying to teach the illusion away, he wouldn't be talking about antibodies for the last 20 minutes.
He would have started by saying they really misled you about the importance of antibodies.
And in actuality, the antibodies are the signal that they knew they could get if they transfected you and that's why they use it as a proxy.
But he's not trying to lead you out of the cave.
I'm not even sure if he's holding the flashlight.
And if he is, he's shining it back down deeper. That's for sure. This is incredible.
The level of neutralizability of the circulating strains.
Then, of course, if some of these variants happen to be more infectious, they will take over and they will dominate.
So immune pressure can be the cause or immune selection pressure can be the cause of dominant propagation of viral variants, but it is not always the case.
And so, that is something that is very important to distinguish because the question then is how can I distinguish between a variant that becomes dominant due to immune selection pressure, or a variant that becomes simply dominant
due to high intrinsic infectivity.
And the explanation is very simple.
And there's many publications that document is that in case the population is exerting immune pressure on the virus, for example, viral infectiousness, you will see that the evolution of the virus, the mutations,
they all go into the same direction.
So that's what we call convergent, convergent evolution.
That means that, for example, if you have immune selection pressure exerted by the population against SARS-CoV-2, you will see that the immune selection pressure is directed primarily against spike protein.
And it is essentially within certain domains of spike protein that are responsible for enhanced infectiousness or neutralizability that you are going to see those mutations.
So those mutations are convergent as they all respond to the same environmental influence, namely the pressure of antibodies on viral infectiousness.
So, for example, in the case of SARS-CoV-2, that spike is responsible for the infectivity of the virus.
So if you put pressure through antibodies against spike on viral infectiousness, then you will see that the mutations that start to dominate in the population, they all converge to domains within the spike protein
that are responsible for infectiousness of the virus.
Whereas if you have viruses that happen to be more infectious that have a high intrinsic viral infectiousness, but it's not due to a new immune selection, you may see several different mutations in several different parts of spike protein
or even in other viral proteins, and the addition of all these mutations makes so to say the virus more infectious, but it's not a convergent evolution of these mutations.
So the authorities have been saying at the beginning, well, you know, we need to do mass vaccination because we can reduce viral infectivity, which was the case at the beginning, which really was.
And they say the list of viruses going to replicate, well, the higher the likelihood that we will be able to restrain or to restrict the occurrence of more infectious variants, or the opposite, the more on the better device replicate, the more likely more infectious variants will dominate.
So with that only applies in the absence of immune selection pressure.
And this is so what I mean is that, yes, if you have, for example, no immune selection pressure on viral infectiousness, then of course, the more the virus replicates, the more likely some of these more infectious variants will pop up and take over and dominate.
But on the other hand, even if the virus replicates at a lower pace, and even if the replication is diminished, you can still have the dominance of more infectious variants provided provided you have immune selection pressure.
So, and that was what, what, what was happening at the beginning. So when we mass vaccinated the at the beginning, the infectivity went down decreased.
Despite this decrease and less replication of virus, we saw that more infectious variants were taking over and better, gamma, delta, omicron, et cetera, which can only be explained.
So in the absence of reduced viral replication, you can only explain the occurrence of more infectious variants that dominate if there is a new selection pressure on that particular characteristic characteristic of viral infectiousness.
So another thing that can, in the absence of enhanced replication that can lead to dominance of more infectious variants is, for example, when you have, and I will come back to this, it's a phenomenon that we call antibody dependent enhancement of viral infectivity.
And what this means is that you have, for example, antibodies that have low, allows the neutralizing capacity.
And even if the intrinsic infectiousness of the virus is relatively low, these viruses by binding to this, neutralizing to these antibodies that have a very low neutralizing capacity, they can become more infectious.
And that is a phenomenon I will come back to this that can be explained by the fact that simply binding of these antibodies to these viruses with low intrinsic infectiousness can enhance viral entry into susceptible cells.
And so by way of this antibody intervention, I would say the virus becomes more infectious.
And what an interesting thing to say when this doesn't say that at all. This says, anybody dependent enhancement of viral infectivity and curves after the first wave of a natural pandemic can confer sterilizing immunity to those who are initially asymptomatically infected.
The second and sometimes third wave is, or are critical in ensuring full fledged herd immunity.
These are some of the worst slides I've seen in a while, I mean, you know, if you're just going to read stuff, I guess, and you're not going to read what's on there but at least talk about something to do with what's on there.
The antibody dependent enhancement is best looked up for dengue fever.
The idea is that for whatever reason, the antibodies that you produced to your, to your previous exposure, enhances the disease upon second exposure.
The dengue fever, what happened was they vaccinated moms, moms had antibodies in their breast milk, and the antibodies in the baby when the baby was exposed to dengue fever, cooperated or assisted the antibodies in creating a worse infection.
Now, you can imagine that happening in a lot of different ways.
One of the ways that he is saying is it can infect other cells because the antibody allows entry, that's a very good way.
Let's just leave it at that, but let's just note that this isn't going very well because we are still, and I mean still talking about antibodies, antibodies, antibodies.
So antibody dependent enhancement of viral infectivity occurs, for example, after the first wave of a natural pandemic of natural pandemic we have seen as well.
I wasn't there, but people have reported this that this occurred during the Spanish flu in 1918, where there was a natural pandemic.
So no intervention with vaccines after the first wave, we had a second wave, and this second wave affected primarily younger people.
So what happened is that, and I will also come back to this phenomenon that the younger people at the beginning, they got asymptomatic infection.
So because of this asymptomatic infection, they only developed very low titers of neutralizing antibodies with low neutralizing capacity, because most of the virus was dealt with by their innate immunity.
So they, they only develop very low titers, short-lived antibodies that had poor neutralizing capacity, but these antibodies were able to bind upon next exposure, upon subsequent exposure to the virus.
They were able to bind to the virus and make the virus more infectious, so that the virus broke through the innate immune response of people who were initially asymptomatic infected, made them ill and enhanced spread of the virus, which is a very important phenomenon because to enhance spread of the virus, the population acquired it ultimately.
So, yeah, let's, for just a second, come to acute self-limiting infection, the definition thereof, and how it generates sterilizing immunity and protection from infection.
So what are acute self-limiting infections?
Well, acute self-limiting infection, I give you a number of examples like parvovirus, like endrovirus, coronavirus, influenza virus, etc.
So the virus infects the host cell, and it will initially, when the virus is released from the host cell, which you see on the left side of this cartoon, the virus will be bound by early antibodies.
We call these antibodies IgN antibodies. You see a picture of an IgM antibodies in the left corner at the bottom.
These antibodies, they are pentameric. These are basically five antibodies that are joined together through sulfide bridges, it's not that important, but you have to know that these early antibodies, or have more specificity,
but they can extensively bind to the virus, and they can build kind of immune complexes.
So with the virus, they're built immune complexes, these immune complexes are then taken up by antigen presenting cells, and then these antigen presenting cells, they will stimulate what we call cytotoxic T cells.
And that is important to know because these cytotoxic T cells, these are the guys who are going to kill, this is the red arrow that you see, to kill the virus infected cells.
And by killing those cells, they sterilize infection, they eliminate the virus because the virus can only replicate, of course, in living cells, in the living cell that is infected is killed by those cytotoxic T cells.
The infection ends, that is why we call these infections self limiting, and they are acute, but they are self limiting.
In the meantime, while this happens, the IgM antibodies, this is the number three on the top that you see, will evolve, so to say, into IgG antibodies.
And other isotype of antibodies that is characterized by higher affinity, and higher specificity, and also longevity memory.
So that means not only during acute self limiting infections, will the virus and virus infected cells be eliminated, but at the same time, the individual will be protected against upcoming,
or next exposure by virtue of IgG antibodies that have high specificity and longevity, so that can basically prevent the individual from being infected and contracting the disease next time around.
So this is important to know, because what results from this is, if you have, for example, a pandemic of a self limiting infection, such as coronavirus, influenza virus would be the same, you will automatically be dealing with a pandemic that will also be acute self limiting.
And that is what we see, for example, if you look at the curves of previous pandemic, best documented, or of course the influenza pandemic, you see that this started all of a certain acute, but then after one or two waves, it was in fact almost under control,
and it was self limiting that pandemic came to an end and transitioned into endemicity. So very typically for acute self limiting infections, when they cause a pandemic, you will have also pandemics that are self limiting, and that end after a few months and transition into into endemicity.
So, so I just kind of, I got to go back a little bit this.
So it would be nice if you would explain this, this basic immunology a little more, it would be nice if you would say that this target host cell is likely a dividing barrier cell like an epithelial cell.
It would be nice if he would say that there's a mucosal layer here with IgM and IgI sorry IgA antibodies in them that have the same poor specificity, but they would bind to the virus, get rid of it.
It would be nice if he would say that the proteins which are expressed by the infected cell are presented on MHC molecules on the outside of the cell, and it's the MHC molecules that are read by the cytotoxic T cells.
It would be nice to for him to say that antigen presenting cells have already presented viral proteins to the cytotoxic T cells of previous infections to the helper T cells from previous infections so that any target cell that was expressing an RNA,
an RNA polymerase, would surely be presenting a protein that would already have a cytotoxic T cell aimed at it.
And so yes, there are IgM antibodies which will mop up any viruses that go systemic, but the T cell memory that's required to get rid of these cells already exists, especially anybody older than six months old.
Certainly anybody older than three.
So the idea that somehow we need to augment this, of course it's ridiculous, but more importantly, the idea that this is an attempt at teaching this, this is frustrating to me.
He's using stars to represent IgM antibodies.
He's got a target cell here that looks like it was drawn with a, what is this?
Really?
We're supposed to pay $160 a person to take a 12 week course with this guy drawing pictures?
$160 for 12 weeks of immunology.
Can I get people to pay that much money that I'm doing the wrong thing?
It better not be thousands of people paying for his immunology course, or I'm going to go bananas.
But I think I should register for it.
I think I should do the whole thing with you because either he eventually teaches immunology or it's going to be 12 or 20 weeks of fraud.
It's not that all of this is necessarily wrong.
It's just, it's not well taught.
It's omissive.
It's insulting.
It's not well planned.
If this was going to be an overview, you know, think about the overview that I've been doing of the immune system over the last few lectures with the drawing that looks like a kidney beat.
I mean, I don't, I don't get it really, but I'm just going to keep watching because I do want to go to bed at a normal time and there's still 30 minutes left. Maybe I'll see.
In an immunologically naive population, acute self limiting viral infections.
Yeah, that's the abbreviation I will use during my course.
Yeah, one needs to get a little bit used to this or a cell.
The IQ self limiting viral infections or acute self limiting viral diseases.
They lead to self limiting pandemics or in the case of acute self limiting viral disease to self limiting epidemics.
So what is the difference? For example, Pirona, SARS-CoV-2, I should say, is an acute self limiting infection.
But for example, MERS and SARS, also grown viruses, they cause acute self limiting viral disease.
So what does that mean? Well, when you get MERS or you get SARS, you will have symptoms.
So you will, the infection will be symptomatic. And because it is symptomatic, people are either seriously ill or they need to go to the hospital or they could even die.
People are almost like naturally automatically isolated from the rest of society.
And therefore, it's easy to stop these infections because people only shed the virus when they have the symptoms.
So when these people are removed from society because they are in bed, because they die or because they are in the hospital,
well, automatically the transmission of the virus will be dramatically diminished even to an extent such that the virus can no lower exist in that it gets eradicated, for example.
And therefore, these diseases like MERS and SARS, and we have seen this, will not cause pandemics.
Pandemics, we will come back to these notions, of course. Pandemics means global spread worldwide.
But these diseases can relatively easily be controlled, because as I was saying, even almost like without public health measures,
people will isolate or they will be removed in one way or the other from society.
Transmission will dramatically diminish and before the virus can further spread, it will, it will, you know, virus will be eradicated or anyway, transmission will be stopped.
So the virus can in general spread to a number of countries. We also call this multi-country epidemics, but never ever develops into a pandemic.
This is different from coronavirus because sorry, SARS-CoV-2 virus, because SARS-CoV-2 virus also being a coronavirus can asymptomatically spread.
So that means a number of people can spread the virus without showing symptoms.
And that, of course, is very tricky because that easily leads to worldwide spread of the virus because, you know, people also say healthy, have only mild symptoms.
They travel, they are in contact with nature, they don't isolate, they don't want to eat, et cetera.
So, but anyway, in case of self-limiting infections, you have self-limiting pandemics in case of self-limiting viral diseases like MERS and SARS, you have self-limiting epidemics.
And that is thanks to herd immunity, we will come back to this in the case of pandemics.
Or thanks to infection prevention measures, what I mean with infection prevention measures is that human behavior being in bed or being hospitalized or even dying is a measure to prevent infection.
Of course, you can add also public health measures that will further prevent the spread of the infections.
They will be very efficacious, of course, because we are dealing with symptomatic infections.
And that is what will make those pandemics or epidemic self-limiting.
So in the case of acute self-limiting viral infections, herd immunity will enable the virus to transition into obesity.
So, okay.
But not prevent asymptomatic infection, I already explained this.
It's strange. I don't know.
I have trouble with this.
I have trouble with this asymptomatic spread means it's an easy pandemic.
I really have trouble with that.
I also have trouble with them mentioning IgM, and they're not really explaining what the deal is with that.
But this asymptomatic spread stuff is pretty much nonsense.
And I think we can all agree on that.
But asymptomatic spread could be a way of them covering up for a mass clone release, for example, now I'm just shooting from the cuff here.
But if you sprayed clone all over Pittsburgh over the course of three weeks and only a few people got sick, but a lot of people tested hot positive for a PCR test, that might be considered asymptomatic spread.
A much more likely scenario is erroneous, nonspecific PCR primers, PCR diagnostic tests being used to create profit, to create illusion of confusion, spread, fear, doubt, whatever.
So asymptomatic spread is a wonderful, wonderful, very simple, but fancy sounding, you know, asymptomatic spread.
With no symptoms, you can't smell it, but it's there anyway.
This is a typical Giordano technique.
There's going to be the symptomatic people that complain of the symptoms and they're really sick.
And then the really way we get them is the internet.
And we tell people that our other signs of what did he call it, antidromic spread, something like that, where they get anxiety, sleeplessness.
And so symptoms that a lot of people have from stress end up becoming symptoms of the asymptomatic spread.
And that's exactly what they did to us.
Every little sniffle, every little cough, test, positive, bang.
I'm going to test positive. I'm going to test too because my wife tested positive. I better test.
I must, I'm asymptomatic. See, it's me.
It's definitely a game. It's definitely being played and it's definitely being perpetuated here.
In 2023, this is the second half of 2023.
And someone is teaching us immunology and it's all about antibodies and it's all about asymptomatic spread being one of the key aspects of the potential pandemic potential of coronaviruses.
To jump from being a self limiting infection to a pandemic, flying free.
Hope you can see it. It's pretty bad news here.
I don't want to tell you, I was hoping there would be a little more, a little more sacredness in this, in this video, a little more reverence for the, the divine.
But this is just the TV stories, the crappy immunomethology that's been pushed out us for the last three years that they're, they're deceiving our children with.
Is he any different? I don't think so. It doesn't seem like he's any different.
So not prevent asymptomatic transmission. Whereas in the case of acute self limiting viral disease, infection prevention measures will even enable eradication of the virus in the affected population.
So, of course, if you have animal reservoirs, like, for example, for, for, for MERS and camels, for example, you will not be able to really eradicate the virus because the virus can come back from this reservoir and spill over again to the human population.
But if you think about how diabolical it is, if we made a camel specific coronavirus and tried to infect camels in the Middle East, just because, you know, we can.
A real, a real nice infectious clone.
Think about that. Who would have and virus that cannot be harbored, that cannot survive, let's say, in animal species, like, you know, back in the 19th century, small books.
And it was put exclusively infect humans. Then it wasn't, and it was an acute self limiting viral disease. You really get eradications or no animal reservoirs.
Endemicity of viruses call causing acute self limiting viral infections will enable regular flare ups, because the virus can still circulate.
And with enhanced infection or morbidity rates, that's what we are basically seeing with influenza viruses, they are endemic.
And from time to time, because the virus can circulate asymptomatically from time to time, if immunity wins, you can have a flare up a breaker and outbreak with enhanced infection and morbidity rates.
So, if you are okay, I propose to have a break for, like, five or ten minutes, and let's say, well, let's, let's come back maybe in ten minutes.
I imagine that this is a lot of stuff for you guys and that's going to have a break before we continue.
So let's, let's, let's connect again in.
Understood herding unity. When talking about pandemics and epidemics is, of course, what is hurting unity. Herding unity is a notion that is not well understood.
And it is key. So you have to bear in mind that no pandemic can be ended without hurting unity. So in the context of acute self limiting infections.
So let's just make one thing very clear. Please, everybody must hear it. Please hear it.
Everybody must hear it. Please hear it.
Clint, why aren't you listening to me? Listen to me. Listen.
Yes.
We are talking about the immunology or the immune biology of pandemics.
With a guy who's one of the leaders on the dissident side, the speaking upside, the Malone team.
About this gain of function, possibly lab leak virus.
And after talking about the immune biology of this pandemic for more than a half hour.
We haven't talked about the PCR testing as the fraud that it was.
We haven't mentioned masking and how that damaged people or the shutdowns and how that damaged people.
We haven't talked about the lack of evidence for spread in New York or any of these other large cities.
We haven't talked about the death certificate fraud or the protocol frauds that included do not resuscitate orders.
Remdesivir, Madazalam, that probably killed hundreds of thousands of people.
And from here at Funden Bosh's perspective, the way to start talking about this is neutralizing antibodies,
antibody-dependent enhancement, and immune selective pressure.
I mean, I don't know, he's going to say all he says all kinds of things.
It is an absolute exercise in stupid complicated.
Because it is stupid complicated. It's not sharp complicated.
It's not useful complicated.
It's not thoughtfully complicated. It's stupid complicated.
With slides full of text, illustrations with bad symbols and bad shapes so that no real information is conveyed.
And except for the fact that it's so complicated that it's really hard for this very nice gentleman to distill it down to anything that I can understand.
But you know it's not his fault. I'm just dumb.
I mean, it's extraordinary ladies and gentlemen because people are going to pay money to take this course and to follow along and to be told how antibodies and how antibodies work and how antibodies are selected and how antibodies are fine-tuned.
How come he didn't say anything about original antigenic sin yet?
Isn't an original antigenic sin kind of a related to antibody-dependent enhancement in the sense of once you go down a certain, you know, memory cell, B cell pathway?
It's kind of hard to go back.
Oh, boy, ladies and gentlemen, I'm not sure really what to say other than this is this is going to get.
Oops, sorry, I guess I did that wrong. Where are we going here?
I just need to get rid of the.
Get rid of this. There we go.
Or acute self-limiting diseases hurt immunity refers, in fact, to a level of protection against the transmission of the infection or the disease within a given population.
So you can already see this has nothing to do in principle.
It has nothing to do so to say with antibodies.
It has to do with a level of protection of the population against transmission, transmission of the infection in case of acute self-limiting infections or transmission of disease within a given population.
So both natural infection and vaccination, primarily with life attenuated viruses can contribute to herd immunity.
So I've been describing and mentioning several different contributions that vaccination during a pandemic can not generate herd immunity.
Well, it all depends on when you do the vaccination if people are vaccinated in advance before being exposed to the virus.
Vaccination as well can of course contribute to herd immunity.
It depends when you perform this vaccination and we will see why this is so important, the moment at which you perform vaccination.
When you do this during a pandemic, you will never generate herd immunity.
When you do this outside of a pandemic, of course, vaccination can contribute to herd immunity.
So optimal herd immunity is achieved.
So again, here we have another example of someone who doesn't seem to be on our team.
No mention vaccination works fine and that shouldn't surprise you. He's a vaccinologist.
He's worked on the flu vaccine. He's worked on animal vaccines, which is also interesting, right?
Because he knows about the feline coronavirus vaccine. He knows about the HEPA virus vaccine and horses.
He knows that vaccinating against these types of RNA viruses generally goes south.
He knows that. He knows that. Don't you see? He actually knows that.
He knows it.
Hair fun and Bosch knows that in veterinary science, vaccines don't work very well.
Not all vaccines are bad.
I've been vaccinated against rabies.
I think that was a that was an intramuscular injection.
I tested positive for the titers.
I don't know if I would be protected against rabies if I got bit by a bat, but I was recently vaccinated for rabies.
But rabies is a protein and an adjuvant.
So it may work a little bit.
It may have also made me vulnerable to to other problems.
It may be the reason why I'm losing weight for the last three years.
Because I got vaccinated for rabies and then didn't eat right or something like that.
Developed auto immunity to my gut floor.
And now I have different gut floor that isn't healthy for me anymore. I don't know what happened.
But I know that when I landed here in 2016, I used to weigh about 205 pounds and I was 6 foot 5.
And now five years later or whatever.
Oh my God, it's terrible how many years later it is.
I told my wife it would be in the United States for five years.
Now I weigh like 170 and that's so can wet.
So I don't know what's going on here.
Ladies and gentlemen, when I reflect on my history and my health history,
my rabies vaccination sticks out pretty highly in my mind now.
Because I don't take the flu vaccine. So the last vaccine I had as an adult was the rabies vaccine.
And the last time I weighed more than 190 pounds was when I got off the plane in 2016.
And I'm not blaming the rabies vaccine, but I have not been healthy in a very long time.
And here just told us that herd immunity is vaccination plus infection and it just demands the real trick here is, you know, the time when you do vaccination, you know, if you vaccinated the wrong time, it might not give you herd immunity, it might just push the virus around
and you'd create more infections.
But if you vaccinated the right time, it's great.
It's sufficiently large portion of the population develops, sterilizing immunity towards the circulating virus or the circulating publishing.
So again, sufficiently large, not everybody needs to develop, sterilizing immunity, but a large portion of the population and sterilizing immunity. What does that mean?
That means that you develop a kind of immunity that is able to eliminate the infection. That is very.
I think that this has to be said for what it is.
Two and a half years ago, I was teaching sterilizing immunity as a as a fact or as a known phenomenon. It's not a known phenomenon. It's not a fact.
It is a concept that perfect immunity would result in sterilizing immunity that the virus wouldn't be able to replicate.
A much more likely scenario is something very, very different. And I'm sure you can imagine it. This is biology.
And so you just get rid of limited or reduced infection or you get limited and reduced infection that is tolerated.
Where the immune response of inflammation, etc. is dampened after each exposure.
But the virus is able to make little copies of itself sure and tell the T cells come in and find those cells and eliminate them because they're dividing anyway. Of course that's works. That's fine.
Sterilizing immunity, I think, is something that has been more recently pushed to give the idea that that is a goal.
That is a biologically achievable goal. And we should have that as a gold standard for what we expect for immunity. And if you can't prove that you're sterile, then you're infected.
And that's why I think he's pushing this and he's been pushing it for a very long time.
And in fact, I think that sterilizing immunity as a concept is something that just spontaneously appears in the literature. And certainly during the pandemic, this is one of the first guys pushing that concept regularly.
And how in the beginning, he was saying that the transfection wouldn't give us sterilizing immunity. And I even wrote a review based on this guy's stuff in May of 2021, where I said that where I wrote that that sterilizing immunity wasn't possible with this, with this
observational vaccine. So don't get me wrong. I'm still crawling out from underneath this rock. I'm not some kind of, I told you so a long time ago with this aspect of the things.
I was fully under the spell of care at Funden Walsh. Absolutely, I was.
And that's important and critical to understand. Here, herd immunity, however, will not prevent asymptomatic transmission in a population, because to prevent asymptomatic transmission in a population, you would need to eradicate the virus.
I just told you before that if the virus becomes endemic, for example, we have this with influenza virus. We have this, for example, in many countries with for diseases like measles, for example, you can have asymptomatic transmission.
The virus is still there. It can transmit without, you know, without causing any disease. So, you know, you don't, you don't see this, there is no outbreaks, but the virus can be transmitted.
It will not prevent transmission, but and this is almost with regard to pandemics with regard to COVID-19, the accurate definition, it can diminish the level of viral transmission down to a level where individuals who have not been immunized.
And for example, for lack of exposure to white virus or to live attenuated viruses are nevertheless protected from symptomatic infection. So you to herd immunity by the fact that a large part of the population will be able to eliminate the virus.
This will result in levels of transmission that are so low that individuals who have not been exposed to the virus are nevertheless protected, not necessarily from infection, but from symptomatic infection, because the level of viral effectivity will be so low that it is not able to cause the disease.
It can cause asymptomatic infection as I just explained.
He is really contradicting himself though, right? Because the asymptomatic infection is the variance that will, from which is more infectious variants emerge.
You can't have it both ways. If the immune system being trained by the mRNA can push the virus into more infectious variants in one scenario, then if there's asymptomatic transmission in this scenario, then it should be evolving as well.
So something is really very contradictory all the time when you try to tell the story about viruses that can go around the world and that sometimes stop and sometimes don't.
Sometimes the RNA has the staying power of many decades and sometimes the RNA has the staying power of a puffball mushroom.
It's very, very strange. It's very, very strange.
They really think that they have most of our families and friends so bamboozled that they can just say whatever they want to, as long as it roughly lines up with what the TV has said for the last three years.
Not symptomatic infection, no disease. That is a definition of herd immunity.
So herd immunity is the cause of the self-limiting nature of pandemics triggered by viruses causing acute self-limiting viral infection.
So to control the spread of infectious viral disease, public health strategies have often simulated have often mimicked natural infection induced in unity by using life attenuated vaccines to fill the gaps in herd immunity.
So what does that mean? Well, because natural infection is so efficient in establishing or reestablishing herd immunity because it induces sterilizing immunity.
Public health authorities have learned from this and in cases, for example, there are gaps in herd immunity.
For example, when newborns, they are immunologically naive.
They are born, for example, in populations that have herd immunity, but they themselves are immunologically naive so they cannot contribute to this herd immunity.
So there is a gap in herd immunity. How can you fill up that gap in herd immunity?
Well, we know that live viruses can induce the sterilizing immunity.
Of course, you don't want to infect those children with veteran virus, but you can infect them with live attenuated viruses that will prevent the disease from developing, but that will enable the virus to infect this cohort of immunologically naive individuals,
for example, young children, and by doing so, you fill up that gap in herd immunity.
So the prophylactic immunization with live attenuated vaccines is the cornerstone of the childhood vaccination program aimed at protecting infants from measles, for example, mums, rubella, varicella, and polyovirus.
As a vaccinologist, I'm the first to say that, of course, in certain children very rarely, this can lead to adverse events because nevertheless you're still using a live virus.
The world has a weak immune system. It could still trigger disease and cause sick value, but it's the best we have right now to fill up gaps in herd immunity, not to protect just an individual.
That was some weak mealy mouth stuff right there, trying to say that live attenuated vaccines are causing something and that, you know, I'm acknowledging that occasionally there's injury.
That's some rich stuff right there. Live attenuated vaccines are not the ones that are causing the problems, a single shot of measles, a single shot of mumps, single shot of rubella.
None of these things were ever being cited as being part of this problem.
And he knows that. He knows that. It's the recombinant vaccines that are the problem because they require an adjuvant.
Goodness sakes care. Goodness sakes care.
Come on, these live attenuated vaccines are often oral or, or, or subcutaneous, you know, they're, they're, oh my gosh, come on.
But to protect an entire population. And I'm also the first as a vaccinologist to advocate for new methods to vaccine children in a way that we can strengthen their immunity without the need to use live attenuated vaccines, but that is, that is definitely for the future.
So by filling up gaps in herd immunity.
We're seeing that we should get rid of live attenuated vaccines and go to some other method, which is what, mRNA really safe genetic vaccines, because the recombinant vaccines don't work.
That's intramuscular injection of a combination of substances to augment the immune system. We already said that was dumb.
You've got to augment the immune system at a barrier.
We've got that at all. He's actually saying the live attenuated vaccines have hurt kids. And so we, I do agree that in the future, we should move away from live attenuated vaccines.
You know, the live attenuated vaccines that Krista seems to bell Ben and her colleagues have shown lead to five times less all cause mortality rate than the recombinant vaccines.
We've got vaccines to bell Ben's work. Man, oh man, this is, this is crazy.
Put immunization with live attenuated viruses, not only protects the immunologically naive infants themselves or children, but also indirectly.
That is very important protects other vulnerable people, such as the elderly and individuals with weakened immune systems.
The immunity renders these individuals and elderly people, people with underlying diseases, more susceptible to severe illness or complications from these infections.
And that is where herd immunity comes in. If you have herd immunity, these people can benefit from the herd immunity, despite the fact that they have a weakened immune system.
The threshold of zero conversion for the herd immunity varies depending on the level of preexisting population level innate immunity, viral infectiousness and viral shedding.
Well, this sounds complicated. It isn't. So if you get infected, for example, you will develop antibodies. If you are immunologically naive, you didn't have contact with the virus.
You certainly didn't have antibodies against the virus. All of a sudden, you get infected. You will develop antibodies.
If you are from white to black, you go from no antibodies to antibodies. That's what we call zero conversion.
So now you could say, well, if we have a pandemic, that's what authorities tried to do at the beginning. And that's also what they did in Sweden.
For example, when the pandemic came, they were looking how many people developed antibodies and based on these antibody levels, they were trying to make an estimate or whether or not you would have hurt immunity.
Because the more people get infected, the higher the likelihood you get to hurt immunity. And of course, the higher the likelihood that people develop antibodies that they still convert.
However, this very much depends the level of zero conversion, the rate of zero conversion in the population, of course, very much depends on the level of preexisting population level innate immunity.
For example, young children have innate antibodies that can protect against infection. So they are protected to a large extent by natural innate antibodies.
And of course, they will not zero convert because they are already protected. On the other hand, if you have, for example, a virus that has low infectivity, then of course fewer people will develop antibodies.
They will get infected, but primarily develop asymptomatic infection. They will develop a little bit of antibodies, but these antibodies will disappear within a few days, a few weeks.
So the zero conversion rate is also quite low and will be much lower compared to the cell conversion rate in a population that is exposed to a virus that is very infectious.
And that will, of course, spread rapidly and will, of course, lead to the elicitation of antibodies in many, many people. And also, it depends on viral shedding.
The amount of virus that is shed by an infected person, if that amount is pretty low because the shedding is pretty much under control, then again, it is an additional, an additional way, so to say, of protecting the population that requires less herd immunity, less immune responses because the shedding is low.
So also in populations, exposed to viruses that are shed at low rates, you will see that the cervical version rate is also pretty low, despite the fact that the research immunity.
So you cannot say, you know, for all kinds of populations, regardless of age, regardless of the infectivity of the virus, regardless of the transmissibility of the virus, you cannot say you need to have like 50% of cervical version to conclude on herd immunity.
That is impossible. Highly infectious viruses, for example, will spread more rapidly. You could say, wow, that's fantastic, because then we will have very fast, we will have very fast herd immunity.
Yes, that's true. So they enable the population to more rapidly reach herd immunity. However, the more infectious the virus, the higher also the incidence of disease and also the incidence of severe disease.
So it's so, remember that he told us that Omicron was going to be really handy because it was so infectious that it might vaccinate the whole world.
Carried funding bullshit is one of the guys that really said that first.
He seems to be describing that here, which is a little strange.
He's used the threshold of serial conversion to define where herd immunity begins, which means, again, he's defining herd immunity simply by antibodies.
It's all antibodies, serial conversion rate, viral shedding phenomenon that are very scary to somebody who doesn't really understand this biology, but completely reinforcing the Scooby-Doo of a novel virus that we had to do something for that the mRNA certainly helped.
And then it was definitely going to come again. This old talk has been about how it's coming all the time.
And previous acquired immunity is meaningless to hard-funded boast. There's no previous immunity to this, any other, no meaningful, nothing.
It comes with a price to pay. So fast herd immunity usually implies a higher level of viral infectivity, but a higher level of viral infectivity, especially if it is due to high intrinsic efficiencies of the virus will cause more cases of disease and severe disease.
In case the population benefits from some preexisting innate immune protection. That's what I explained a minute ago. For example, due to preexisting from preexisting, sorry, I'm trying to.
Okay, sorry. In case the population benefits from preexisting innate immune protection, for example, due to the preexisting innate or natural antibodies in young children, or, and we will come back to this, to reign innate immunity in healthy people that got infection.
So people can also train their innate immunity and make it so strong, basically, that they can be protected against infection, eliminate infection without having to rely on antibodies.
See, so here he's selling his product, because he's interested in modifying natural killer cells. And so he's saying that trained cell-based innate immunity, which is not T cells, innate immunity implies natural killer cells.
So what he's saying here is that besides innate immunity, there's antibodies. So he wants you to forget about T cells completely. Even though he did say cytotoxic T cells earlier, there are no previously activated and instructed T cells, which have any bearing on this virus that he's talking about here.
Otherwise, he would say that. That's why he chooses cell-based innate immunity.
And no antibodies in these people will be elicited or at most very, very low titers. So herd immunity in those cases will be achieved at much lower cell conversion rates of neutralizing antibodies.
So herd immunity versus herd immune selection pressure. So what is the difference? Well, when a sufficiently high fraction of the population exerts immune pressure on the virus, but that immune pressure does not suffice to kill the virus, to eliminate the virus.
If it's suboptimal, then what it does, it does not generate herd immunity. I was just saying, in order to generate herd immunity, a substantial fraction of the population needs to offer sterilizing immunity.
If that the immunity that is raised in the population is suboptimal and not inducing sterilization of the virus, what you get then is what I call not herd immunity, but herd immune selection pressure.
Remember, that was what we were saying at the beginning. If you exert immune pressure on the virus, but it's not sufficient to kill the virus, then you will give the opportunity to that population to select viral mutants that are able to.
What if I explained it this way? I hope this is going to work.
You are in, you're a dog, and you want to, you're afraid of people.
And so you're afraid of people, you're a dog, and your owner that made you afraid of people wears a red hat.
And that red hat means that every time that that dog, you, you, the dog sees another person with a red hat, you're especially stressed.
It's not good.
Now, the only way to get rid of that would be to have somebody with a red hat be really nice to the dog really, really often, while nobody with a red hat should hurt the dog anymore.
That learning that I just described with a dog is impossible in the immune system.
So, in other words, what you have done in this scenario is rather than let dogs become accustomed to their owners.
We have taught all the dogs in the world, no, this is going to go wrong here, this is probably going to go wrong here, this is not going to work right.
It's a bad analogy, sorry.
But the first part isn't wrong. A dog could become afraid of a certain type of person or with a certain person with a certain uniform on, and you could rehabilitate that dog by changing its experience around people with that uniform.
With the immune system, if the immune system is instructed to force to focus a complement of immune cells, T and B cells, to a particular protein, that memory is permanent.
And any time that memory is provoked, then T cells and B cells will go into an orchestration and attempt to further modify and specify that memory complement, that linked recognition associated with this epitope or set of epitopes.
What he's describing here, this immune selective pressure that could be raised as a result of transfection assumes that the immune system completely normally produces zero prevalence and therefore B cell and T cell memory to the spike protein and its epitopes as selected by your immune system.
It assumes no damage, it assumes no errors, it assumes no mimicry, it assumes no autoimmunity, and it assumes no other T cell or B cell or immune, sorry, innate memory matters for this virus.
It's really talking about a blank chalkboard and how that chalkboard needs to be filled in before people have herd immunity, nothing else previously matters.
And this is such a foundation for the faith because the faith is based on this is a novel virus that wasn't here before and everyone is vulnerable.
And so what he's doing is very carefully, and it's taken me a long time to get to this point.
I apologize, he is taking his through this hypnotic discussion, but he is laying down the mythology, the very foundation of what it means to be novel, what a novel response to a novel pathogen is in the cartoon representation of the simple immunology
of a pandemic.
And that is that you need to build antibodies and the antibodies are two certain targets.
And it's not a good idea to push one target at the start of a pandemic. That's all he's got.
And this cartoon does not question the faith at all. In fact, what he's pushing right now is exactly the faith.
Because the population has no meaningful fraction of immune response to a novel virus. That's the story he's telling you.
And so we've made a mistake by trying to augment the immune response to a particular protein when everyone was vulnerable.
A novel virus for which everyone was vulnerable.
Overcome this optimal immune pressure. And if that occurs at the population level, you will select variants that start that are more infectious and start to dominate in the population.
This sharply contrasts with the situation where a sufficiently large fraction of the population exists optimal immune pressure device optimal means sterilizing, then you have herd immunity.
So people are often confounding. Not at least our health authorities hurt immune selection pressure. This is, you know, referring to a population that may have, you know, high levels of antibodies that may have been vaccinated boosted, et cetera.
But that is not capable of killing the virus that is exerting some optimal immune pressure. That is hurt immune selection pressure, which only derives the propagation of more infectious variants.
A natural pandemic of always when at all talk about a pandemic, it's always a virus causing a new self limiting viral infection eventually generates optimal immunity in a sufficiently high fraction of the population to generate herd immunity against viral infectivity.
And that is what simply in a natural way and pandemic very, very logical mass vaccination. However, during a pandemic generates suboptimal immunity in a sufficiently high fraction of the population mass vaccination sufficiently high fraction of the population could be 40% 50% 60%
to generate not heard immunity, but heard immune selection pressure of viral effectiveness, which is not something we want. What is the key message really? Well, you know, the key message I mentioned it already is the only way if there is one thing that you, you know, keep in your head and for the rest of your life is that the only way for a population to end a pandemic is to establish
immunity. If you if the population cannot generate herd immunity, you will not end the pandemic. I would say in a friendly way. Okay, so this is the story and I'm afraid we're going to have to knock it down.
Or at least very much question the idea that my immunity affects your immunity.
That my vaccination status affects your potential health risks.
That heard, I mean, we are part of a herd.
Is not very far away from community health.
Not very far away from communal health, not very far away from public health.
And that is this illusion of everybody's vulnerable. Everybody has a role to play in this.
Everybody has an obligation in this.
That's where this is going. And I know that herd immunity is an old concept, but it's an old concept based on very bad epidemiological models of how disease passes.
And it doesn't take into account many, many other factors and with reasons why there has been an ever decreasing incline infectious diseases in the last decades.
But let's keep listening. I want to get done.
This requires a substantial part of the population to acquire sterilizing immunity. This can only occur if the population level in your response or population level in your response is the overall in your response of the population to the virus does not drive viral
immune escape. If you have not heard immunity, but you have a herd immune selection pressure, you will drive the propagation of more and more infectious variants.
And that drives viral immune escape and the antibodies, even if people were not vaccinated, but naturally infected cannot deal with this because the antibodies are no longer a good match to the new variants.
So now he's saying that even people who are naturally infected, their antibodies also can't handle the evolution of the virus being driven by the people who are vaccinated. Listen carefully to what he said, because this is important.
Because the antibodies are no longer a good match to the new variants that are now dominantly circulating.
So hurting unity naturally occurs during a natural pandemic, which is nice. And then you could ask the question again, why does natural pandemic not result in viral immune escape? And I will explain this in a second.
It's very important of course to understand. Vaccine coverage rates or vaccine induced antibody rates.
Is he saying this is not a natural pandemic then? Is that where he's going with this? Why does a natural pandemic not result in viral immune escape?
A such or not a reliable metric of the level of herd immunity generated during a pandemic.
So very often people say, wow, we have 80% of the people vaccinated or we have 20% naturally infected, 60% vaccinated, 20 and 60 is 80%.
So we should have herd immunity. In fact, that has nothing to do with herd immunity, as I said, it all has to do with sterilizing immunity and reducing the level of transmission of viral population.
And in the human population, and I will come to the explanation as to why a natural pandemic does not result into a viral immune escape.
But we should first maybe elaborate a little bit on the definition of of ethnicity, pandemicity and epidemicity because very often I see that these terms are mixed up and sometimes people refer to epidemics when they're talking about pandemics and vice versa.
So it's important to have very clear definitions on this that also makes sense and that one can use, you know, over and over again, you will not need to change those definitions as we have seen in the past, according to the evolution of the virus.
They are carved in stone, and they are like, you see them here, they are correct.
And the necessity refers to an infection that can spread asymptomatically in a specific geographic area or a specific population, and it's consistently present, but usually at a relatively low, but stable rate.
And it's only under certain conditions or in specific geographic areas or populations that endemic infections lead to outbreaks of disease, for example, measles in developing countries, for example, influenza also in our regions.
It's seasonal, so it's also due to a specific situation, but basically the virus is always there, right?
And it points to a gap in herd immunity and combined with a relatively high viral infection rate because gap in herd immunity, people, for example, elderly people in developing countries, I was talking about the measles, I was talking about the newborns, the immunologically naive people.
And if you combine this, for example, with a high viral infection rate, as we have in the winter season, because people are spending more time indoors, and for example, with measles, you have in certain countries due to poor hygienic conditions and also crowding, you get high viral infection rates.
This combination, the gap in herd immunity and relatively high viral infection rates can lead to outbreaks in countries in areas in populations where the virus is endemic.
So what is a pandemic or a pandemic refers to a sudden and a global spread of the infection with predominantly cases of asymptomatic and mild infection, that is the predominant mild infection means, okay, you can have mild symptoms, you can maybe be in bed for a day or two, but certainly not severe.
And fewer cases of moderate and severe disease, these are, you know, not necessarily the exceptions, but the vast minority of cases develop moderate or severe disease, the vast majority is asymptomatic and mild infection.
That's what we have seen at the beginning of this pandemic.
And this is simply due to the fact that there is no herd immunity population is immunologically naive, and therefore also the virus can spread very rapidly, and therefore it's a global spread.
Epidemic or epidemic refers to a sudden and widespread spread of the disease. I was saying, for example, MERS, SARS, acute self-limiting, viral diseases where the infection automatically causes symptoms, but because it causes symptoms, it's also relatively
easy to contain, to some regard, already spontaneously, because people who are in bed are, of course, not, you know, certainly things, so to say in society, they are not having contacts or they are hospitalized or when some people die, for example.
So it will automatically have a self-limiting effect just by the inherent nature of the disease, and it is easily too easy to intervene because public health measures can be very, very efficient, simply because you can, you only have to, in fact, track people who have symptoms because these
and only these are the people that are also shedding the virus and responsible for transmission.
So in those cases, there is no herd immunity, and there is a relatively high viral infection rate because it would not be a high viral infection rate, and the disease would be symptomatic, then, you know, most of the time, the virus would not spread, would not spread to several different countries because you couldn't immediately contain it.
It's because it has a high viral infection rate that, despite the fact that it's symptomatic, it can nevertheless spread to several different countries.
That's why we are often talking about the multi-country epidemics, but they are not evolving into pandemics.
So in order for a pandemic to classify, this is a direct consequence of what I'm saying of these definitions, to classify as a health emergency of international concern.
Remember, the WHO declared the SARS-CoV-2 pandemic as a health emergency of international concern, a health emergency is when you have a really major impact on people's health and of international concern.
It would need to involve a rapid and global spread, not of the infection as such, but of the disease, of symptomatic infection, because otherwise it would not be a health emergency.
So now, I would just say, if naturally a disease is symptomatic, it will be easy to contain it, and it will never evolve into a health emergency of an international, of a global concern, so to say.
So that is normally, normally impossible, because the symptomatic infections, as I was just saying, are rapidly self-limiting.
Unless, of course, unless the new response and or the virus are evolving to a more pathogenic form.
So that means that you could have a pandemic, the virus spread everywhere, if it's a natural pandemic, it will not be a health emergency of international concern, because vast majority of people will develop asymptomatic or mild infections.
Unless there is maybe an intervention that all of a sudden renders this virus that has spread worldwide, more pathogenic.
So I'm thinking of a new escape, for example, that could be responsible, or you would have, you know, abnormal immune responses, no lower, natural immune responses, but maybe immune responses that have been influenced, and that have been derailing,
maybe also due to some kind of external intervention, but nature doesn't do this. Nature will not make a pandemic a health emergency of international concern.
If that would be the case, you know, there would be a risk of disseminating or even eradicating the full human population, which has never ever been documented with any, with any natural pandemic.
So how does a natural pandemic end? Well, to ensure a sufficiently high percentage of the people develop stabilizing immunity, the virus needs to widely spread across the population.
As those susceptible to symptomatic infection will mount high antibody levels after the first wave, there is a risk that viral infectivity could fall below the minimal threshold required to ensure viral transmission towards the reminder to the remainder of the population.
So what I'm saying here is that during a natural pandemic, people get infected and will, you know, those who get symptomatic infection will mount high antibody levels after the first wave.
So now, because they have antibodies, they have, they are very well protected against the infection. And so there would be a risk that the infectiousness, the viral infectivity, stops there that the transmission of the virus stops there because it is controlled by people who have developed high levels of antibodies.
That of course would not be a good situation to develop herd immunity because in order to have herd immunity, you'd have herd immunity because the virus would be gone. What is he talking about?
What a weird story this is. If viral infectivity falls below the minimum threshold, then it fizzles out like every RNA virus has in the past.
It's like he's now fumbling the ball because he realizes, oh, yeah, wait, I already told you that RNA can't do this or I didn't tell you, but I'm telling you it.
What the hell is this? High antibody levels.
You need to widespread of the virus. And so there would be a risk if that would happen that viral infectivity falls below the minimal threshold that is required to ensure viral transmission to the remainder of the population.
So the remainder of population would no longer be infected. So this would of course prevent herd immunity from being established.
So there is a mechanism that during natural pandemics prevents this and that will ensure that the infection and the transmission of the virus continues despite the fact that already many people have developed protective antibodies after the first wave.
And this mechanism is very unique. I think this is really a fantastic phenomenon.
So those people who during the first wave developed asymptomatic infection, I told you, most of the people during a pandemic will develop asymptomatic of mild infection.
So how can nature then proceed in a way that these people will also have durable protection against infection to have durable protection against infection.
They need to develop antibodies. But if there is symptomatic in your mind infected, they will barely develop into any antibodies and they will be very, very shortly.
So well, these people who previously developed asymptomatic mild infection during the first wave, they become now more susceptible to infection. How does that work?
Well, this is because the antibodies that those people developed, I was just saying short lived and low titers and low neutralizing capacity.
They will enable non neutralizing antibodies to bind with low affinity to spike routine. That is through the internal domain of spike routine. That is a very conserved antigenic domain within spike routine.
And by binding to this internal domain, they will of course not neutralize a virus. I was just saying that a neutralizing capacity of this antibody is very, very lousy, but they will enable enhancement of viral entry into susceptible
host cells. And therefore, this part of the population, the largest part of the population that was previously asymptomatic infected will now become infected, predictably infected.
They will even develop disease and they will develop antibodies and they will promote a further spread of the infection so that the population can now acquire herd immunity.
So this antibody dependent enhancement of iron infection contributes to herd immunity and therefore reduces viral infectivity and transmission as a definition of herd immunity.
So this reduced viral infectivity and transmission prevents infection in experience individuals so individuals that haven't yet been infected at all from developing symptomatic infection and hence provides transition of viral infection into the endemic phase.
So that is how a natural pandemic ends. So I think.
So that's how a natural pandemic ends.
In other words, we're not having a natural pandemic anymore because we pushed it around.
In other words, we're not having a natural pandemic anymore because it was a lab league.
We're not having a natural pandemic anymore for any number of reasons but he's not really explaining it.
And it's driving me mixed nuts.
It really is driving me crazy.
This is the worst lecture introductory lecture to pandemic biology I've ever heard.
And they want you to pay $160 for the course that follows it.
I will stop here to leave time for a couple of questions and yeah, we will just continue with the rest of my slides in the next session.
But please also after this session. Don't be shy to send me comments because for me, it's also a new experience when you experiment. I don't know. I'm going too fast to slow.
It's what I'm saying redundant. I'm not making myself clear enough. I don't know. So I will be grateful for any of your comments. And if there are questions, I'm, of course, more than happy to take it.
Thanks.
Cut.
That was it.
So, of course, if you were in the course, you could have asked questions. And if I was in the course, I could ask questions.
I'm not sure what I'm going to gain from that, though. I gotta, I gotta see if I can do it. Maybe I can send an email to James Lyons while Aaron Hill let me take the course for free.
Maybe I can audit it.
I don't want to waste too much of my time, but on the other hand, I am very curious as to what people are going to learn because I have the feeling that the immunology course that was taught there by James Lyons Wilder is also pretty heavy on the antibody side of things.
And it's that tilt toward the role of antibodies and defending you from an a respiratory virus or from a virus that infects your gut.
And more importantly, the role of seroprevalent antibodies, which Dr. Joseph Lee is one of the guys making this argument first.
And foremost, me as the guy who made this argument first and foremost, that these IgG antibodies can't enter the lungs. They can't enter the mucosal layer. They can't pass into the gut.
So it's not really clear how an infection, which is occurring at these epithelial barriers, is going to be really helped by having seroprevalence of antibodies in circulation.
In the case of extreme viremia, perhaps in the case of exposure to an infectious clone, perhaps.
But if you have a normal respiratory virus that is productive in your lungs is shed into your mucus and that mucus goes down into your gut and a compliment of T cells in your lungs that's intolerant and a compliment of T cells that's tolerant in your gut.
Combine to orchestrate a systemic immune response to the exposure to that RNA seems pretty cut and dry.
And that's how that works.
And we're not talking about that. We're talking about immunity based on antibodies.
IMM, UN, ITY, that's what I got, bodies anti. That's what we're talking about here.
And that's unfortunate because we know that that's garbage, right? We know that that is garbage.
Ladies and gentlemen, they have misled us about a laboratory or a batcave zoonosis.
And I think that Herod Fund and Bosch plans to mislead us about the role of antibodies in our defense against a laboratory or batcave zoonosis.
We can dismiss this because we know there's a conflated background signal. We know he should have started by explaining all the PCR made this really bad.
He should have started by explaining that the sequencing could just be altered by the systematic change of the primer sets, of which there are at least 99, but up to 106 that are generally used in order to sequence a coronavirus from beginning to end.
And so the conflated background signal of previous coronavirus conflated background signal of RNA sequences that we don't understand
has been used to create the illusion of spread of variants around the world.
And it is actually the protocols and the transfection that have caused the vast majority of the excess deaths, all of them.
So the protocols are murder and transfection is in medicine.
If you think that an infectious clone was used to seed a few cases around the world, or thousands of cases around the world, it doesn't really matter.
If you think that a transfection agent was released, where people were just transfected with the spike protein and then that signal was conflated with a coronavirus signal,
because the WHO test used RNA-dependent RNA polymerase, and the United States test is currently using the N protein.
So the protein that is very specific for SARS-CoV-2 isn't even part of the testing protocol. It may never have been.
So in reality, we're talking about a whole bunch of different ways that a conflated background signal added or not added, enhanced or not enhanced,
could have been used to create a situation where doctors were tricked, coerced, and bullied into executing protocols that were essentially murder and transfection is in medicine.
I think we can safely say that this no-virus group has been a distraction for a while, and if they convert to the right story now, that's great, but let's not forget they didn't help us for three years.
Let's not forget that Kevin McCarran was saying Andy Kaufman's name and Bailey's name out loud all the time.
Let's not forget that that was one of his primary missions from day one was debunking the no-virus people, and the list of them was short.
So rather than ignoring them, he promoted them. He made memes of them.
Protocols are murder and transfection is in medicine.
These people lied to us about biology, including the biology of gang-of-function viruses in order to invert our rights to a set of permissions.
And the thing that they inverted was the very basic biology of our immune system, and they've had this plan of inversion in place for a long time, and it is evident in the childhood vaccination schedule of America when compared to other countries.
The nuts have not gone down well in my constricted throat, and that's what this change in our way we think has allowed them to do, and we have been duped into believing that this was caused by a dangerous virus instead of a dangerous, a dangerous plan.
And I think that we have come up with the biology that explains how this was a dangerous plan rather than a dangerous accident.
And the dangerous plan is continuing. I'm going to need to cut it short. I can barely talk.
The dangerous plan is continuing because this is how they plan to govern us.
They plan to govern the world with a mythology that unites us.
A mythology about gang-of-function viruses and the danger of pandemics.
And a mythology about AI and how AI can control us, but also help us.
A mythology about how we're about to, we're on the cusp of, we're just crossing the hill where we're going to be able to augment our genome.
And the personalized medicine is an almost realized reality.
And the climate change is something that needs to be fought because within five years everything could fall apart.
This is the new mythology that they want to govern our children with, that they are misleading our children with, and that we have to fight until our very last breath.
And this has been GIGO and Biological, a high-resistance, low-noise information stream brought to you by a biologist.
You can get me in touch with me at GIGOOM.BY or GIGOOMBiological.com.
I thank you very much for supporting the stream at GIGOOMBiological.com.
You can see it there. All the people that support our scrolling above.
Thank you very much for joining me. Sorry, my voice is given out.
Intramuscular injection is not a valid means of immunization. You can say it's shorter by same transfection as an immunization.
But it actually applies to more than the current shots.
Please stop transfection in humans because they are trying to eliminate the control group by any means necessary.
This has been GIGOOMBiological.
Twenty-three days in a row I think. Keeping it going. I'm going to try to get to 600.
I don't know how to grasp my voice. I might start coaching my boys basketball team. That's not going to go well for my voice.
I'll tell you that. I'll tell you that much. But my boy did really well in the first tryouts and I don't know man.
If I can coach my boys basketball team, I might have to stop streaming a little bit less.
Honey and vinegar, Pamela. Love you babe.
Honey and apple cider vinegar. Maybe a little lemon in there too. I'll do it. I'll do it, I promise.