Geert_infectiousness.md 49 KB
Meeting of Giants
Ambiguity So there is, in my mind, there is still an unresolved question of whether, even with the additional jabs, we aren't seeing some vaccine enhanced replication, at aminimum.
Before you go on, I want to ask Geert, does that make sense that the vaccinated could in effect be superspreaders
Geert: So my understanding of this whole thing is the following. In countries where you have high vaccine coverage rates, like UK like Israel like US. You will see that there is some movement of waves around the plateau that is really very high. The average infection rate is high, if you compare these countries with other European countries, you will see that the plateau is much higher.
So we know the effect of mass-vaccination. That, indeed, in vaccinated people they exhert a lot of immune pressure on the virus. This is, in fact, an ideal breeding ground for more infectious variants. The more you vaccinate, the more you're going to see that you'll not succeed in bringing down the infectious pressure.
However, if you still have a substantial proportion of the population who is non-vaccinated, you will see that these people will of course get infected, but will happen is that, a lot of them still up until today, is not going to have any kind of the disease. They get infected, they will shed the virus for some time, but they will eliminate the virus.
So basically they're going to reduce infectious pressure. And those who get the disease will build life long, well at least long-lived immunity, and also contribute to diminishing infectious pressure. So that is important, you will see in those countries where there is still a substantial amount of non-vaccinated people who can get asymptomatically or symptomatically ill, they will contribute to diminishing the infectious pressure, and hence you will see that the average level in countries with relatively high vaccination rates is relatively high, but you will still see some substantial waves every time you get unvaccinated people get the disease will reduce the infectious pressure when they mount antibodies, and the more you vaccinate people, the more you're going to see that this will disappear.
So, in other words, what I'm expecting in Israel to see is that this movement will come down, will calm down, you will end up with this high plateau, a little bit of movement, still around it, and then what I expect is a huge wave.
In other countries, where there is much less vaccination, for example where there is still a substantial amount of non-vaccinated people. Again, the average level of infectious pressure is still way way above where we were a year ago, and you will still see movement, because there is still unvaccinated who can get a disease when they get infected, for example, asymptomatically, I call them the vacuum cleaners. They will eliminate a lot of virus from the population, those who get the symptoms, they will mount long-lived immunity, and also contribute to the reduction of the infectious pressure. So the wave will stop again, you will have diminished infectious pressure. But then there is still other non-vaccinated who can get disease, it will go up again. And the more you vaccinate people, the more you're going to see that the waves become smaller and smaller, but the average level of the infectious pressure will still be high, it will become as high, fo example in countries like Germany and my country, it will become as high as the countries that have now already high vaccine coverage rates like the US like the UK. And then we are just waiting for the huge wave.
And that is my prediction, and this is what I interpret when I see these data in Israel, where you see there is not big waves anymore, but the plateau is very very high, right? And what else do you expect, you have vaccinated almost all people, and we know that the vaccinated people are not going to contribute to the diminishment of the infectious pressure. The only people who can do this are the non-vaccinated. And the fewer unvaccinated, the less impact you have on the average infection rate. This is my prediction, people can follow this.
Malone:
Can I comment? I'm going to try to paraphrase what Geert just said in a real simple way.
The truth is that it's the vaccinated who are creating the risk, and not the unvaccinated. The unvaccinated are, like he said, serving as virus sinks for the most part, unless they are in those high risk groups.
The probability of them having significant diseaes and death is minute, particularly if one administers anti-inflammatory drugs early.
And the whole risk in this whole equation is not being generated by the unvaccinated that then develop broad-base natural immunity to multiple antigens and epitopes that's typically long-lived. It's the vaccinated that have received these very focused spike-vaccines that all have, basically, a common epitope structure, and are driving through selective pressure, evolution to escape those key epitopes that are present primarily on the receptor binding domain.
Geert, am I understanding you correctly?
Geert: Ya, there is one thing, Robert, and I'm sure you're getting this right, but I want to emphasize this because this is so important, again as I am saying all the time, we should not stigmatize people, we should not blame the vaccinees as individuals and, therefore, let's put up the slide.
It's not because someone is vaccinated and is exerting an immune pressure that this person is a problem. It becomes only a problem when everybody is in a similar situation because, then, you give the opportunity to that more infectious variant to really adapt to the population and to dominate.
So, again, this is the most important thing that I want to convey, it is not a problem of individuals being vaccinated. We know all, Robert, you confirmed this - what we should have been doing at the very beginning of this pandemic with the vaccines was to vaccinate the vulnerable people. A segment of the population. That wouldn't have done any harm in terms of evolutionary escape, etc.
So, the problem, are not the individuals who are vaccinated, the problem is the mass vaccination. To push a whole population to exert this widespread immune pressure. That is how, finally, the more infectious variant can adapt to the population and become dominant. And, of course, this population can no longer reduce infectious pressure.
The fact checkers are saying, you guys are talking nonsense because the vaccination is not driving mutations or mutants. Nobody ever said this. It's so important that we explain to people where the confusion comes from. There is no other way but with these slides to give a little bit of clarification on what exactly is the probelm.
Two individuals, one who is vaccinated, one who is not vaccinated. (or two groups)
You always have a proportion of mutants, more infectious variants for example, and you have, let's say, you take one variant and you have the originals.
Let's say we have 100 viral particles. The ratio is 80 wild virus and 20 variants.
It is a ratio of 1 : 5. 1 variant and 4 wuhan lineages. 1 in 5 for the variant.
So what happens when this innoculum will be put on a vaccinated person vs a non-vaccinated.
Well, the vaccinated, if he's vaccinated, will have antibodies against the spike protein. And, therefore, there will be a selection of this different viruses, because only the variants will pass through the small hole.
So that means, there is a resistance, which is a smaller hole of contractive opportunity, the smaller hole representing the immunity against the S spike protein. And if that resistance exists, then there is only those viruses that can overcome this resistance by passing through this small hole that will be selected.
So you can, for example, from 100 particles, through selection, reduce them to 10. You have a reduction of 10 times the total amount of viral particles.
As a matter of fact, this reduction ends up in 10 particles of the same nature. They are all infectious, more infectious variants, because these are the only ones who managed to pass through this small hole.
So now exactly the same situation with an unvaccinated person. So let's assume we have the same level of reduction from the 100 particles we are going to go down to 10 particles. Is that possible? Of course.
Because the unvaccinated people, let's not forget, they have immunity. This is the reason why when we got the Wuhan strain, the vast majority of the people were protected from innate immunity, so that is really a protection, it's not like the unvaccinated have no protection whatsoever, and this protection is conferred by immunity and more specifically by innate antibodies.
So you have a reduction, as well, from 1 to 10. let's say the same.
So what's the difference? Well the difference is that the innate antibodies they do not, they are not selective. They do not discrimintae against more infectious particles, original particles. They are non-selective, so they reduce the viral load, but they do it in the same way for the more infectious variants as for the original strains. So that means that, of this 100 particles are going to end up by a reduction of 10, but I'm going to have the same ratio, 1 to 4, that I had at the beginning, 1 variant for 4 original particles, so the 10 that I have here, there are 2 variants and 8 wild-type viruses.
So the end effect , I'm still having 10 infectious virus particles, but the difference is that in the individual who got vaccinated, I will have 10 particles of the same nature, all more infectious, whereas in the one who did not get vaccinated, and who did not put this immune-selection pressure on the virus, I have 10 particles, 2 of which are the variant, and 8 of which are the wild strain. Exactly the same ratio that I had at the beginning.
So, now, what does that mean? Immune selection, if there is only 1 individual in the whole population who does this, then there is no problem, because this variant will never ever be able to dominate in the population.
So the probelm is that if I am going to mass-vaccinate, then I do have a problem, and I am giving here the example of a population being 25% vaccinated.
So 25% means that 1 in 4 people will fit into this scenario with the smaller hole, and 75% will fit in the other scenario where the hole is much larger where there is no immune selection against the S-protein.
So you can see there is 25% with the smaller, and 75% with the larger hole.
So let's compare in a situation where we go to 75% vaccination. 3 out of 4 people are in the scenario where immune seleciton pressure is exerted against the S-protein, and only 1 in 4 fits into this scenario. So what is going to happen? If I know make the calculation, how many more infectious particles do I have in total?
SO here you will see that I have 1, 2, 3, 4 variants out of 7 in total. Whereas here, with the 75% vaccination rate, I have 1, 2, 3, 4 variants out of a total of 5 viruses. So you see the concentration effect that is taking place, 4 out 7, is like 60%. 4 out of 5 is 80%. So you can imagine the more I vaccinate, the more I will have this selection, and I will end up with basically with only more infectious variants.
When that happens, this selection, this reduction doesn't take place anymore. This selection doesn't take place anymore. Hre I had a reduction, why did I have a reduction? Because I had a selection factor against S. But if all of them are already more infectious, I'm not going to have a selection anymore, so I'm not going to reduce the infectious pressure anymore. This can be seen in the Israaeli curve, where the more you vaccinate, you have a higher plateau and you will not be able to bring it down anymore.
The interesting thing is that if you look at the non-vaccinated, you will have something which works the other way around. How do you go from 75 to 25? You have to bring in non-vaccinated people. The baby-boom does this. It's very interesting because in the UK, for example, the lockdown measures were lifted in July - what did we have? Well, people wwere again mixing, there was still a fair amount of non-vaccinated people, and people had close contact again. So you bring people again in contact with fully-vaccinated people, what will you have? You will have no selection,y ou have a dilution of the infectious pressure, because the competitive advantage that exists here, that the more infectious variant has, has a tremendous competitive advantage, will be weakened, mitigated when you have more non-vaccinated people, when you intensify these contacts. If everybody gets vaccinated, you won't have this anymore, and yo ucan see that in the infectious rate curve of the UK. Nobody could explain this, Boris Johnson was just gambling, he was trying something, why does he trying something? Because he was saying, well for teh first time in the pandemic we see a disconnect betwen the number of cases and teh number of deaths, so let's take advantage.
Let's lift the lockdwon measures? Within the next few weeks we saw quite a substantial decrease, because we had close contact between a number of non-vaccinated people, despite the fact that mass-vaccination continued during this time. These are the kind of examples that i'm trying to ask people to explain. Within 2 weeks, this has nothing to do with vaccination, this has to do with contacts with non-vaccinated, and I call tehm the vacuum cleaners, because they will reduce infectious pressure without putting pressure on the infectiousness of the viruses, because it's not selective, the innate antibodies will go after themore infecitous variants as the less infectious variants, the mechanism is completely difeen, it's through multivalent binding.
Robert Malone:
Hate the game, nto the player. It's not hte individual, it's th epolicy. If i'm understanding Geert correctly, the policy of universal mass-vaccination is the problem here. It's not targeting any individual because of what they have or have not elected to do. So, hwo do I explain it to the average person? The problem I have in the US is that a large fraction of the population is unfamiliar with Darwinian selection. That's the starting point, I can't really have a conversation about selective pressure with many people. So you have to have that kind of understanding before you can go further.
To explain what Geert has just shared - the nuance of how to relate the dilutive effect of the unvaccinated is new to me, so I thank him for sharing that and walking me through it, so now i have to think about how I can simplify that into a tweet nad walk people through this. I like teh idea, so basically what he's saying is that the unvaccinated serve as a dampening function, a sponge in the distribution of the virus mutants, and because they have a more diverse immune response, and so are not going to be selecting for a specific variant, that's the key in what he's saying in a metaphor of a thin channel, what he's realy focusing on is that it's not just an immune response, but a very selective immune respone that's going to result in a particula type of phenotypes that rae going to circumvent that. I
I'm often given the same challenge that he did, why isn't the unvaccinated the ones that are selecting for the mutants, and it's hard to express the idea that diversity of immune response in the diversity of each of us in terms of our MHC molecules, makes it so that I guess in his model, in the unaccinated population that hasn't been driven to this common endpoint, in terms of the education of their B and T respones, they have a wide diversity of how they are responding to the virus and so instead of really one narrow pore, he has a metaphor of a large pore, it has a lot of pores. The selection is on a lot of different proteins and a lot of different epitopes. So the virus doesn't converge, this mass vaccination will not be driving to a commonly adapted final endpoint, and this is what he's warning us about the explosion from.
Geert: Yes, of course
Robert: We are going to see convergent evolution towards a final endpoint.
Phillip: Based on the research that I've been doing as well is that one of the difficulties is that this virus is largely bening in the sense that if you get a nenonate and ge tthem infected with it, they don't get severe disease. So the question is, the huge problem is when someone gets infected is in the interferon response, and the virus is abl eto Block that. In someone who is vaccinated, what was interesting is that they finds that they produce a weak IgA respones. So they do produce some IgA against the virus, but not enough to stop the replication of the virus. Additionally, it's tuned to the original virus, and therefore you will only end up with replication of the virus that can evade that weak IgA response. An dso you are right, it does select, and this is what I found in a very interesting paper that was shared, in a prison population they had a huge uotbreak of COVID-19 when they were all vaccinated . And so it's as though they selected virus that could evade the antibodies and then you end up with a mutated virus that can infect everybody, the vaccinated and the unvaccinated.
Robert: Geert has made the point that under this scheme, using Marek's disease as a metaphor, and this is something that we had disagreed with previously, but im' coming to his point of view, the risk is nto only that we're generating escape mutants, but we're generating mutants that are more highly replication competent, more highly infectious, and potentially more pathogenic, this is his point that it's not just that we're culling the elders with the prior waves of infection in the migration of the virus to more pathogenicity in the younger cohorts, but that the fundamental biology of the virus and its replicative effect is shifting, and that's creating more risk in those younger cohorts?
Geert: Well my opinion is slightly different in the sense that we really need to distinguish between infectiousness and virulence. When we're talking here about immune selection pressure, very very clearly because these are S-based vaccines, and so the immune pressure is against of course the S protein, and the immune pressure is sub-optimal, because otherwise we could have really sterilizing immunity, which is certainly impossible if we vaccinate in the midst of ap andemic, so we put sub-optimal pressure on the spike protein, and the spike protein is responsible for the infectiousness. And so, again, we put sub-optimal immune pressure on viral infectiousness.
And so the question is what is the effect on virulence. I am not aware of any pressure that is exerted on the viral pathogenicity, the virulence, and if we would have seen such spectacular mutations it would have been published and shared. So far there is none of this. And so nobody can explain why is it that all of as udden that the younger age groups are getting disease and getting susceptible because the virulence is not changing. And then my explanation is that we do have, becuase of the circulation of more infectious strains, we do have, on average, and we see it on the curves again, on average we have higher infection rates, we have higher inectioun rates so the likelihood that somebody gets exposed shortly after the first infection becomes higher and higher, and so the likelihood that somebody becaomes exposed again to the virus just a few weeks after he or she has been exposed for the first tie becomes higher because of the high infectious pressure.
There are really interesting publications that show that people like youngsters young people who teh fifrst time were not showing any symptoms, that they develop S antibodies that are short-lived that do not induce B-cell memory, so they are not really primed, but these short-lived antibodies are still capable of binding to the virus, without necessarily neutralizing it, and they prevent the innate antibodies that have much less affinity, they prevent them from binding, so they suppress, in fact, the innate immunity, and that is the reason why young people are now getting the disease, and as a matter of fact, pretty fast. So it's not a matter of the virulence, it's a matter of the increased infectious pressure that increases the likelihood for somebody who got infected to become re-infected within a short time frame after this first infection, whie still sitting on short-lived antibodies that are not sufficient to really neutralize, but that can suppress the innate antibodies, and that they do not neutralize, why - it's very clear. These asymptomatically people have already eliminated the virus before the short-lived antibodies start to peak.
So the short-lived antibodies have no function at all in the elimination of the virus. This is completely, so why are they there? I mean, when such things happen, we can not afford to leave any stone unturned, and this is a very interesting trick of the virus, becaues in doing this it can take another part out of this reservoir, out of this young people you will see the more this virus becomes infectious, the more we will go down with the age groups that become susceptible. That is my fear, the more we vaccinate, the higher the infectiousness of the dominantly circulating virus, and the more we will go down in the age groups that will become susceptible to the virus.
So it's not a matter of intrinsic virulance mutations, it's really a matter again of the high infectious pressure that is built up because of adaptation of more infectious immune-selected variants, thanks to mass-vaccination.
Philip: Can I point out something that I think is important when we think about how the viru sworks. With children, one of the issues that I've been having is that we've stopped doing autopsies, we've stopped studying the details. And when yuo have a virus, the delta variant is producing I think 1000 times more viral particles. The question is simple - are we dealing with a cytokine storm, or are we dealing with a viral pneumonia? And you can't know unless you're doing autopsies because that would explain why the younger age groups are being infected now - they are now having a viral pneumonia, where there's lots of virus all over the lungs and they're getting sick with it, as opposed to the original problem with COVID-19 which was a cytokine storm. ANd we seem to be missing, doing these critical things. I just want to ask Robert about his thoughts on ADE - any thoughts with regards, what would you say about that?
Robert:
So, from my standpoint you just jumped from one topic to another. You were talking about the viral replication, the viral pathology, intrinsic viral pathology, and then bridging that to the cytokine storm viral pathology, and then you introduced the thread of antibody enhancement.
I caution with the primary viral infection, the virenia phase, your language suggested that you were focused mainly on the pulmonary tract, and so just to hammer the point home, this thing goes everywhere. I have friends that are primate virologists that have been doing detailed autopsies, and they're seeing that this pathogen is infecting virtually all tissues, including reproductive tissues at very high levels and also, by the way, setting up chronic infection in the gut. So I just caution focusing too much on the respiratory tract, when we seem to have spike-mediated effects on coagulation, on endothelial damage, on renal disease, on lung yes, but on a variety of other tissues, including teh reproductive tract, and if we're having higher viral loads because we have selected mutations that enable high levels of virenia, it totally makes sense to me that we'll see more of a primray viral pathology in all these tissues.
In terms of the cytokine storm, the cytokine storm thesis seems to be less of an issue except in those who have the preexisting conditions. It's like they don't move into that second phase, we clearly have a 2-phase disease, and that second phase that I'm told with delta instead of starting at about day 7, it's more pushed up to about day 5 when it does occur. And I'm perplexed as to why the vaccine should be dampening that. The phenotype that there's less severe disease and death associated with the vaccinated because that for me is troubling how to makae sense of that because what's killing us is that hyper inflammatory response.
So why an antigenic specific vaccine would be dampening the reactive hyper-inflammatory response in patients that have just as much viral load, if not higher, doesn't make sense to me- I'm looking forward to reading that manuscript in an upcoming issue of cell, I'm sure, but I haven't seen that yet.
Then the Antibody Dependent Enhancement - so I got the FDA specifically called out antibody-dependent-enhacnement in its various communications as a risk that was uncharacterized and unknown still at the time that they issued the emergency use authorization. It still remains unresolved, to what extent it occurs, Geert will probably tell you and I can share with you that in the case of, say Dengue virus, which is the classic example of ADE, one has the greatest risk during the waning phase of the immune response, because the slop, there's a more protracted duration in which you move through the threshold where you have enough antibody around that it's binding the virus, but it's not blocking its ability to infect.
So it's that waning phase window which seems to be the setup for ADE. Here's the rub, and this has been pointed out to me multiple times by others - is that, even though the FDA has used the term in all the prior literature on corona vaccine development used the term ADE as the risk - in fact, this virus is not replicating in macrophage and monocytes, so that data is not there. And so, for the purist, antibody dependent enhancement ADE is defined as facilitation of uptake through FC receptors into monocyte derived populations like macrophages, and so you get this explosive replication in cells that otherwise don't have the right receptor, and so they say "you can't call this ADE, robert, you've been fact checked you're wrong".
And so I think that's a bit of nomenclature thing, tomato tomato - I prefer to use the term vaccine-enhanced infection, replication or disease. Because it's a broader category, ADE is a subset, so how might we be having vaccine-enhanced infection or replication? If the antibodies that are being generated are able to bridge and enable use of receptor pathways that aren't being used - notivce I'm saying the same thing, but with different words, the presumption is that ADE has to occur through FC receptors - well FC receptors aren't the only way to pick the lot to get into a cell - there are other antigens and receptors and so the idea is that potentially vaccine-induced antibody responses may be enabling viral infection through alternative receptor pathways than is happening otherwise.
So they key question in my mind is people are saying "well, we're not seeing enhanced disease post-vaccination, we're seeing attenuated disease" I'm saying yeah, btu the disease in the inflammatory response to the virenia it's not the virenia itself, generally speaking, that's what we justestablished earlier when you were talking about the inflammatory phase. So then in my mind the phenotype that we need to watch for is the enhanced loads - viral titer loads, because that would be the true sign of a vaccine-induced enhancement - because that's thte kind of proximal things that we could look at - now, do we have decent tools for lookign at viral loads? Well, if we look ourselves in the face, the answer is no. As Kary Mullis, prior to his untimely death liked to point out - PCR is not a quantitative asset. And so we're not having people do classical virology, like Geert and his veterinary colleagues do - where you're actually looking at virus titers, and you're culturing them in cells and micro-titer plates.
We're relying on the surrogate assays of what is the cycle number as an indirect measure of viral load. So if you were able to detect the virus after a much lower numbe rof PCR cycles, that suggests that there's more nucleic acid there and so we use that as a crude surrogate for viral load. So the problem, in my mind, is that we're not asking ourselves the question and we haven't really taken up the task of looking at it rigorously. A skeptic could say that we're avoiding the question studiously, but that's why I'm very eager to see from my Israeli colleagues data, even if it's PCR threshold number, where they parse by weeks post-vaccination or months post-vaccination so that we could see what are the relative viral loads in the infected vaccinated at, say, 3 months when you have peak, or even 3 months, vs 6 to 8 months. And look at load then, and I think that would b the indicator of whether or not we're having vaccine-enhanced replication, but right now, I don't have those data, I haven't seen it, and I've asked for it and I think the problem is that there's just a lot of disincentives to asking those kinds of questions, no one wants to fund them, and so we're in a world where it's knowable but unknown. And so that's my sense of the whole vaccine-enhanced replication disease ADE spectrum of things.
Philip: And so it brings us to a very important phase of our discussion. You guys understand how the regulators think and you've interacted with them at different levels. What will they be thinking now, and if you were in the room with them, what would you be saying to them? I will start with probably Geert.
Geert: Well, what I would be saying is that what I'm trying to do since the beginning of this year is trying to explain what the impact is of mass-vaccination and making it clear to them, because I think that even the regulators, the regulators are used to looking at vaccines that have been tested in clinical trials, in a very well-defined environment, where you don't have what we see now during the pandemic, what we see is that you start vaccinating lots and lots of people, you start developing a kind of dynamic of population-level immunity. And that dynamic, that changes of course, the more you vaccinate people, that dynamic has repurcussions on the evolutionary dynamics of the virus. And those influences and interactions are having an impact on the effectiveness of the vaccines, etc. I've been seeing this thing evolving, right?
This is something these guys, in fact, have no experience with. That is not what you typically see during a clear well-defined clinical trial where almost everything is standardized. So they are trying to deal with this like with any other vaccine that has been tested in efficacy trials, and we already see all the difference - my goodness that we see in terms of effectiveness, in terms of safety, in terms of the dynamics that are evolving as well in terms of immunity in terms of viral infectiousness, and that is something that is completely absent in their reasoning, and so I think that is why they are completely puzzled and I think there is a huge need for them to learn, really to learn, but it's very difficult if you are a regulatory authority to say "well guys, but we first have to dive in our books and in a number of publications and listen to a number of experts who can explain those dynamics before we can reasonably make an assessment of those dossiers". And I think one of those regulators, I happen to know one of those regulators who left FDA. And I think this si kind of like, this uncertainty and anxiousness of not knowing and not understanding what is going to happen.
Because if you understand these things, you can act in good faith and you know these are the risks an these are the disadvantages. But if the beast is unknown and you do something at such a large scale, authorization at the large scale, and you go into children - something we rarely do right away with vaccines - then it becomes really something tha tlooks very scary to people. And I think, personally, you're going ot see other folks leaving, that's waht I think.
Philip: And your thoughts Robert, what would they be thinking, what would you be thinking and doing?
Robert:
And so I feel the need to parse your question once again, and forgive me for that, I guess I'm being a reductionist now.
I personally feel tha tgeert is giving the benefit of the doubt too much. An dI can't speak for the european medicines agency, or the individual regulatory authorities in Europe and how they think - I can speak to what I see in the United States. Your question infers that, if you're talking about regulatory authorities I ifner that you're talking about FDA.
FDA operates based on checklist. And they are kind of rigid in that way. It's like a punch list, like you're going to go shopping and you have to ge tthis thing and the other thing and they all have to be done. The list that your spouse gives you on the weekend of chores. So that's how the FDA approaches that - they're not a whole lot of thinking. They don' tset policy. So your question is really a kind of policy question, but it presumes that policy decisions are happening at the FDA level - they're not. At the FDA they're looking at a dossier and saying "does this meet our predefined criteria, if so, then yes".
Now, one of the things about that in that regulatory space is they're looking at potency,efficacy or effectiveness, safety, purity and adulteration. That's kind of the main checklist that they're looking for. And so they are hobbled, right now, and they admit it in the BioNTech licensure letter, in that they flat out at the FDA state that the existing database structure that exists in the United states - so that's VAERS, VSAFE and the databases from medicare medicaid and VA and army medical system etc. They're not sufficient, they're not structured in a way and they're not sufficient to allow them to detect rare adverse events. And so they have directed BioNTech that they have to perform more rigorous studies to evaluate the safety signal.
So the FDA is admitting that they can't evaluate the safety very well. And, yet, they are still moving forward with market authorization - why are they doing that? Why did we see two of the top regulators in the vaccine branch resign, over the issue of the third job? The boosters?
The reason is because the FDA is no longer independent from the policy-making apparatus which exists in their executive branch.
So it's the White House that's setting the policy, which is to say that because Tony Fauci is appointed basically the czar of this disease, it mostly comes down to Dr. Fauci's personal perspective.
And then you float, and you just saw a great example of this kind of process flow with this decision about the third jab, the booster experience, in the United States, we had the independent academic reviewers looking at the data on behalf of the FDA, this is the verbac panel - and they made a clear unambiguous decision that despite the lack of sufficient data to make a Go decision, in terms of safety an efficacy in the elderly and high-risk populations, they were going to go ahead and authorize that because the risk to those populations was already sufficiently well-documented because of the Israeli data na some American data showing that the vaccine durability was so poor. And so these people are now at higher risk and they were already at higher risk and now their vaccine protectio nis dropping. And so they're saying, in teh balance we should go ahead with that.
But then you had the director of the FDA, Janet Woodcock step in and say "Well that's all fine and dandy, but I'm going to add in another group which is basically - we think that anybody that has contact with the public, so this is nurses health care personnel all the way down to grocery clerks - are at significantly enhanced risk of severe disease and death" There's actually no data supporting that. If you're 55 or 45 or whatever, that's your risk stratification - there aren't data saying tha if you're a grocery clerk, you have a much higher probability of death and hospitalization if you're 25 than someone who isn't a grocery clerk. So they made that political decision because they watn to impose universal mandates.
And so this gets tossed to the CDC, to show you how the US works - it gets tossed to the CDC. And the CDC independent panel, called the ACIP, evaluated the same data and said no we reject this added 3rd group taht the director of the FDa has added in. That's all those with public contact. Wt reject that logic, there's no data to support that assertion, and we just think you should go ahead with the same recommendation that the verbac gave. And then we had, within 2 days, the director of the CDC overruled that, and went back to the same policy that Janet Woodcock of the FDA had rolled out, which is basically coming from Tony Fauci, as I explained. And so that's how things rae working here. There are other wrinkles to this.
We are at a situation where we are operating in a way that is independent of science - the science no longe rmatters, really. It's public policy by FIAT. And, int he case of the CDC in particular, I think it's important to understand that CDC is a classic case of aregulatory group in a sense, tehy're not really regulatory - they're policy advisory -a dn they have authority to purchase vaccine, that's part of why they do this. So they set standards for care in the UNited States, or they attempt to establish standard of care. And it's important to understand about hte CDC that they have a dual function. They are specifically tasked with vaccine efficacy. They get a large amount of money to promote vaccination, yet they also have an internal mandate to ensure vaccine safety and regulate vaccine safety - these two things are in conflict - I think that's self evident - there's an intrinsic conflict of interest within the CDC in that it is funded largely to promote vaccines, but it has also the underfunded mission of evalutaing their safety.
So that's the situation int he states, so ynow I've parse that part out. Given this question, assume Biden calls you up that's not going to happen - an dsays, dear Robert, what shoudl we do? We have a problem? Red lights are flashing? I'm so concerned about what you're saying on Twitter.
That hypothetical was presented to me and Peter Navarro - and so we did come up with a set of policy statemnets and publish them in the washington times and they amount to 4 key policy items, and they're very very informed by Geert's thinking. Frankly, when I finally got my head wrapped around what Geert has been trying to teach us, I realized that we had a big probelm and we had to change course.
So what I advocated and I advocated by the way with Cardinal Turkson at the vatican 2 weeks ago, I was granted an audience. I've advocated in Portugal, I've advocated in Italy and I"ve advocated here in the UNited States through those op-eds with Peter Navarro - is a 4-point strategy.
Reserve the vaccines for the elders and the morbidly obese and the high risk population, and make it available globally. Right now we're overusing vaccine in the WEstern World - we're basically beign vaccine pigs, but we are hording the resources in the West unnecessarily. As Geert has kindly taught us, we're actually doing damage through our policy of overusing vaccines in the west, and meanwhile vaccines are not being made available in populations in less economically advantaged countries that don't have the ccapital to buy - it's not just buyiing the freezers, it' sthe cold chain is enormously expensive and difficult. And it's the elders in those countries that represent the memory - the wisdom and knowledge of each of those countries' villages and townships etc. And, it's a huge crime that we're not providing vaccine coverage for thos epeople who need it just as much as the elders do in the EU and the US and Israel, for example. So, spread it out, use it where it's really needed, don' thorde it or use it as an economic weapon.
Make early interventions widely available. The agents that are out there, including the monoclonal antibodies, are very effective when adminstered early and aggressively. A number of those agents are considered controversial and yet they are beign used widely often in emergeing economies tha tare having better outcomes in terms of morbidity and mortality than we are in the west, certainly where we arein the US. THe most recent example of Uttar Pradesh with their wide use of Ivermectin in India and suddenly collapsing the incidence rate of death and disease from COVID. We saw from before some fantastic examples in Peru, and that as kind of a challenge re-challenge experiment, where they deployed ivermectin and then they changed policy and didn't deploy it, and the morbidity and mortality shot up. We have a number of agents, not the least of which is Vitamin D which makes a big difference in the morbidity and mortality, os make those available early.
I believe that rapid test kits that are biased towards false-positives, because any test will have a bias - an dso acknowledging that home test kits be made available that have a bias towards false-positives, because there has to be a bias one way or the other. And then, available, more specific tests in physicians' offices - so people have a good idea that they don't have respiratory syncitial virus, like whta was ripping up the pediatric population this year an deverybody thought it was SARS-CoV2 it was RSV.
I really think that we need to address the fear. There has been too much fear promoted, and Geert has pointed out your risk currently with the current circulating strains, if you're not in one of those high-risk groups, you're not one of the elderly, is a fraction of a fraction of a percent. That you would get death or severe disease from this virus, inf act what you will get for most of us is broad-based long lasting immunity, as Geert has kindly shared with us. So, we don't have to be afraid and I think that we can address the fear using apps or other computational tools that allow you to make an assessment of what your own risk is.
So those are the four policy points that peter navarro and I had come up with. And of course after we published it in the Washington Times so that everyone in DC would be able to read it, we got nothing but fact-checked from Facebook, but other than that virtually no responses. So I don't know what to say, I'm trying to influence policy, but I feel like it' sa labour of sisyphus.
Philip: Anything to add, Geert?
Well, for me I think that the most important thing to do, if tehre is one thing that I really need to point out, it's to reduce this infectious pressure. And that is, for me, something nobody has any kind of idea how we are going to get rid of this highly infectious variants, and they are not going to calm down spontaneously. It's not like this virus is going to say Enough is Enough, I am going to insert a number of mutations that will diminish my infectiousness. And, as I was saying, for me this is really a huge threat to those who were previously naturally protected, we have seen young people all these younger age groups, below 65 etc, having almost no problem whatsoever when the pandemic started, and now we see increasingly younger age groups that get the disease. For me this is clearly due to the high infectious pressure as I already explained, so how can we reduce it? Well, first of all, we have to stop this mass vaccination - the worst thing ever. The worst thing ever that we do is to vaccinate younger age groups. As I tried to explain, this is the buffer. The younger age groups, you bring them in, for example, the unvaccinated, you are going to see a diminishment in the infectious pressure. They are the vacuum cleaners. ANd even if they get the disease, most of them resist relatively well to severe disease because of their younger age, because of their stil fairly-high rate of innate antibodies. Vaccinologists know very little about innate antibodies. Go on my website and look at the publications, it' svery fascinating.
So if they start vaccinating these people, they lose this potential. When people get vaccinated, they are going to breed, in fact, those more infectious strains, and through immune selection pressure, there is no longer this elimination. We lose, completely, this buffer. The people get the disease, they build long-lived immunity, so this is really our hope for herd immunity. Nobody talks anymore about herd immunity, what is the objective still of the mass vaccination campaign? Can anybody tell me the objective? If tehre is no objectivity, there is no strategy, of course. There is only tactics. There is no common objective, and every country is doing its own thing, so this is really a disaster, because the only way to solve this, still, we don't change biology - we don't change immunology. It's still the interplay between the virus and the immune system, it's still herd immunity, so where are we going to get herd immunity from? Certainly not from vaccination, and even less when we do mass vaccination.
So if we could reduce this infectious pressure, we could say back to the younger age groups, go out and do your thing. Because this goes back to the beginning of the pandemic where we had the wuhan strain with a much lower intrinsic infectiousness, and nothing was happening with these age groups. There's always people who have an innate immune defect, etc, but we didn't see these incidences now higher rates of morbidity in younger age groups. So we need to bring donw the mass vaccination, of course, because we are just turning all this potential to build herd immunity, we are just converting this into the opposite. People who cannot contribute anymore to herd immunity, and it's not really only from a public health standpoint, but it's also from an individual health viewpoint, because this thing is evolving and I pointed this out in a number of articles that I have posted. It's not me saying that there is now high pressure from the population in driving mutants that escape neutralizing S-based antibodies. These are molecular epidemiologists who are describing this, of course they're not saying that this from mass-vaccination the mmune pressure, btu they are clearly point out that there is a fast mounting immune pressure and that drives, increasingly, mutations that are escaping from neutralizing antibodies. So this is evolving, so that means that we know one day that some of these resistant variants are circulating, it's just that they have not necessarily become the more dominant strain, or the more infectious ones, but that is what we're going to end up with. Let's not be naive with resistance, right?
And also, from an individual viewpoint, you can be happy that today you are still protected. But don't we ask ourselves the question how long is this protection going to last? How about 3 months from now? Where is this limitation, we know already that this protection is limited, and we hav already seen how it has been evolving, initially there was an impact on transmission, certainly, and then in fact it was lost but then there was still an impact on disease, prevention of disease, now it's only severe disease. So all this rhetoric and the narrative that is changing about the claims of the vaccine is merely reflecting the evolutionary dynamics of the virus during this pandemic, so we need to bring down this infectious pressure and the only way it can be done, if you would like to Ivermectin or not, frankly speaking, I don't care, but we can only do this with antiviral prophylaxis. How else are you going to do this?
And stoppping of course, mass vaccination, and what I would say that is very important as well, according to my humble opinion and humble interpretation of the data we also need to avoid overcrowding. Personally, I think that infectious strains have started circulating in the population even long before mass-vaccination had started, was due to a large extent in certain ideas to realy overcrowding. Because when you have overcrowding you have high infectious pressure, of course that's almost by definition. So the likelihood that somebod who gets asymptomatically infected gets reinfected during the time where he or she is still sitting on antibodies is very very high.
So what does that mean? Immune pressure of course. Immune pressure on S-protein, so higher infectiousness, right? So that is something hygiene but essentially overcrowding, stopping mass-vaccination, and dramatically reducing this infectious pressure. And we can not do this with the vaccines, in all the countries where we have this high vaccination rate, that is where we have high infection rates. For me this is a complete no-brainer. This is simply common sense and it could be done. it could be done. But if we continue the mass vaccination, nature will win. We will end this with herd immunity, but we will pay a huge price, of course.
And what I don't understand, Philip, is that initially I have been begging to compare the ratio of mutants shed by vacinees, vs the original strains. To see whether there was a shift towards more mutants shed by vacinees compared to non-vaccinees. Btu then all of a sudden they said well if you're vaccinated, we don't do the sequencing anymore, we close this chapter, we dion' do this anymore. So that was not a criterium
Now my next criterium for demonstrating the detrimental impact of continuing these mass-vaccines, would be to compare the ratio of severe disease and death