Mass Vaccination and Natural Immunity: Bret Speaks with Dr. Geert Vanden Bossche
Bret speaks with Dr. Geert Vanden Bossche in Bath, England, together for the COVID Better Way Conference 2022.Geert Vanden Bossche is a Doctor of Veterinary Medicine who has specialist expertise in virology and vaccinology, Geert has worked in industry in the construction of vaccines, and in the non profit sector working to bring immunity to larger numbers of people.Find Geert:https://www.geertvandenbossche.org/https://twitter.com/GVDBosschehttps://www.youtube.com/channel/UC_yhGQiJ5lTmOaoIQA9...
This type of balance between a pathogen and an immune system has been shaped over thousands of years through evolution, like natural selection, all these type of things.
What we have done here, literally, is we have thrown a bombshell On this thing, you know, on this delicate balance that has been established for many, many, many years, right?
And then, would we expect that this thing is just going to die out?
It's not going to have consequences?
It's the end of the pandemic phase, as our friend Fauci is saying, you know?
How can you ever end a pandemic without cutting dramatically the infection rate?
What you are seeing right now is exactly the opposite.
Hey folks, welcome to the Dark Horse Podcast.
I am sitting, as longtime viewers of Dark Horse will know, with Gert Vandenbosch, who is a vaccinologist and virologist.
I talked to him on Dark Horse in... geez, what month would that have been?
Do you remember, Gert?
I think it was maybe June?
June.
Yeah, that's quite possible.
We talked about your hypothesis regarding the impact of the mass vaccination program against COVID On the pandemic, and you said some very stark things about the likely outcome.
In effect, you described the likely proliferation of escape variants of the virus, and you implored us to stop the program because you believed it would do more harm than good.
I think before we get to your current view of the pandemic and the vaccination program, let's talk about how the progress of the epidemic has matched your expectations and in what ways it might have departed from them.
Yeah, well, first of all, I think what I have been predicting and what, you know, was completely correct is that by doing mass vaccination during a pandemic, that was my point, that we would drive the expansion, the propagation of more infectious variants.
And I think that evolution we have clearly seen, we have seen dominant propagation of, you know, alpha, beta, gamma, delta, omicron.
I think the common denominator was that each of these dominant variants was more infectious than the previous one.
So back in those days, I thought that the higher level of infectiousness of the virus would automatically imply a higher level of virulence or a higher level of damage, you know, in terms of the incidence and maybe also the severity of the disease.
So let me just clear this up for our viewers.
So you've got two different parameters, right?
One is how transmissible it is and the other is how harmful it is.
And so you can have a very transmissible disease that can have a very minor effect or you could have a very transmissible disease in the worst case that also was very harmful, right?
Or you could have a very harmful disease that didn't transmit very well.
All of these are possible.
Exactly, exactly.
And, you know, the harmfulness, we call it often the virulence, right?
The capacity of the virus to cause, you know, more severe or even deadly disease.
Right.
Now, I have to stop you there because, evolutionarily speaking, it's confusing to have these two terms because, from the virus's perspective, the virulence is not positive, right?
It's neutral or negative.
In general, the virus is only interested in propagating, and in general, it is propagated best when the creature that is infected is most capable of walking around and spreading it.
So, virulence is like an unavoidable downside of the pathogen's mode of existence, whereas transmissibility is sort of the objective of the exercise from the evolutionary point of view.
Is that fair?
Yeah, the only thing I'm always worrying about is that people often, especially virologists, do this.
They talk about the virus as if the virus had a plan or the intrinsic properties of the virus would be changing.
We, of course, often forget that when virus becomes, you know, causes less harm, That it is because the immunity of the population is growing, is keeping the virus better and better under control, and that therefore, so to say, the virus is becoming less harmful and less infectious very often.
So that is something which is very often misunderstood.
People think, you know, the virus, you know, wants to survive, the virus wants to do this.
No, the virus has no plan.
All the virus can do is to replicate.
It can mutate and it can hide in the genome but that is not relevant for coronaviruses in this case.
So I want to defend my language for a second.
The problem with evolutionary biology is if we speak in this ultra rigorous way where we do not imbue A desire to propagate, for example, a plan.
If we do not project that onto the virus, then we will have an impossible time making any headway.
And so we speak with a kind of shorthand, and I follow Dawkins in this regard, where he says it's just simply very important that any time you make an argument that the tree has grown tall in order to shade the The competitors, right?
That you are able to correct.
If you have to describe the same thing in the perfectly rigorous but not very useful terms, you can do it, right?
You don't ever want to describe this in a way that you can't get back to the highly rigorous version.
So, I think we have to use the shorthand.
Obviously, the virus doesn't have a plan, but it certainly doesn't have an interest in doing harm.
It is not served by doing harm.
And what we are looking at is simply that there are numerous copies of these things.
I mean, impossibly large numbers of copies.
And those that happen to be transmitted best are the ones that come to dominate the population.
It's very standard selection at this level.
It's natural selection.
Yeah, and so what that means is that features that enhance the transmissibility are fostered.
Sometimes those features that enhance the transmissibility are a reduced virulence, right?
That the creature is more intact and therefore the creature's ecology facilitates the spreading of the virus.
So in that way, I do think we have to be mindful of this thing.
The objective of the virus is to transmit, but the other thing you said is very important, which is that, and I remember learning this when I studied immunology, which is that in general, yes, viruses do become less virulent over time, but the evolution takes place on the part of the host for the most part.
Right, which is a disturbing discovery, right?
Because what that means is that the virus is actually exerting a selective effect on the host, right?
So in any case, it's an important point.
But so far I think what you've said is that the vaccination program was going to exert a selective pressure on the virus that was going to cause a proliferation of mutants that would have increased transmissibility.
Yeah, a natural selection of mutants that can overcome that pressure and we put the pressure on the spike protein obviously through the antibodies and the spike protein is responsible for infectiousness.
So we put pressure on the infectiousness of the virus.
So we got natural selection of more infectious variants because the more infectious variants obviously could overcome the suboptimal pressure that we put on this characteristic of the virus.
And the suboptimal pressure came, of course, from the fact, first of all, you put pressure by doing mass vaccination and it is suboptimal because you do it during a pandemic.
So people get already exposed to the virus before they have full fledged immunity.
We do it in fact with prophylactic vaccines that we use normally before we get exposed to the virus when we travel to a foreign country where we know there is a disease we can protect against.
You make sure that you get your full vaccination course completed before you get exposed.
So we are not quarantining people that we vaccinate, right?
They get their first shot and their antibodies are immature.
It takes time for them to mount the antibodies.
But at the same time, the pandemic is ongoing and they can get exposed and a number of people get exposed while the immunity is still suboptimal.
So the fact the mass vaccination is one important point.
And the other one, doing this during a pandemic is also very, very important in terms of, you know, Exerting this suboptimal immune pressure.
So I want to try to make that clear, too There's several errors here as I see it.
You've listed two of them here One of them is the mass vaccination program and the other well, actually maybe you've got mass vaccination Into a pandemic that's already raging which means that there's several different places where we now guarantee evolution, right one of them Is that if you're just vaccinating everybody, you don't know who just caught the virus at the moment you vaccinate them, who's about to catch the virus.
And so what that means is, you know, immunity takes time to develop.
The immune system is learning something and it actually learns this through an amazing process.
One of my favorite facts in all of biology is clonal selection, right?
Because we are a static target that lives for 80, 90 years and we are up against pathogens that evolve on the scale of hours.
We have a population of cells that have been adjusted by evolution to evolve in the same time scale.
I find that just an utterly stunning fact, right?
So, we have these cells, B and T cells being the examples.
So, B cells make antibodies, T cells have something like antibodies that never leaves the cell.
It's not a free-floating protein.
But the process of clonal selection requires cells to produce cells to produce cells and each generation of those cells gets closer to the formula, which means there's a period of time over which your immunity is developing.
And the problem is That that period of time over which their immunity is developing may interface with a pathogen that is so widespread that you are likely to get it.
And at the point that your immune system is exerting this selective pressure before you've developed immunity is you have partial immunity.
Partial immunity is like a training program for the virus.
And that is really the key error.
Absolutely, yeah, that is really the key error and I'm always comparing this to, you know, it's just so amazing to me that everybody knows this from the field of antibiotics.
And the only difference is we all know that viruses depend on living cells.
But if you have a bacterium, for example, and you have a medium with a suboptimal concentration of an antibiotic, The bacteria, they can replicate on themselves.
So there is no need to change the medium.
You have the suboptimal concentration of the antibiotic and then you have the bacterium and of course you will have a selection of mutants that can overcome this, you know, this hostile environment.
If now we have like viruses that, you know, depend on living cells, and of course they will destroy the cell, so they will come out of the cell.
So with that also, you know, when they get transmitted, for example, to another individual, it is very, very important that you keep that suboptimal medium.
If the virus gets transmitted to somebody who is not vaccinated, this person is not going to present that hostile environment to the virus.
And you got the natural selection in one person, but that advantage gets lost if it is transmitted to somebody who does not have the suboptimal immunity.
But if you do the mass vaccination, it's like this suboptimal medium is going to be conserved just like with, you know, the bacterium, because it gets transmitted to somebody else, but in the same situation.
Because this person also is presenting this suboptimal immunity.
And if you have like 60-70% of the population in that situation, you will of course, you will promote this natural selection and enrich of course this variant in the population.
So it is largely, largely comparable to the situation with bacteria and suboptimal antibiotics, just that the virus depends on a living cell and, you know, it needs to be transmitted to perpetuate its cycle.
But every single time in a massively vaccinated population, it will encounter the same medium, just like the bacterium is proliferating under hostile conditions of suboptimal antibiotic concentration.
Right.
So in effect, what we did, which you're pointing out, is we ran an insanely large gain of function experiment that we didn't mean to run.
We set up a selective environment and we basically said, here are the tools that we are going to deploy against you in a very weakened form.
That gave the virus the ability to, you know, experiment in the way natural selection does and discover vulnerabilities of that system.
But your point is it goes from one person to another person and it keeps finding people with the suboptimal immunity.
So it keeps finding the same puzzle again and again and again.
It's gonna get good at it.
And there's another flaw here, which arguably Maybe they didn't know.
I suspect they did, but the fact that these vaccines are, well, and we probably should not be calling them vaccines.
Robert Malone scolded me about that earlier, and I believe he's right.
I at first wasn't convinced that the terminology mattered, but this is sufficiently novel that we should probably use a different term.
But these inoculations do not produce sterilizing immunity.
Yeah, that's the point, of course.
So on the one hand, even if they did produce sterilizing immunity, you've got a problem if you're vaccinating into the face of the pandemic because people on the way to having full immunity are still a gain-of-function experiment effectively.
But in this case, even people who have reached the final stage, haven't encountered the pathogen, have had two weeks or a month to develop their immunity, are still a gain-of-function experiment because the immunity isn't sterilizing, meaning they can catch the virus and they can transmit it It's not shutting down the virus in their system.
Is that fair?
Yeah, yeah.
The problem is, you know, from the very beginning, that's what I said, don't use these vaccines that do not induce sterilizing immunity
During a pandemic and in the form of mass vaccination, so these three elements are absolutely critical and there is very often some misunderstanding about the sterilizing immunity because imagine if you would get vaccinated by a vaccine that induces antibodies on the antibodies, and you would have, you know, a full-fledged vaccination course.
So you end up with high titers of antibodies.
And I would say when the antibodies reach the peak, when at that very moment you get exposed to the pathogen, there is a reasonable likelihood, depending, of course, on the viral load, that all of the virus you got exposed to get neutralized by these antibodies. that all of the virus you got exposed to get And then people say, well, you see, there is sterilizing immunity.
At that point, the vaccine induces sterilizing immunity, but if you would have the same encounter with the same exposure at a point in time where the antibodies would already be declining, or whether the antibodies would still be very high, but you would have a much higher viral load, Then the quantity, the concentration of the neutralizing antibodies would nevertheless not suffice to completely neutralize the virus.
And then the very same vaccine against the very same disease would not induce sterilizing immunity, you see.
So that is important to understand.
That is the disadvantage of the antibodies, of protection that relies completely on antibodies.
Right.
Actually, that's the next thing I was going to say, is that one of the things that has been very clear in the Very confused informational environment that we have faced is that there's almost an obsessive focus on antibodies and I almost feel like that is driven by the fact that the public knows that term and has some relationship with the idea of an antibody, but they don't have a relationship with the
The other types of immunity, T-cell immunity, for example, is playing such a strong role.
And really, my understanding, and you're the vaccinologist, but a vaccine that induced durable T-cell immunity would be much more effective in this battle, and you wouldn't necessarily be able to read that it was there in the antibodies, because frankly, Even if the response was entirely on the T-cell side and therefore you didn't see an antibody titer, it would still potentially be very effective.
Now, it is likely that you would have an antibody response that you can easily measure and a T-cell response which is much more difficult to measure.
Yeah.
Is that fair?
Yeah, yeah.
But, you know, unfortunately, none of these vaccines, none of these vaccines are inducing A sterilizing T-cell response that has memory.
So you can induce T-cells but if you don't have memory it's not going to help you because that's the purpose of course of vaccines that the next time around the immune system would remember this.
So in none of the vaccines but even during natural immunity there is no evidence there is plenty of publications on T-cells with coronavirus but there is no single evidence there is no single study That shows that you have cytolytic T-cells, so T-cells that can effectively kill virus-infected cells and that have memory induced by natural infection.
So, this is very typical for coronavirus, also for enterovirus.
And what happens most likely is that because when you get a disease, you recover from the disease.
You know, some people recover after 3, 4, 5 days.
That is much shorter than it takes for developing the kind of antibodies we were talking about.
You were just talking about, you know, before you get this maturation, isotype switching, etc.
It takes several weeks sometimes.
So, the question is, how then can you recover from the disease after 3-4 days?
And if these would be memory T-cells, then you would expect that next time around, you know, you are completely protected against the disease.
So what we know is that there are Epitopes in the spike protein that we call them, they are universal.
They are completely conserved and they induce cytotoxic T cells, but that have no memory.
So that means if you get infected, And the virus will be presented, of course, by antigen-presenting cells because it's a foreign body.
It will be, you know, presented by antigen-presenting cells.
That is the purpose.
That is the goal of the, you know, the objective of those cells.
Then, this universal epitopes, so it means that regardless of your genetic background, you know, you notice the MHC complex, it is not restricted by the genetic background, so it works in everyone.
But it binds with very, very high affinity to these MHC complexes, and that induces the cytotoxic T-cells, but without memory.
So you will cure out the disease, you will eliminate the virus-affected cells, but there is no memory.
If there were memory, because it's a universal epitope, You would expect that whatever coronavirus you have been infected with before would be completely protective because you would have long-lived cytotoxic T-cells that would be even, you know, if you have induced memory, even five years, ten years later, They can still be recalled and do the job.
And that is not the case.
And that is a big misunderstanding.
Many people have been saying, yeah, previous coronavirus protect you and etc.
Of course, they can to some extent protect you, but you're not recalling previously induced memory T cells because they don't exist.
They don't exist.
Yeah, you will have memory T-cells that will produce cytokines.
That, of course, plenty of cytokines and the cytokines can dampen the infection and the disease.
But there is no study whatsoever, whether it is with the vaccines or as a consequence of natural disease, that has been able to demonstrate the presence of the induction, I should say, of cytotoxic T-cells, memory T-cells, that work universally in everybody.
And that's what you need for a vaccine because, you know, that is the reason that why up till today we don't have vaccines that are based on T-cell immunity.
Of course, T-helper cells.
If you don't have the T-helper cells, you don't have good antibodies.
But in order to have, you know, the problem with the T-cells It's the same as with the antibodies, but it's the other way around.
The problem of the antibodies is the antigen variability.
That's what we are seeing right now, that the antibodies that are induced by the vaccine do no longer match with the circulating.
But with regard to the T-cells, we have another limitation, which is the restriction by the genetic background.
Your MHC complex is different from mine.
And of course, if you come with a T-cell vaccine with certain epitopes, These epitopes, by your genetic background, your MHC haplotypes, will be presented in a way that you induce maybe cytolytic T-cells, but it will not be the case with my haplotypes, because the same epitopes that are in the vaccine or not will not be presented in an immunodominant way.
So, see, that is where we have severe limitations also with regard to T-cell vaccines.
Well, up till today, we don't have any vaccines that eliminate or that abrogate the infection.
Abrogation because the cell should be first infected and then you could kill the virus-infected cells.
So, there's abrogation of the infection.
That's also the reason why we don't have therapeutic vaccines because it means that the cell is already infected Can you then abrogate?
Can you stop the infection?
Can you kill the virus-infected cell?
No, we don't have those.
So, that is something which is very important to know because people still think, well, you know, we are focusing this on the spike protein, we should have had, you know, more T-cells, you know, yeah, you can induce plenty of T-cells, but if these T-cells are not capable of, to your point,
killing virus infected cells and when you kill the cell since the virus needs to rely on a living cell if you kill the cell that it infected it cannot propagate anymore right so that is sterilizing immunity as well right it's it's not by neutralizing All the virus particles before they can enter into the cell.
So once they enter, you let them enter into the cell, as many as possible, and then you come and you say, you know what my criterion is?
I'm going to kill literally every single cell that got infected.
That is also sterilizing.
I distinguish very often between sterile immunity Where you prevent infection from taking place by neutralizing all the viral particles, you know, before they can enter into the cell in the first place.
Compared to sterilizing immunity, you allow the invasion into the cell, but once the cell is infected, you're going to kill the whole thing, right?
This is sterilizing immunity.
That's a very good distinction.
I've never heard that one before.
Is that yours?
Yeah, well, I don't know, but I've taken it, you know, deep.
You know, vaccinology has been confronted with so many shortcomings.
We have no, you know, and people are asking, why do we have all these limitations?
Why can we not?
I mean, there's so many things, but, you know, When you have an antibiotic, we think it's completely logical that you can kill several different bacteria, even if phylogenetically they are completely unrelated.
Everybody thinks this is very normal.
And with vaccines, with antibodies or with immunity, can you believe it?
If there is an antigenic shift or an antigenic drift, we have already a problem.
Look at the influenza vaccine.
You know, every year we need to do an update and very often we come to it.
So we have these severe restrictions.
So that is also genetic, HIV, all these chronic diseases.
We have no vaccines against us.
We have been testing.
We have been trying for 20 years to make a vaccine against HIV, for example.
We have been failing.
And therefore, I've been deeply involved when I was working at the Bill and Melinda Gates Foundation because they're essentially concentrating on very difficult diseases that become chronic, Tuberculosis, malaria, HIV.
So yes, I've taken a very, very deep dive into this because people have been trying to solve this with adjuvants, with new delivery technologies, etc.
We have turned it upside down and that is where you get, I think, quite deep insight into the limitations of current vaccinology.
It's like the difference between fusion and fission power.
Fission isn't that hard.
Fusion turns out to be incredibly difficult to get right.
That I'm less familiar with.
Well, let me ask you this.
I take your comparison between bacteria, where we can have an antibiotic that is broadly effective against bacteria from different clades, and we just consider that normal, and your comparison to vaccines, which, you know, you make a vaccine that works and then a slight antigenic shift makes it useless.
Why the distinction?
So, I'm gonna guess the distinction is actually the reason that viruses are what they are, right?
Viruses have gotten a huge evolutionary benefit from shedding all of their biology and borrowing it from their host, right?
Because what it does is it reduces the attackable architecture, right?
Because the architecture is you.
Right?
So, in effect, what you have are antigens, right?
And the point is those are amenable to being shifted out from under whatever you point at them.
So, that's sort of a built-in problem.
It's a reason... Yeah, it's a built-in problem, yeah.
A built-in problem.
I also wanted to go back and just point out that your example of a medium with suboptimal amounts of antibiotic really makes this point.
And you can imagine, if you throw Bacteria on a medium that has twice as much antibiotic twice the concentration necessary to kill it.
Well, then no individual survives So there is no next phase of the experiment and the problem is that selection gets very effective when something lives and it almost becomes I mean it really is more effective if you really bottleneck something down to a very the most, you know unique members of the population then the next iteration is entirely born of those unique members of the population.
So you've done a very effective job of finding the ones who are resistant.
So we have this issue, and then I would add to the issue of vaccinating into the pandemic, the non-sterilizing immunity creating a gain-of-function experiment, even in people who've developed their full immunity.
There's also the issue that this extremely novel mechanism for delivering a vaccine has narrowed what the immune system is exposed to so much that it actually makes a much easier puzzle for selection to solve.
Right?
I have not really heard this discussed anywhere.
Maybe I've been missing it.
But if you use, let's say you used a live attenuated virus or a killed virus, right?
Between the whole virus.
Then you get antibodies to various different epitopes, right?
You get some antibody to the spike, you get some to the nucleocapsid, and the point is this.
Let's say that you're vaccinated with such a thing, right?
Now you have memory cells That are producing several different types of antibodies.
If some virus figures out, if it has a mutation that allows it to escape the immunity that was generated to one of those antigens, it doesn't necessarily create an advantage because as long as the antibodies to the other antigens still managed to effectively shut down the virus.
The point is that successful change doesn't get transmitted.
And so I think there's another mistake here, which is that to use one antigen means that there's no fail safe and that effectively the more antigens your body knows the formula to, the less the chance that any innovation that would defeat one of them actually lives to pass on the less the chance that any innovation that would defeat one of Is that fair? - Yeah, well, no, it's not fair in this case.
Because, of course, this is the argument that immediately comes up and that we have been, you know, we have heard this so many times that, you know, what is the problem of the antigen?
Because, as you're pointing out, we are just using one antigen.
But then I'm saying, you know, what is the benefit of An antigen of having antibodies induced against an antigen that, first of all, is not accessible to the antibodies, like a nucleocapsid.
It's not accessible to the antibodies.
Because it's blocked by all the spikes on the surface?
And, as you're pointing out, what is the critical thing?
It is the protein that enables the infection into the cell, you know?
That is the one you have to target.
Which is why they picked it.
Yeah, of course.
So, I do think it is the right target, but if you put it under immune pressure, and I bet whatever you want, you can come with plenty of other antigens.
Of course, you're going to induce many, many antibodies, but they are not going to prevent the infectiousness of the virus because they are directed against Proteins, you know, that are not involved into viral entry that will also to a large extent not be accessible to the antibodies because they are inside of the, you know, they are not presented necessarily on the membrane, the cell.
Well, okay, maybe you just answered my question, but doesn't this raise your distinction between sterile immunity and sterilizing?
Was that your two terms?
No, for me, the sterile immunity, but that is a definition that I made just to distinguish, because I think we need to distinguish between a situation
Where antibodies in exceptional situations as I was explaining if you are really you know boosting somebody you have high titers of antibodies and at the peak of their antibodies you are exposing them to a mild viral load you may be in the exceptional situation at that very point where you have reached the peak that the antibodies would be able to neutralize all the virus so that none of the particles can even enter into the cell.
Sterilizing immunity is once this process has happened, the virus has already invaded the cell, so it's no longer a sterile situation, but you can make it sterile again by killing the virus-infected cells.
But doesn't that solve the problem of, let's say, the nucleocapsid proteins not being available to the antibodies?
Because the infected cell will still That's what I'm saying.
infected.
And so you can't generate the sterilizing immunity that prevents the invasion of the cell, but you could have an effective response that would kill all of the infected cells.
That I agree with.
But then we should be able, that's what I'm saying, we should be able to generate vaccines because in the infected cell, of course, I mean, these proteins, these other proteins that are hidden in the virus before it gets into the cell, when it gets into the cell, several these other proteins that are hidden in the virus before it gets into the cell, when it gets into the cell, several different viral proteins that are normally hidden within the
But then you should be able, and that is what I'm saying, that current vaccinology is not capable of doing it, you should be able
To induce cytolytic T-cells that are specific, let's say for example the nucleocapsid, okay, that are antigen-specific, nucleocapsid-specific and that are capable of inducing antigen-specific cytolytic, because they need to kill the cell, T-cells and they need to have memory because if you get vaccinated and it's not memorized and it needs to be in order to be a vaccine that is useful In a universal way.
If it works with your MHC complex, but not with mine, you have the restriction, right?
I mean, we have done all this homework, right?
And that is what I'm saying, even during natural infection with coronaviruses, same with enteroviruses, nobody, nobody has ever demonstrated that there is, even through natural disease, induction of universally, you know, functional Cytolytic memory T-cells that are antigen-specific, right?
You have plenty of memory T-cells that will produce cytokines and of course they can modulate, they can of course mitigate the disease and all these type of things.
But if you want to have sterilizing immunity, that's our point.
And certainly during a pandemic, you need to be able, for God's sake, to kill that cell, right?
Oh yes, 100%.
Okay, let's get out of the weeds because I have a feeling we will have lost some people.
Let's bring them back.
No, that's not your fault.
All right, so we have a vaccination program and a An inoculation that effectively creates an inadvertent gain-of-function experiment where we are setting up the hurdles for the virus to solve this problem evolutionarily and to re-emerge on the basis of the alteration of the spike protein, which is the only protein we targeted.
So that, last time we spoke, you said this is going to produce escape variants, that that's what we should be looking for.
And you believed that we were going to see escape variants that were both more infectious and more virulent.
Is that right?
Yeah, I was in fact not distinguishing that much at that point between, you know, the higher level of virulence and infectiousness.
I almost thought, you know, when the virus is going to become highly infectious, that was really my conviction, then automatically it's going to spread much faster and doing much more harm in the population.
So, that has come out, I guess.
I think everybody acknowledges that this mass vaccination now has really promoted, I should say, the expansion of highly infectious variants.
I've never been saying that the mass vaccination induces the mutations because, you know, mutations But it enables the virus, you know, to do a natural selection between all the different mutants that are produced anyway and to select those that are most appropriate to overcome this pressure, you know, on the infectiousness of the virus.
This is to say, we'll select the more infectious variants and enable those to become, through the system that we discussed, the mass vaccination, the same medium everywhere, to become predominant, of course, in the population.
So, that is true, but at the same time, and that is probably maybe the next question you want to ask, it did not automatically, on the contrary in fact, imply a higher level of virulence.
So, that is something that I also learned.
And that is also why I'm saying it's not the end of the story.
There will be a second step that the virus will take if we continue, you know, well, continue mass vaccination by for example vaccinating children or by boosting people.
And boosting people is like an automatic process.
We have Omicron circulating.
That is far more, you know, stronger as a boost than coming with a new Omicron vaccine for example, right?
Yes, well, it does raise the question, and I think many of us have scratched our heads over it, why we are still transfecting people with Wuhan version spike protein.
Why has the, I mean, if there's one There were so many downsides to the way they chose to vaccinate here.
If there's one upside, it's that you could swap out the antigen that you've targeted for an updated version without changing anything else.
And yet we haven't updated this, which is an odd fact.
Do you have an interpretation?
Why did they continue?
Why are they still recommending boosters with the original version of the spike protein rather than an updated one?
Well, you know, it's interesting that even in, you know, 2022, where we have all this access to, you know, science and technologies, that vaccinology has remained an extremely empirical thing.
And as a matter of fact, and the answer is as easy as that, they continued and they found out, well, you know, I mean, seems like the efficacy is going down.
But for some reason, for some reason, this thing, believe it or not, still seems to protect against severe disease.
So now I'm asking you, do you know about any vaccine, any vaccine, That in fact makes even the vaccinee more susceptible to infection, right?
And nevertheless protects against severe disease.
Do you know any vaccine that does not protect against disease but that protects against severe disease?
So it's not a logical approach but as a matter of fact They continue and they find out, even if the duration of that protection, even against severe disease, is declining.
Everything is declining.
Initially we had an impact on transmission, then that was no longer the case.
We had an impact on disease, no longer the case.
We had only an impact on severe disease for a duration of a couple of months.
Now we have impact for a few weeks on severe disease, right?
And so empirically they say, you know, In fact, what they're saying is, we don't understand how this works.
I'm just telling you, I don't know, after all these years of vaccinology, I don't know of any vaccine that has these characteristics.
It protects only against severe disease, not against disease.
It enhances even the susceptibility of the vaccinees to infection.
Nevertheless, they are protected against severe disease, right?
Well, how convinced are you that that work is to be taken at face value?
Because I've seen at least one analysis that suggests it may not be a robust fact.
No, I agree with you that it's not robust.
That's why I'm saying it's... Oh, so you're saying this is suspicious?
Oh, yeah, absolutely!
Suspicious rather than remarkable.
Well, remarkable, no, it is suspicious, but you're asking me why they're still continuing this, and I'm answering you, it's an empirical business, right?
And they found out that, you know, it's still protecting against severe disease, so they're saying, you know, let's continue with this Wuhan thing.
Well, I understand why they're continuing the vaccination campaign, because, unfortunately, it would appear to be a straight-up business decision.
Right, that they are obsessed with putting more vaccines in more arms.
I can say there's a... obviously they're being paid on a per-vaccination basis at some level, so they have that interest.
I think they also have a perverse interest in getting rid of the control group because there's so much...
Adverse signal adverse event signal.
So anyway, there are lots of reasons they seem to want to vaccinate people, but I'm not yeah, I'm what I'm curious about is why as long as they were going to do this, they didn't update The antigen.
And I can think of a business reason that they might have.
You know, there's this funny business around the emergency use authorization came with special liability protections.
They then got FDA approval, but they are still delivering the emergency use authorized version, even though they are supposed to be essentially the same.
Why are they doing that?
Because it preserves their special protection from liability.
Maybe if they updated the antigen under the FDA-approved version, they would lose that.
So I could imagine that that would be the case.
Yeah, it would also take time.
They know that the antibodies, as you know, are directed against the receptor-binding domain, which has a high level of variability.
And I think the main criterion for the public health authorities is to keep the hospitalizations under control.
And that is, so to say, what a vaccine, according to them, still does.
Because they are just looking at what is happening today.
They are not interested in the evolution.
They are not interested in seeing what is happening tomorrow, what is going to happen in a few months from now.
So they are making these snapshots.
Okay, what are the number of hospitals?
We continue with this vaccination.
Okay, infection rates go through the roof.
It's the first time that we see, see all this is very suspicious, it's the first time that we see that the morbidity and mortality rate is no longer following the infection rate during natural epidemics is following.
Now it's completely disconnected, right?
But they're saying, you know, don't care, don't care, because we still have the hospitalizations under control, right?
So there's no need for, you know, for an update or whatever, right?
Right, where, you know, one of the things that I, I don't want to get us too far off track, but one of the things that I've been, of course, wondering about is I agree.
What I see is that we did essentially the inverse of what we should have done on every front.
I would flip almost every bit the opposite direction.
I agree.
None of the things that have been done could be scientifically justified.
Right.
So, and to me, this is very alarming because you can get, incompetence can give you something like a random response.
It can't give you the inverse of a great response.
Right?
That's something else.
So, we can leave that be for the moment.
So I have this question in my mind, though.
Let's say that we, you know, just the thought experiment.
Suppose that we hadn't done the mass vaccination campaign, right?
And then there's sort of two versions of that, okay?
Let's say we did nothing and we just, behavioral modifications and nothing else.
What would the world look like today?
How much loss of life would there have been?
And then the second version of it, the one that I would favor, and I think you would favor, is Without the vaccination program and the aggressive development of protocols based largely around interventions that are known to work, supplementing vitamin D for people who are deficient, reproduce drugs, early treatments, hydroxychloroquine, ivermectin, the other stuff that seems to be so effective, where would we be today if we had done
The A and B versions of the don't use these vaccines.
What do you think?
Well, first of all, for me, it's, you know, I cannot, I can simply not imagine because people are always saying, yeah, you're saying stop mass vaccination.
What would you do?
You know, let people die?
No, of course not.
We have these, you know, treatments and it's not that these treatments were new.
Some people have started early on like Peter McCullough etc showing that this was really very effective and as you know I'm coming from the veterinary field what you often what you sometimes do with certain diseases you would infect the animal deliberately and then you would treat the animal.
So, in that way you can immunize.
So, if somebody, in other words, gets the disease and you do the early treatment, of course, also with the animal, you will not wait till it's moribund, right?
So, you will treat Then this, you know, they will recover from the disease automatically, they will build antibodies, they will contribute to herd immunity, right?
And of course, there's also this thing about, you know, all the other age groups, I mean, you know, the elderly, of course, they would have had to intervene, also people with underlying diseases, with comorbidities, we know the groups, the vulnerable groups.
All the other age groups, I mean, of course they could have had some asymptomatic, some mild or moderate disease, but what is wrong with getting the disease and being in bed for a couple of days, right?
You recover from this, It then provides a large part of the population with immunity, with herd immunity.
Once this herd immunity is established, it means that the likelihood that somebody who is vulnerable, who has a weak A weak immune system gets infected with a viral load that would be sufficient to make that person ill is very, very remote.
In other terms, once you reach that herd immunity, you can just skip all the infection prevention measures, etc., that you had put in place during the time where herd immunity was in the process of being built up in order to protect these people, right?
That is what would some people have died?
Of course, right?
But the pandemic, you know, I mean, I can only that's also something which is very stunning to me, astonishing that if you are confronted with a pandemic, I mean, our generation has never seen this.
The first thing to do is you look what happened in history, you know, what happened with the Spanish flu, for example, how long did it last?
I've been checking all the pandemics that have been documented.
None of them lasted longer than 18 months, for example, right?
And some of them, you know, 8 or 10 months.
Now, you have to realize, back in those days, you know, the world was still a very large Please, it took time, you know, because people, you know, we're not that interconnected, etc.
as now, but now the world has become a very small place.
So, I even suspect... It'll be faster.
Absolutely.
Absolutely.
Right.
So, this matches my sense of where we'd be.
If we had done nothing, There would have been a massive loss of life.
It would have burned itself out and we would be lamenting the loss of life, but we'd be effectively done with it.
If we had done the right thing, which is to skip the transfection campaign and to aggressively use the tools that quickly became apparent that they worked... For the vulnerable population.
Yes, well, really, I mean, we've seen examples where these things have been deployed well, like Uttar Pradesh, for example.
Probably Japan, although it's a little harder to figure out what they did.
Well, Japan, we can discuss this, but I have a lot of very strong information, trustworthy information from real insiders.
It's not Ivermectin that did the job.
But they are talking rather about, you know, the TB vaccine still being part of the childhood vaccination program.
And you have heard about these studies where, you know, a lot of immunity gets stimulated by the TB vaccine.
And they are saying it's rather due to this fact rather than to the ivermectin.
But anyway, put that aside for the moment.
So, if we had treated aggressively Protected the vulnerable prophylactically, maybe we protected everybody prophylactically in light of the fact that ivermectin worked that way in at least the initial variants.
I mean one of the things that troubles me here is that ivermectin's efficacy has dropped, right?
I actually didn't expect that but it did.
Since when did it drop?
Delta?
Delta and Omicron.
Right.
Yeah.
I think I have an explanation for this, but we can come back to this later.
But you can keep it in mind.
Yeah.
Oh, yeah, yeah.
I'm very curious.
I know why you're interested.
But in any case, I do think that we have these two other scenarios.
Both of them are better than where we are.
We've had a very high loss of life and we've had basically a collapse in our belief in our medical apparatus because it has revealed itself to be incompetent at protecting us and it has revealed that it's willing to lie egregiously and all of this so yeah all the collateral damage and bread it's not finished well and it's not finished which is really conspicuous
because and this this has been bugging me for for a year now which is you know we look at these rates right and And, you know, the rate is rising.
It's rising in a population, more than half of which has already had the virus.
So the point is, we are not seeing the accumulation of the immunity that would normally be accompanying anything like this.
And we're seeing such rapid proliferation of these variants.
You know, and we're seeing people get the disease multiple times within months of each other.
There's a lot here that's non-standard and, you know, we will of course never know what would have happened if we had behaved in one of these other ways, but I'm reassured to hear that you see something of the same picture.
Absolutely, absolutely.
I mean, what is also very interesting is You know, they have been doing analysis, PCRs on corpses from people who died from the Spanish flu back in... and they have pretty compelling evidence that there has not been, you know, a shift in variants, right, during that epidemic.
Yeah, right.
It was stable.
Yeah, so the variant or the lineage that basically, you know, caused or was there at the beginning of the pandemic was still the same that entered into endemicity.
Right, but this is, well, you tell me if I've got it wrong, but this is what I'm saying about If you have multiple antigens and the body has responded to them, then it is much harder to solve the problem of escape.
For the virus escaping the immunity, if the immunity is multifaceted, it's much harder because even if Even if some virus comes up with the perfect solution for one antigen, it still doesn't escape because the other antigen shut it down.
Yeah, but it's the infectiousness that counts.
So, I will tell you what the reason is.
If you have natural immunity, and we are not talking about mass vaccination, back in the Spanish flu.
So, what happens is that I was just Talking about, you know, the cytotoxic T cells, for example, the same with influenza, that have no memory.
But they will kick in pretty fast.
They will, you know, take out the majority of the viral load.
And by the time your antibodies start to rise, most of the viral load will already be cleared.
So you're not mounting antibodies in the presence of the virus, which, you know, is of course avoiding immune escape.
That is so important to understand because that is very different from a situation where people get immunized and then get, you know, exposed to sometimes a high viral load.
You know, that is what is so frustrating when people compare vaccine-induced immunity and naturally-induced immunity.
They only look at the antibodies and the capacity of the antibodies, but they forget That before getting acquired antibodies as a result from the disease, that the virus first need to break through the previous stages of the immunity, for example, these cytotoxic T cells, right?
And the training of innate immune systems, right?
And that you cannot analyze this.
You know, the cytotoxic T-cells that have no memory, you know, normally you re-stimulate in vitro with peptides, but if there is no memory you cannot re-stimulate this.
Trained innate immunity, we have no tools to examine this.
So, we are only looking at part of the natural immune defense if we look at the naturally acquired antibodies and compare those to the vaccine-induced antibodies, right?
So, the natural immunity, in other words, is much more powerful and the part that we are analyzing and comparing to the vaccine-induced antibodies, which do not go through these previous stages of immunity, is completely unfair, right?
And the system is so sophisticated, you as an evolutionary biologist should be very interested in it, that in fact, You know, by the fact that most of the viral load gets taken out by the cytotoxic T-cells, which are not, you know, they are not very specific.
So, they are not leading to natural selection.
And by the time you reach the peak of the antibodies, that takes time, most of the viral load has already disappeared.
So, there is no pressure on the virus.
There's no immune escape, right?
It's extremely interesting.
So, you need all this detail.
I'm always saying, if you study this phenomena, You cannot afford to leave any stone unturned.
You have to ask all the questions.
Why?
Why?
And unless you have an answer to all of the questions, you cannot, you know, draw conclusions and certainly not extrapolate to, you know, this is the same as with the vaccine.
Antibodies or antibodies?
Acquired antibodies or acquired antibodies?
You understand what I'm saying?
Oh, I do.
And it is a classic mistake when people with some other kind of expertise walk into a complex system.
A complex system requires that you have humility about what you don't know, which is almost everything.
I like very much that word.
Yeah, it's really important.
And I must say, in speaking to you the first time, You certainly opened my eyes to what was right in front of me and I wasn't seeing it, which was the implication of so many people who had never been exposed to this pathogen who weren't vulnerable to it, right?
That they had a completely effective response on board.
Now, it does leave me with the next question, which is, whatever that innate immunity is, why does it decay so rapidly in life?
I know a lot about senescence.
This surprises me how quickly... You mean the innate immunity?
Why does it decay?
Well, I know why it decays.
I don't understand why it decays so precipitously.
Well, I'm not sure that it's true provided the innate immunity gets strained, right?
You know, this is something which has been pretty well described essentially over the last 10 years, that through epigenetic changes you get, it's not the classical memory where you have a memory marker, but the epigenetic changes will lead to a kind of functional reprogramming of cells So that when they produce the antibodies next time around, they will, you know, better recognize the pathogen.
Okay, so then what you're telling me... I think I get it, but I don't know it.
So, help me out here.
A five-year-old has pretty good innate immunity to COVID because their system has not been programmed to very much.
Because it has not encountered very much.
The more of that system that you narrow into responding to some pathogen that the child encounters, the less of it is available for general use.
Is that what's going on?
That this is a trade-off?
As you get specific, you lose the general.
Yes, I mean, it's taking a few shortcuts, but I mean, that is certainly the way to explain it to the audience.
Okay, now explain it to me.
And in fact, that would not at all be a problem if the narrow targeting, which has high specificity, for example, in form of, you know, adaptive antibodies.
Right.
If it was targeted at COVID, but it's not.
Right, so I get this now.
So basically the point is you've got some beautiful system that could in principle see anything, and it will see a bunch of things, and the point is it can't do that forever.
And so that, I never understood this before, and this has been a key feature, this has been one of the things that people don't understand about your model.
And I'm not saying that I understand whether your model is right or wrong, but when people talk, when sophisticated people Talk about Gerrit van den Bosch and his view.
They say, why is he so focused on the innate immunity and these peculiarities of it?
I think this is a pretty satisfying answer, right?
The effectiveness of an untrained immune system against COVID is shockingly good.
Yeah, but the only limitation is, is because of the affinity of these antibodies is lower, you know, they interact, what they recognize, in fact, are patterns on the surface of the virus, on the surface of the cells, patterns.
And that is the beauty of this system, that patterns, these most likely glycan patterns, are shared amongst a broad spectrum of different viruses.
Not only all the variants of SARS-CoV-2, but all the coronaviruses.
Most likely all the glycosylated envelope viruses, like even influenza, etc.
But because they bind through multivalent binding, Their affinity, because in that case you talk about avidity of the antibody responses.
So they have the strength of binding is, you know, inferior to the strength of binding of specific antibodies.
So you could say, well, we do this all the time when we vaccinate our childhood vaccinations, for example.
But, you know, there is no problem, as you were pointing out, if the specific antibodies that you induce do a perfect job, because they have memory, they have strong affinity, that means they will strongly neutralize.
The innate antibodies, they are perfect, but they cannot cope with a high viral load.
But if you break through that innate immunity, you will have the phenomenon that we were just describing.
You will get acquired antibodies.
And guess what?
These acquired antibodies will be a perfect match to the virus that caused the disease.
Whereas now we are with the Wuhan.
The spike is not at all a good fit, obviously, to the virus we are in.
So, you see how powerful this natural immunity is, the different components.
And, you know, that's why I'm saying, to your point, you know, I'm always saying I'm not a top virologist, top immunologist or a top vaccinologist.
But you know, it's so multidisciplinary.
I've learned to bring these fields together, even biophysics.
If you don't understand the difference between a polyvalent IgM binding, you know, antibody and a specific IgM for a specific antigen, you know, you will never ever understand this, right?
So, it's so many different aspects that need to be put into consideration.
And I'm always saying, the value I'm adding, I hope, I guess, is putting the different pieces of the puzzle that I find in publications, etc., to put them together.
And obviously, you know, today science is no longer capable.
That's why I love the thing you were saying at the Better Way Congress, We need to rebuild the science and to some extent for these complex problems, I think we need to also have a different approach to science in the sense that not thinking in silos, but a multidisciplinary approach.
Well, here's the funny thing.
I mean, I agree with what you said entirely and I'm frustrated to no end that the way Scientific education has evolved has caused this obsession with specialization.
Yeah, and right and technologies technology and specialization and no doubt these things have their place, but the problem is synthesis is the natural partner of reductionism right and It is not rewarded in our system.
So what you're saying, well, I'm not a, you know, a great this, a great that, but what I can do is bring the things together.
Well, to me, all of my favorite evolutionary biologists were involved in synthesis.
That's what they were doing, is taking all of these isolated things that don't seem to tell a story and figuring out where you have to stand in order to say, ah, that's what this is, right?
You know, and that's really...
It's such a it's such a crucial part of the process and what we've effectively been watching I mean if we give the benefit of the doubt and we say well, okay, they really screwed this up, but it was an honest error Well, if it was an honest error, it was an honest error created by a committee of specialists where nobody remembers how to put the whole thing together, right?
And it's a it's it's tragic and it's tragic at the level of like a million American deaths You know, it's unbelievable.
Yeah, I fully agree with you.
You know, it's just unbelievable that in, you know, in 2022, where we have access to all this science, all these technologies, you know, all these, you know, institutes put like millions of taxpayer dollars into it.
And we are not, we are not, we have no clue how to tackle, you know, a complex health problem.
So, that also means we cannot give anything back to society from all the money that got invested, right?
So, all these publications is in fact, you know, they are essential, they are important, but when you start to have publications, you know, if it becomes an objective in its own right, I've learned to use science as a tool And if I don't see any added value to the kind of problem I'm studying, I will not dig very deep.
But if I think, you know, even a molecular detail, this could bring a piece of the puzzle, then I will take a deep dive, right?
And so it's a completely different approach to, you know, to science.
But, you know, you see, it's needed in a situation like this.
The public health authorities, even the key opinion leaders, they don't know what's happening right now.
Do you agree?
They have no clue where this thing is going, right?
It's like the worst of all possible worlds.
They don't know what's going on and they have no idea A. that they're in the dark and B. that there's another way that wouldn't leave them in the dark, right?
We've just lost the understanding of this and everybody who does it, all of the generalists are driven out because frankly you can't compete as a generalist inside of the system.
So, yes, it's a tragedy, and when you think about the immense costs of this, I mean, they're not even all quantifiable.
This week, at this conference, the one that I am reminded I am reminded of how frightening this is, but the gaslighting of the vaccine injured, I cannot think of anything more diabolical than this, right?
You injure people and then you tell them it's in their head.
Right.
And then you tell other people that they're part of an anti-vax movement.
You know, we are living in a surrealistic world right now.
It's nothing, nothing makes sense anymore of any, you know, this is, yeah.
I'm always saying, you know, it's, uh, it makes me and it takes something to make me speechless, but that, that makes me speechless, right?
I find myself also at a loss for words pretty frequently.
All right, we have just paused to close the curtains to prevent the darkness from leaking in.
I want to ask you though, all right, we've looked at what you thought was going to happen.
There's been a surprise.
The surprise is that the evolution of greater infectivity did not come with greater virulence.
So that's interesting.
I guess we have to talk about the question of Ivermectin and its dropping effectiveness, but before we do... Yeah, yeah, yeah.
Well, don't forget that question, yeah.
Well, maybe we should do that and then let's return to where you think we are in the pandemic and what you think is coming.
Okay.
So, and I'm not saying that, you know...
What I think is right, of course, but it might be, it might point into the right direction, which is that right now we are facing a situation, it started already with Delta, but now it has moved to an extreme situation where the virus has become resistant to the vaccinal antibodies, to the potentially neutralizing antibodies.
And there are interesting studies from Professor Fantini, the University of Marseille, who is a biochemist.
This has been published.
It's also in the document in the manuscript that I gave you.
I'm referring to his publications.
who has shown that if the neutralizing antibodies, the potentially neutralizing antibodies, I should say, are no longer able to bind to the virus, then non-neutralizing antibodies can bind.
So in a sense that it's always like this, if you induce antibodies For example, against the protein, you may have, if that protein is responsible, for example, for infectiousness, you may induce antibodies that can, you know, neutralize the virus, but at the same time, you are also inducing antibodies, we call them ELISA antibodies, that have not neutralizing capacity, but that could potentially bind.
So now, what he has found out is that when the neutralizing capacity dramatically diminishes, That the non-neutralizing antibodies can bind to the spike protein.
And you could imagine the following situation where the neutralizing antibodies they bind to the virus, to the spike protein, that you have a kind of like a conformational structural change
which prevents the non-neutralizing antibodies from recognizing their binding site because that also he has been he has documented that the binding site for the non-neutralizing antibodies is not situated within the receptor binding domain but is situated within the N-terminal domain.
That is one thing.
What he has also shown is that this domain is very conserved amongst all the variants in contrast to the receptor binding domain which you know is very very variable.
Yeah.
The receptor-binding domain has been under intense pressure from the vaccines.
Yeah, therefore we had omicron 20 mutations or only in the receptor-binding domain.
Right.
This other domain is highly conserved, which you would expect because there's no advantage to altering it, presumably, or very little.
It is very conserved, yeah.
Okay, so go on.
Yeah, so what he has, the most spectacular thing he has demonstrated, or he has shown, is that when these non-neutralizing antibodies bind, so preferably in people, you know, who have antibodies that are no longer functional, so to say, then the binding of these antibodies to the spike will lead to an enhanced infectiousness of the virus.
Yeah, it's enhanced, you know, antibody dependent, but it's depending on the non-utilizing antibodies enhancement.
So now, this is... So, we need to unpack that a little bit.
Yeah.
So, the point is, you've got a virus, it has a molecular structure that allows it to enter the cell.
You've got immunity generated by these transfective agents that is producing antibodies which stick to this thing.
But the problem is at this scale you can always get a situation where what sticks to the protein is actually creating a mechanism.
It's creating a new mechanism potentially to get into the cell or it's creating some change that actually facilitates the entry.
Well, the explanation is, in fact, the spike protein, all this is dynamic, right?
Very often in biology, things are not static, it's dynamic.
So, the spike protein has two different positions, open and closed, or up and down.
So, this thing is going like this, right?
So, to bind to the AC2 receptor, the spike needs to be in the open position, then it can readily bind.
But if it is sometimes closed, you know, depending on the number of statistically, you know, contacts, sometimes it will go to the AC2 receptor, it's closed, it will not bind, right?
So now what the non-neutralizing antibodies do by binding to the conserved domain within the N-terminal domain it will force the spike in the open position.
Got it.
And therefore it now becomes very infectious.
What has been shown in peer-reviewed journals is that therefore the susceptibility of the vaccinees Two infections, you know, is much higher than the susceptibility of the non-vaccinated people, right?
Right.
So, that is something very important to understand.
Now, and I will come to the point of ivermectin, but look, I think this is fascinating.
What we are seeing right now, if you think about this, the fact that these non-neutralizing antibodies can now bind to the spike
All of a sudden, what that means is that the behavior of the virus, the infectious behavior of the virus, is no longer dependent only on the intrinsic properties of the virus, but is to a large extent determined by the immune response of the host, the non-neutralizing antibodies.
We are seeing more and more that the behavior of the virus is no longer determined by seasonality.
Right, yes.
Look what is happening right now.
I mean, in my country over the last four, six weeks, an enormous drought, unusual for Belgium, sunshine, nice temperature.
Infections, you know, are all over the place.
Secondarily, we know that normally younger people are better protected against infection than, you know, elderly people.
What you're seeing right now is that youngsters as well, young people, they get reinfected all the time.
So age, When you have these antibodies, it doesn't seem to play a role anymore.
You see what is happening?
That is unprecedented.
We have never seen this, that the behavior now of the virus, unless you neutralize it, but then it's gone, but that the behavior of the virus, the infectious behavior of the virus, is now largely determined by the binding of the virus to these non-neutralizing antibodies, right?
It disconnects the whole thing from seasonality, it disconnects it from age, etc.
This is a repair, because people say, yeah, Omicron, this and this and this.
No, Omicron, you know, the behavior of Omicron is to a large extent determined by the immune response, which is anything but effective.
It's on the contrary enhancing the infectiousness of the virus.
So, you've got my evolutionary brain racing, because In some sense, if I understand what you're saying correctly, the mass vaccination of the population of planet Earth created a synonymized new species.
I mean, in effect, what we had was a human population with wildly different susceptibilities to this virus, right?
So the virus was trying to solve different problems.
And also depending on the individual, you know, age and etc.
And we know that, you know, people were vulnerable, others were not vulnerable, etc.
But what we effectively did was install the same port On a huge population of people.
Mass vaccination does this.
And so by doing that, then the point is now the virus does not need to solve the problem of how do I infect old people and young people.
That's a tough problem to solve if those two systems work differently because to work better in this one, you give up something in that one.
You're harmonizing the whole thing.
Right.
And by synonymizing them, by saying, well, you know, look, old people and young people, they're going to have the same port.
If you can figure out how to use that port, Boom!
That's exactly.
Well, I have not understood that before.
And I mean, this is not, you know, there is, that's why I'm saying, you see these pieces of the puzzle?
Somebody demonstrates that it's enhancing the infectiousness, right?
Others demonstrate where exactly this is binding.
Others, you know, clinicians, they show, for example, that the susceptibility of the vaccine is much higher to infection.
And then we observe that, you know, the behavior of the virus is no longer bound to seasonality.
That it is independent of age, that it becomes more and more independent of age, etc.
You see these pieces of the puzzle and then you fit all this, you pack all this together.
Now what you're going to have, to your point, and I'm not saying that this applies, this is the truth, but I think that it started already to some extent with Delta, which already was to some extent more resistant, you know, to the vaccinal antibodies.
Now you have an extreme situation where in fact you are in an artificial way because of the binding to these non-neutralizing antibodies pretty dramatically enhancing the infectiousness of the virus.
So, for me, you know, that would automatically require a higher dose, you know, of ivermectin.
Not because the virus has evolved, but because now you have a new component that synergizes with the intrinsic infectious behavior of the virus and that dramatically increases the infectiousness.
That's why we call it You know, antibody-dependent enhancement of infection.
Right.
So, in effect, this is fascinating, a virus is a creature that has surrendered its biology and gotten a tremendous advantage by borrowing the biology of its host.
In this way, it is borrowing the updated biology produced by the immune system, right?
And it is developing.
I mean, this is exactly what biology does.
This is exactly why You know why I have to shake my head at people who thought they were going to simply solve this pandemic with simple tools they had no idea the complexity of the thing they were interfacing with.
Yeah well you know this is this is typically biology you know everything is dynamic the the virus is is evolving the more you put pressure but also the immune system we talked about training of the so that means if your innate immunity got not compromised the unvaccinated you know they also get more and more exposed to the virus but they can train their innate immunity so it is
It is like and that is why I cannot understand why like public health authorities they look at this oh look at the hospitalizations they don't understand that this is a dynamic right that this is evolving and it will evolve as long as we have not achieved a new equilibrium, a balance.
You know, if you have, after a natural pandemic, you have a few waves and then all of a sudden, you know, there is herd immunity, the population controls the virus, that is a kind of meta-stable equilibrium because, you know, people will age, some people have underlying diseases, for example, so immunity may wane a little bit.
The threshold, as soon as, it's a very delicate balance, as soon as you get over the threshold, you will have a few people who get the infection, who get the disease, that will immediately increase the infectious pressure.
Other people will, you know, but if there's still sufficient herd immunity, You can get this thing again under control.
That's why we are talking about an outbreak sometimes or a small epidemic like we have with flu.
But as long as you have not achieved this kind of equilibrium between the immunity of the population and the virus, you know, this thing is evolving.
And you take a snapshot and you say, That is what, you know, that is what this vaccine does.
It will, it will, you know, prevent hospitalizations and severe disease.
We are already seeing that even that situation, you know, it was, it had a duration of at least several months at the beginning.
It's now down to a few weeks, right?
And yeah, so.
All right, so several things.
One, your hypothesis on what happened to the efficacy of ivermectin is pretty interesting, so let me just recap.
Well, that's my explanation, but... It's a hypothesis, but I like it.
And your point, if I understand it, is that effectively the antibody-dependent enhancement has increased the capacity of the virus to infect people, which is not a story that involves ivermectin.
But what it means is if you're dealing with a new pathogen that has a new tool, and that tool is one that borrows from your immune system when it arrives from your system.
Which is, you know, the place where it replicates.
It depends on the host.
Right.
The point is it's like a cat burglar arriving at a house where it knows there's going to be a ladder.
Right?
That's a cat burglar with some extra capacity.
So you're going to need a bigger, better security system to defeat that person.
And so the point is, ivermectin worked.
It still works, but you need a lot more of it to get the same effect because the virus has learned a few tricks along the way because we taught it.
We trained it.
Yeah, yeah, absolutely, absolutely.
So, when this entry into the cell gets expedited, it's logical that you need to come, you know, with a higher concentration at the very beginning.
You cannot, you know, if 20 particles enter at the same time, more or less, instead of five particles, The concentration at that very surface of the susceptible cell needs to be higher, right?
That seems very, very logical to me, but I think there is no molecular proof of this, but there is, yeah, I mean, at least I think a hypothesis is plausible for as long as there is, you know, there is some evidence that it is wrong, right?
Yeah.
All right, let me ask you another question.
I wondered about and worried about what would happen to something as useful as Ivermectin, and I'm troubled by the fact that you need more of it, although I'm heartened to hear that that's not really a failure of the drug that's actually on the virus side, if that's what's going on.
Absolutely, absolutely, yeah.
But, here's the other one I worry about.
The virus did not transmit outdoors essentially at all.
Has it learned that trick?
And if it hasn't learned that trick, is it going to learn that trick?
Because that will be a whole new disaster for humanity.
To transmit outdoors?
Yeah.
So, what do you beat exactly?
The evidence was quite good that people did not catch the infection outdoors.
And the model that Heather and I built, which I think is pretty robust, is that the mode of transmission is highly dependent on what we call the effective volume of the space.
Right?
So, in a car with the windows closed, it transmits pretty darn well.
Right, in the car with the window open it's a lot slower to transmit and you know the volume of a room and then you get outside and effectively the volume of the room is infinite and it doesn't transmit.
Now, I can't think of a reason that this virus shouldn't be able to, if humans use the outside environment to evade the virus, I can't think of a reason that it shouldn't be able to evolve the capacity to transmit outdoors, especially since presumably its wild ancestor did.
Yeah, but does it really need to evolve to acquire that capacity?
It all depends, of course, on the viral load.
In the past, for example, before this happened with the non-neutralizing antibodies, you maybe You required an inoculum, or for example, just as an example, 10 viral particles to have, we call this a take of the infection.
If you had, for example, less than that, fewer particles, they would get onto your mucosa, but there would be no take of the virus.
I wouldn't have replication in my body.
Exactly, exactly.
But now, if you have these antibodies, Right.
It can make these antibodies, of course, will bind before viral entry to this virus.
And it makes the viral particles more infectious.
Then five particles, three particles could be sufficient.
So that means it's all a matter of concept.
We know this very well.
Well, certainly when we do experiments in animals, everything depends on the viral load.
Of course, you need that many particles.
Otherwise, you're not going to be able to induce the infection.
So now, I think that, you know, that people, especially if people are vaccinated, who become very, very susceptible that even if the virus gets significantly diluted in an open air space, that there is still, you know, A reasonable likelihood that with 10 times less particles on your mucosa that you can still have a take of the infection, right?
This is exactly what I'm concerned about.
I mean, you've given me a mechanism here, but I guess the point is the outside environment has been effectively infinite volume, which means you never rise above that infective threshold.
Yeah, that I don't know.
I don't know.
But it's also, you know, if we are outside and we are looking at pictures on my mobile phone, we are getting pretty close together.
We are still outside, but, you know, that could be sufficient.
But I don't think people who are, you know, walking somewhere in the woods, you know, I mean, that is very different.
But there is a situation where even outside you get pretty close together.
Well, that was the funny thing about this virus at the beginning, was that we all thought, yeah, outside, you still need to distance and all, but then the evidence really reflected the fact that nope, really outside was almost completely protective.
And, you know, and my thought was, oh God, that's a, that's an evolutionary challenge that this thing can overcome.
And anyway, I'm wondering if it has already, if part of what we're seeing is actually that it has learned this trick.
But anyway, let's leave that aside.
I think the final question that we should address is where do you think we are and what do you think is coming?
I think the virus is in the process of crossing the valley of fitness for overcoming another pressure that we are putting now.
Fire the non-neutralizing antibodies because this story and this is another piece of the puzzle.
Some scientists have been doing very very interesting studies and have shown that in fact the non-neutralizing antibodies that we were talking about and that are responsible for enhancing the infectiousness of the virus at the upper respiratory tract and I will explain this in a moment but let me first summarize this.
Now these very same antibodies So what they have shown is that part of the viral particles at the upper respiratory tract are taken up by dendritic cells.
But they are not internalized in the dendritic cells.
They are absorbed at the surface of the dendritic cells.
Migratory, you know, dendritic cells that migrate to distant organs.
Dendritic cells do that.
One of the distant organs is the lower respiratory tract, but it could also be the liver, could also be the digestive tract, for example.
And they have shown that there is a process that is called trans-infection.
And what does trans-infection mean?
Trans-infection is the transfer of the virus that is absorbed on the surface of the dendritic cell to a susceptible alveolar epithelial cell.
That process of trans infection is inhibited.
They have shown this in vitro.
Therefore, I'm saying it's all pieces of the puzzle, right?
This process of trans infection is inhibited by non-neutralizing antibodies.
And that is due to a conformational change that prevents, in the manuscript that I gave you, I'm describing this in detail, but they use a conformational change that makes it impossible for the virus that is adsorbed to the dendritic cell to be transferred to the susceptible cell.
Because once it is transferred to the susceptible cell, The susceptible cell gets infected and will present a spike protein at the surface and that will induce fusion of the infected cell with a non-infected cell that will induce the syncytia.
I don't know exactly how to pronounce this in English.
The syncytia.
You know what syncytia?
Yeah.
Yeah, exactly.
And the syncytia have been clearly correlated with severe disease.
All patients dying from severe disease, you know, you find the syncytia in the organs.
So, and that process is called, not by me, but by this scientist, transfusion.
So, you have the trans infection, the transfer from the viral particles absorbed at the surface of the dendritic cell to the susceptible epithelial cell that will then also infect other non-infected cells through a process of transfusion.
This is the S-protein that, you know, induces You know, when it gets presented, it is like, you know, it gets rearranged so that it gets fusogenic capacity and can make the cells fuse so that you have a syncytium and that is what is basically causing systemic and severe disease.
So, in other words, the non-neutralizing antibodies are suppressing Or suppressing, if you like, virulence, the capacity to cause severe disease at this moment in time.
Yeah.
So, whereas in the first phase of the pandemic, we had neutralizing and we had, you know, suppression or we had immune pressure on viral infectiousness via the neutralizing antibodies.
We have now immune suppression.
on viral virulence through the non-neutralizing antibodies.
I can repeat it if you like.
Well, I'm going to need some help here.
First of all, there's some new things in here that I just didn't even realize were on the map.
So, you're telling me that these infected cells migrate internally to vulnerable epithelial cells.
Well, these are dendritic cells, migratory dendritic cells that have, you know, absorbed viral particles that they have, you know.
So, when you say viral particles.
You're not talking about virions, you're talking about… No, I'm talking about virions.
You are, okay.
It's synonym, you know, viral particle and virion is the same.
Alright, so they take in these virions.
They don't take them in, they absorb them at the surface, they are not internalizing them.
I see, okay.
And so they're… Right.
And this is new, you know.
They have demonstrated this.
The dendritic cells have C-type lectin receptors at the surface.
Obviously, these glycosylated viruses, coronavirus, you know, has glycans that stick to these lectins and that is how, you know, they absorb really to the surface of the dendritic cell.
All right.
And then they're being transported.
Yeah, they migrate.
To epithelial cells, to distant organs, could be anything.
Now, the virus One of the things that's confusing about this virus is it seems to have such high tropism for different tissues that probably isn't really helping it transmit, which I take to be a likely byproduct of a laboratory origin, that basically the rules that usually keep a virus limited to infecting tissues that help it transmit are
largely alleviated by the laboratory environment where the animal that it's being passaged in, for example, doesn't have normal constraints because somebody's feeding it and it doesn't have to walk around.
But in any case, okay, so it migrates to these distant cells.
Distant organs, you know, and one of these distant organs is, of course, the lower respiratory tract.
But you may, of course, know that some people develop and have enteric problems, digestive problems, as a result of coronavirus.
So, it's not really strictly limited to the lower respiratory tract.
So, people will not have respiratory symptoms, but they will have diarrhea and spasms, for example.
Right, which is interesting because it's not transmitting this way, as far as we know.
So, that's conspicuous to me, right?
Well, it's not transmitted, it will be shed, but you know, it's a very fragile, it's not like enterovirus that is very resistant in the environment.
I mean, I studied for a long time environmental virology, I mean, Coronavirus is very fragile.
It cannot really survive for a long time, certainly not in, you know, in wastewater or in sludge or whatever.
Whereas with enteroviruses, this is a primary source of contamination.
That's also why, you know, people are always saying we almost eradicated polio to a large extent.
That was due to water sanitation, right?
And all these type of things.
Right.
Yeah.
Which is quite a can of worms there, but yeah.
All right, so what does this mean?
For a what you expect the pandemic to do and be how we will know if you know What's the prediction of your hypothesis?
Yeah, so what is what this means to me?
Is that we are currently?
facing a very weird situation as I told you already why where we have a A high level of infectivity, of infectiousness, but we have mild, relatively mild disease, right?
Where we know that this mild disease is not due to neutralization of the virus, not due to herd immunity, because on the contrary, we keep saying that We have high infection rates in the population.
It's very infectious.
So, what these vaccines are doing right now is anything but generating herd immunity.
Because herd immunity would mean that you see a dramatic decline of infection rate.
You're seeing exactly the opposite.
So, what we are seeing is enhanced infectiousness But mild, mild symptoms.
And if this is true, what these people suggest based on in vitro studies, but I must tell you, Britt, these people have done this and, you know, it's just a coincidence that I know the group because I, you know, one of these people that I know very well got a grant from the Bill and Melinda Gates Foundation and I was working at the foundation, so I know.
So they have been using cells that are really simulating completely the epithelial cells in a sense that their AC2 expression is very low, whereas we know at the upper respiratory tract AC2 expression is pretty high.
And they also explain why, indeed, in order to infect nevertheless cells that have low expression in AC2, they need some kind of help.
It is, you know, normally, this transfection that takes place is helping the infection because during this, when the virion gets transfected, you get a rearrangement, a structural rearrangement of the spike protein, which makes it fusogenic and which enhances, despite the low concentration or the low expression of AC2, you know, the entry into the cell.
So, I guess what I'm saying is that now these non-neutralizing antibodies are in fact preventing this process from taking place.
And we know, I just explained to you, they are binding to this highly conserved antigenic site, right?
So, to the same extent as the neutralizing antibodies were binding to the receptor binding domain and exerting pressure on viral infectiousness because this receptor binding domain is the part that you know enables viral entry and hence infectiousness.
The non-utilizing antibodies by binding to this you know antigenic site within the N-terminal domain has been shown that they bind are now like exerting pressure on another characteristic of the virus which is viral virulence, right?
And so there is no, they don't prevent the virus from replicating.
So we still have high rates of transmission, higher than ever.
So my guess is, but of course I'm only, you know, Sharing some fragments of the puzzle that I put together.
But is that again, the virus will be, you know, will be capable of overcoming the pressure.
But we know viruses can overcome pressure that is exerted by antibodies.
I mean, we have had the example, we have not learned from the first phase of the pandemic, because what the first phase of the pandemic learned us is that
If we exert immune pressure on a characteristic of the virus without being capable of preventing the transmission, nature will do the natural selection and will give a competitive advantage to those guys who are capable of overcoming this.
And what is the result?
Well, we have dominant propagation of a highly infectious variant which is Omicron.
We have not learned that now we are exerting pressure because the virulence of Omicron is lower than the virulence of Delta.
We have not learned that if we are now exerting pressure, and we know how this comes, it's because there is pressure, you know, of these non-neutralizing antibodies by binding to this antigenic site that is conserved in the N-terminal domain, you know, we have not learned that this immune pressure, it's also an immune pressure just on another domain, is now highly likely, you know, of
Giving a competitive advantage to those guys that will be able to overcome this and I'm describing this in my manuscript that this is I think it's highly likely that this will be possible by additional glycosylation of the virus.
I mean, we can expand on this, but it's also very, very surprising to me that if you read about glycosylated viruses, you know, in every textbook of virology will tell you that, you know, glycans are so well suited to shield Antigenic domains from recognition from antibodies.
And why is this?
Well, remember this, the viral membrane is in fact part of the cellular membrane, you know, with these viruses.
When the virus is budding, it gets enveloped by part of the cellular membrane, the cellular membrane that is carrying self-glycans, right?
So, the virus is carrying self-glycans that are not recognized per definition by the immune system, But they can shield, you know, a whole antigenic domain from recognition, right?
And so, that is what I think is very likely to happen, that the virus will overcome this and that we will end with a virus that is not only highly infectious, but also virulent and that is completely resistant to any of the COVID-19 vaccines.
So, let me understand this.
I see why this model predicts Omicron is not the natural vaccine that many of us hoped it might be, right?
That effectively it's highly infectious, it's going to give everybody natural immunity and we can finally be done with this.
Your model is saying that's not likely.
I'm saying it's the case for the unvaccinated because it's just going to train better and better you know the immune system of the unvaccinated people right and that is a very interesting comment because I need to say Britt that right now when people are saying you know what there is still a number of unvaccinated people that despite Omicron land in the hospital
Every medical doctor, every virologist, every vaccinologist knows that if there is one thing you cannot do with a live attenuated vaccine, so Omicron, is to immunize vulnerable people or people who are not in good health.
Because there is always a likelihood that in those people the virus will break through despite the fact that it's attenuated.
So the people that now land in a hospital with Omicron are people that you would never ever vaccinate with a live attenuated vaccine.
People with underlying diseases, with a weakened innate immune system, etc.
But for all the others, it's just, you know, a training, a training of the immune system.
And you see the thousands, the vast majority of the population, you know, unvaccinated, you know, is not hospitalized, right?
Yeah.
So, okay, I read you loud and clear now.
You're saying that that model, which many of us discussed, I certainly argue that this is a possibility, is logically correct but only functional in those who have not been trained by the transfection I'm trying to avoid the word vaccine because I know it's not right, but the COVID-19 vaccines, right?
So now we've got two populations, one of which is carrying effectively the synonymizing port I described it as before.
I'm just speaking metaphorically.
And then the unvaccinated population is still highly variable and also is being trained by Omicron to be better and better at fighting off closely related coronaviruses.
There is one important thing that I need to tell you.
That is that I told you that the non-neutralizing antibodies are directed against an antigenic site within the N-terminal domain that is very conserved.
Now, so people got vaccinated with the Wuhan strain.
Well, we know what the S-protein, you know, corresponding to the Wuhan lineage.
So, the receptor binding domain of this one, so that means that people have been primed, their immune system has been primed to recognize the receptor binding domain of the Wuhan as well as the N-terminal domain, right?
So now you come back with a virus, Omicron, which has an N-terminal domain.
It's in fact the antigenic site within the N-terminal domain, but I'm going to keep it simple.
The N-terminal domain, so to say, that is very conserved.
Conserved, so the same as Wuhan?
Yeah.
The other is variable.
So antigenic sin tells you that when you have primed with an antigen and you come back with the same antigen, that those antibodies will go through the roof.
So the non-neutralizing antibodies, and you don't need an additional Omicron vaccine, simply by the circulation And people are highly susceptible, the vaccinees.
They get their non-neutralizing antibodies boosted like hell.
For the part of Omicron, the part of the virus that has changed, it's the first priming.
Because in Wuhan, the receptor binding domain was completely different.
Right?
So before new antibodies can develop against the part of the virus that has been changed, dramatically changed, namely the receptor binding domain, that will take time.
Before that can happen, the non-utilizing antibodies in no time will go through the roof, enhance the infection.
You see what I'm saying?
I think I do.
And if you take away this resistance to the non-utilizing antibodies, then the enhanced infectiousness will automatically result in enhanced disease.
So, if I understand you correctly, what you're saying is you've got this N-terminal domain which is highly conserved and therefore... Well, it's a part, it's a part, the part that is recognized by the non-neutralizing antibodies is highly conserved and is situated, has been well described within the N-terminal domain.
Okay.
So, what that does is it is basically a signal to the immune system that activates that fraction which was trained at the same time.
And so, trained on the Wuhan S protein, the receptor binding domain, which has now changed.
So, effectively, this is tailor-made to trigger the immune system to deploy an ineffective response, which now enhances the capacity of the virus to infect.
Is that what you're saying?
Yeah.
It's just that we, in that case, we don't talk that much about the training.
We would rather say it has induced memory.
Has induced memory, okay.
Even the non-neutralizing antibodies are still specific and acquired antibodies, but that's a detail.
Yeah, I'm speaking colloquially.
Yeah.
So that sounds like a recipe for a new phase of this pandemic.
Especially in light of the fact that it predicts that there are two populations, those who have been transfected with these so-called vaccines and those who haven't, who are going to have exactly inverse response to the future variants.
And so, in any case, one, I would just say That's frightening.
It's also proper scientific form.
It's a hypothesis.
It's delivered with a prediction.
We can know whether it's right, you know, and as with your initial predictions might be that there's a nuance where the model is mostly correct and then something surprising interfaces, you know, a lot of things could happen.
But anyway, we at least, you know, I think the thing is Very troubling to hear you say that, because I heard you say your predictions before, and although the world did not unfold exactly as you predicted, it was a lot closer to what you predicted than what anybody else predicted.
Well, it occurs in two phases, right?
And if you think about it, we got variants that were more and more infectious.
At a certain point, the virus became resistant to the neutralizing antibodies.
That enabled the virus to exert pressure on viral virulence.
Because as long as you don't have the non-neutralizing antibodies that take over, you cannot exert pressure on virulence.
So, you have more and more infectious virus, then all of a sudden, you know, the virus becomes resistant, the non-neutralizing antibodies take over and those now start to exert immune pressure on viral virulence.
And what I'm saying is that Whereas at the beginning of the pandemic, the immune pressure was gradually increasing because there was like one variation or two or two or three variations within the receptor binding domain.
Now we are talking about boosting of non-neutralizing antibodies.
So all of a sudden, in a large, vast majority of the population in highly vaccinated countries, we are having a huge immune pressure, right?
By these boosts, right?
And we have been doing mass vaccination.
So it's in highly vaccinated countries, the majority of the population, right?
Because it's always the population that exerts the immune pressure.
When we agreed on that, one single individual cannot do this, right?
So I guess what I'm saying is that whereas you could think of the evolution of the virus, you know, taking a more or less linear course at the beginning of the pandemic, that what we are seeing right now is like, you know, And it's very, very
Strange that now for the first time within one of these families of variants, the Omicron, even within this family, we have now more infectious sub-variants to an extent that the WHO has now decided that, you know, the BA4 or BA5, we need to consider them in their own right as a variant of concern.
Yeah, that actually begins to feel like An adaptive radiation, right?
And so I may be stretching a little far here, but my sense is that when we see an adaptive radiation, basically we see a branch of the evolutionary tree that suddenly sprouts a wide diversity of things.
Because we have not seen this with Delta.
We have not seen this with Gamma.
Right, exactly.
And so my My point is that actually there's something selectively going on that's different and what I would argue it's at least consistent with your model that what's happened is we've crossed a threshold where the opportunity, basically the reward for experimenting has gone up and therefore the virus is now experimenting in effect with different ways of being.
So another explanation could be that the binding of the non-neutralizing antibodies to the antigenic site is still improving.
But, you know, I mean, that can still go on for some time.
But, you know, the pressure is, I think, enormous.
And that's why I'm saying it's the valley of fitness.
You know this from evolution, right?
You have the selection, but then the virus needs to become dominant, right?
It needs to cross this valley to become more and fitter and fitter.
And Yeah, so the situation that we are in right now, I think that is the summary at least of my analysis, is completely unstable.
It's unstable.
The virus has not reached the equilibrium, right?
Yes, we have not reached equilibrium and I think one way of interpreting what you have delivered so far Is that we have prevented ourselves from reaching an equilibrium that we would have gotten to.
And it might have been very painful.
We might have arrived there at an unacceptable cost, but we would have arrived there and we're not arriving there at all.
And we've got to ask ourselves the question, how long are we going to keep interfering before we realize we're creating our own problem?
But you know, the problem is that we have now a load.
A highly infectious virus to circulate and that that in its own right is boosting people all the time.
Yeah.
We cannot, you know, we cannot take this away.
Right.
That is where I'm saying if we are not, because if you think about this, if you think about this, if the infection rate rises in the population.
Yeah.
Then of course you are going to have the prevalence, the prevalence in the population of elevated titers of non-neutralizing antibodies is going to increase.
That is going to increase the immune pressure on the whole thing, right?
The more immune pressure, the higher the infection rate, so both are interconnected.
So what can you do?
Mankind can diminish the infectious pressure, you know, massive mass antiviral campaigns, for example, right?
But if we don't do anything about this, the other thing is to diminish the immune pressure.
Now, who is exerting this immune pressure?
It's not the non-vaccinated population, it's the vaccinated population.
So, if you want to achieve this equilibrium and you don't want to play with the infection rates, you don't want to diminish this, what you're going to get is that the immune pressure needs to diminish to rupture this vicious circle But that means that it's a population that is exerting that immune pressure, you know, that needs to be reduced in order to get your 60-70% of herd immunity.
Because now the herd immunity is like the unvaccinated, let's say 10%.
If you want to increase this, right, if you're going to diminish The contribution of the vaccinated population, then you can increase this to like 60 or 70 percent.
The other way to increase it, that's theoretical, is a baby boom or it's massive immigration from poorly vaccinated countries.
Or it is, you know, the ultimate solution would be a vaccine that prevents, that blocks the transmission, that induces sterilizing immunity.
No, we don't have this.
Now, frankly speaking, I don't know about any other solution, right?
Yeah, that's very troubling.
It's very troubling, yeah.
I mean, that's why I told, you know, Dell Big Tree, do you really want me to convey this kind of message?
To your audience, because, you know, it's not good news, but, you know, you know this as an evolutionary biologist that this type of balance between a pathogen and an immune system has been shaped over thousands of years to evolution, like natural selection, all these type of things.
What we have done here, literally, is we have thrown a bombshell On this thing, you know, on this delicate balance that has been established for many, many, many years, right?
And then, would we expect that this thing is just going to die out, it's not going to have consequences, Omicron is the end of the pandemic phase, as our friend Fauci is saying, you know?
How can you ever end a pandemic without cutting dramatically the infection rate?
What we're seeing right now is exactly the opposite, right?
Right, and I don't know how we got here.
I think it was a combination of hubris, some kind of wishful thinking, the belief that we were entitled to come up with a miraculous vaccine very quickly.
Arrogance and stupidity.
Arrogance and stupidity and greed.
There's also an element of this in which they don't feel the pain because they're financially winning as they deliver us these feeble products.
I agree, I agree.
All right, well, this has been quite a discussion.
It certainly Unnerving.
If you had to give advice to the world, what's the next thing?
Presumably your advice is stop the vaccination campaign.
This has already been my advice almost like a year ago.
The whole time.
Yep.
Yeah.
And I think your view has been borne out.
Obviously, you would favor the widespread careful use of repurposed drugs that work?
Yeah, absolutely.
I don't see any other solution and if that's not going to happen, I can only advise people who are potentially vulnerable, we know Which part of the population we are talking about, as we were saying, regardless of age, regardless of age this time, to get access to antivirals, to protect themselves, right?
At an individual basis.
I don't have a very good feeling with this, because if this whole operation is not coordinated, because every individual will need to care for himself or herself, Then, I do not rule out that we may even start to face problems with these antiviral drugs in terms of resistance.
The higher concentration we were talking about has nothing to do with that, right?
But if now people are going to take this on an irregular basis, or they are just going to take it prophylactically, you know, we heard this also during the Congress, you know, I went to the workshop the first day, I don't know whether you attended this, where people were saying, oh, you can take this prophylactically, etc.
We know what happens if you know if people or if we administer to animals, you know prophylactically Antibiotics for example, I mean, it's some drugs Yeah, but yeah, so I'm not saying it's going to happen, but I don't have a good feeling It's saying, you know Everybody can get this over-the-counter or everybody should you should use this and and and you know You use it the way you think it's it's good for you, etc.
Well, this is a great reason not to have Sabotage the credibility of the entire medical establishment Simultaneously because what we really need is to have the doctors on board with a proper regulated campaign that uses these antivirals in the way that they should that will not exert This kind of selective pressure where suddenly we'll lose the few tools that actually work.
Yeah, right.
That would be a disaster All right.
Well, this has been a great discussion.
I really appreciate your having it with us, and I really appreciate that you are doing this work, because, you know, those of us who have been paying attention know that it has largely been a thankless task.
Nobody wants to hear what you're trying to tell them.
I know that.
Anyway, I appreciate that you're doing it, and at least know that there are some of us out there listening, and that we've gotten a lot from it.
Well that's what I appreciate also that you are doing is listening to it because you are you know one of the few people also is deeply involved in this and has of course the capacity on your background to grasp to a large extent you know the kind of elements that I'm bringing to the table because yeah it's of course Very important.
It would be an ideal situation if more and more scientists would, you know, try to understand and try to think about the consequences.
Because even if, you know, only part of what I'm saying would come out, it's still going to be catastrophic, right?
And and and if you know even a hypothesis that I think if you will read the manuscript I'm I'm really happy to hear you know any comments and and where you think that this is not well documented or or but I think I've put a lot of work in this to make this as scientific as possible And if that is indeed the case, I cannot understand that we can simply put this aside and say, yeah, you know, there is no risk.
Let's just continue, right?
I mean, that is that is just you can debate about certain elements and likelihoods.
But if a hypothesis is, I think, relatively well Documented and arguments are, you know, scientifically reasonable just to put everything aside and, you know, completely ignore this.
I mean, if you think about the consequences at the population level and at an individual level, right?
I mean, it's just unbelievable that Yeah, and that we would force, you know, whole populations to go through this kind of drama, right?
It's crazy.
I will actually go one step further than you here.
I'm often surprised at how important the philosophy of science is in understanding science itself, and in this case you What you've got is a past prediction that is highly accurate, right?
You predicted a pandemic of variance.
Everyone knows that we are now living a pandemic of variance.
So the point is, when somebody gets something like that right, then the answer is, what do they know that I don't know?
Yeah.
Right?
They should be coming to you now and saying, what did you know that we don't know?
Teach us that.
And to the extent that they're not, that is on them.
But somehow we got to get control of the system and we've got to restore reason to it because this is now a massive self-inflicted wound.
Yeah.
Yeah, absolutely.
Absolutely.
Yeah.
Well, as I was telling you, Britt, I mean, it makes me speechless.
And when I'm talking these things, you know, as a human being, I cannot believe that I'm telling this type of stuff.
But when I take a deep dive in the science, as I'm something, you know, I get immersed by and I say, well, this is so compelling.
You know, I miss sharing this with somebody at least, right?
So it's a very strange feeling, right?
Anyway.
Anyway, well, yeah, it's weird.
I don't believe in being called in the religious sense of the term, but there's some analog to it and I think you've been called and I appreciate that you're shouldering the burden.
