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Geert Vanden Bossche and Dr. Robert Malone MD on COVID vaccines, risks, and policies (Transcript/Video)

The following is a transcript (auto-generated) of a meeting between Dr. Robert Malone and Geert Vanden Bossche.

Speaker1: [00:01:35] Hello and thank you for joining us today. It is a tremendous pleasure and privilege for me to have the opportunity to speak with two giants today, two giants of COVID 19 who have been sharing their thoughts and their expertise over the past many months. Now I have to say that it’s tremendous because one I was the first to interview Gert. This was all the way back in March. And also the first to interview Robert Malone, the inventor of mRNA technology. And now I’m also the first to have both of them there with me to discuss. So here we have Gert and Robert. How are you guys doing today?

Speaker2: [00:02:23] Well, we are fine, I guess, but very worried still. But thank you. Thanks for having us, Philip, and organizing this opportunity together with with Robert. Thanks.

Speaker1: [00:02:36] Wonderful, wonderful. I’ll start off since you talking then Gerhardt, I’ll just ask you to do a quick introduction of yourself.

Speaker2: [00:02:45] Well, yeah, as people know, my background is, in fact veterinary medicine, but I worked for many years in the human vaccine industry as well in the for profit as in the nonprofit Bill and Melinda Gates Foundation and Gavi, and took it a long story short. I consider myself as a problem solver. So what I like to do is to put pieces of the puzzle together to unravel very complex, complex phenomena. I think one example here is, of course, the COVID 19 pandemic, where we are drawing from several different fields immunology, virology, vaccinology, evolutionary biology, even biophysics. And that is what I’m really interested in, and that is really what I have been doing with regard to this pandemic since, well, since the beginning of this year or so.

Speaker1: [00:03:47] What allows Robert, if you can do a quick introduction of yourself?

Speaker3: [00:03:53] I’m Robert Malone. I’m a physician and scientist, I’m licensed to practice in the state of Maryland. I’ve been developing vaccines and and developing countermeasures for outbreaks in bio defense purposes for my entire career. About 30 years. And in the case of this outbreak, since January 4th, I’ve been focusing on developing repurposed drugs and also developing a novel vaccine together with my colleagues in India at Reliance Health Health Group. And that’s a more traditional vaccine that is protein subunit based. When I was a young man working at the Salk Institute in the Molecular Virology and Biology Laboratories of India, Verma and others at the Salk, I had a series of discoveries between nineteen eighty seven and nineteen eighty nine that gave rise to initially nine patents that covered the landscape of what we now call mRNA and DNA vaccines. Many of some of those were initially filed from the Salk and then subsequently from a company that I joined called vehicle. So when I say that I’m the inventor, original inventor of the technology, it I’m not the inventor of these vaccines for COVID 19 and SARS-CoV-2. Rather, I invented the technology platforms back in eighty seven and through eighty nine when I was a young graduate student. So, yeah,

Speaker1: [00:05:35] Yeah, I was going to lead straight into that because I thought to myself that we’re on the brink of a transition with medicine. And quite truthfully, I think a lot of that has to do with the technology to do with Miranda. And I just wanted to play a short clip with regard to some of the the work that had been done previously. And I just wanted to know your thoughts, what you would feel in terms of being so influential in the field and seeing the potential of what’s going to happen. So I’ll just play this short one minute and a half here.

Speaker4: [00:06:18] We started working on RNA to try and understand why it was so inflammatory. We were both completely open minded. Any data that we didn’t understand and there was a lot of it. We sat down. We kept doing experiments. We kept getting results. We kept getting excited by the results.

Speaker5: [00:06:39] Middle of the night submitting grants and 2:00 3:00 in the morning, sending each other and you’re, oh, you are still up. And here I am, still up.

Speaker4: [00:06:49] We couldn’t have come to the result without both of us being involved.

Speaker5: [00:06:55] I was making the RNA and Drew was checking whether it is immunogenic, not immunogenic. Then he goes to data and we need we leaned over and we try to understand and make sense of it.

Speaker4: [00:07:15] Finally, we figured out how to make it non

Speaker5: [00:07:17] Inflammatory, and then our mind was all over the place.

Speaker4: [00:07:21] Let’s go in in every direction in a year and in the future.

Speaker5: [00:07:25] We just were amazed that, oh my god, this is what it means.

Speaker4: [00:07:29] And after that is when the vaccine field and other RNA fields took off.

Speaker5: [00:07:38] It was very enjoyable to be a scientist. It’s a joy.

Speaker1: [00:07:53] Yes, so thanks, Robert, I just I just saw that, and I think the reason that I’ve brought that up is because I think that the R&D technology is the breakthrough that is potentially going to transform a lot of medicine in the next few decades. And it worries me that sometimes with what is happening in terms of the controversies about vaccines that we forget how remarkable this technology is. What are your thoughts?

Speaker3: [00:08:30] So the the idea of using Yemen is a drug that that intellectual space is now enabled by certainly the improvements of Kariko and Weissman, in particular, the work of Peter Cullis and his various team members in terms of modifying the Kelenic lipid structure that we were originally using back in the eighties. But the in terms of the broad impact, what we really have is is a new form of pharmaceutical. It’s it’s opens up the opportunity to use this poly nucleotide mRNA for a wide variety of applications. And what’s lovely about it is that normally with the development of a biologic pharmaceutical, one extensive process development, manufacturing optimization, et cetera, that has to go into that development of that product. For instance, if it’s protein based and antibody or anything else, and with the mRNA platform, you basically have the same formulation within general parameters of poly nucleotide size. So you don’t have to redo all that stuff. It’s straightforward. All you have to do is change the sequence. And so what this opens up is the prospect of much more rapid conversion from a recognition of an opportunity, a new biologic pathway or whatever into a product without having to do all of the extensive manufacturing, process, development, characterization, release, etc..

Speaker3: [00:10:16] You can use one set of of of optimized conditions and formulation conditions in manufacturing and release. So what it translates to is is an opportunity to produce things much more rapidly and more reproducibly, and potentially also to enable their manufacture in a variety of environmental conditions. Different countries on a on a much more limited scale, you don’t have to have a huge manufacturing process. And I once worked at a company called Solvay just to give an example that invested a huge amount of money in developing a cell based flu vaccine. So you’d think that’s pretty simple. It was a many, many multimillion dollar plant to to do this manufacturing production, and it was only dedicated to that one product that flu vaccine, which failed in the end and the company lost that huge investment in that manufacturing facility. Now with this platform, we have the chance to have something that can easily be deployed in in environments, in developing nations in a decentralized way with a much more rapid turnaround between concept and end product.

Speaker1: [00:11:36] Wonderful. So that’s that’s tremendous. Actually said something there that I never even realized that both of you had interacted in the past at some point developing vaccines. So I can safely say, then does it? Are you guys, I assume, are not feeling proud that you are almost heroes to anti-vaxxers? How does that make you feel?

Speaker2: [00:12:02] Yeah, well, I mean, for me, this this is not this is not an issue. I think we have no longer the luxury of discriminating between all kinds of different groups. I think I’m making my ideas very, very clear. I’m not stigmatizing people. If there is somebody who is fundamentally against vaccines, he’s open to my reasoning to what I’m saying. I mean, this is this is not the way I’m all the time advocating for solidarity. The only way we are going to get out of this crisis is put our heads together and to overcome this kind of shortsightedness where, how or how, who is belonging to which camp. I mean, I don’t care. We shouldn’t be doing that. I am so sick of all this discrimination and stigma stigmatizing people. I mean, it doesn’t help us at all. So I’m not having a problem at this point with anti-vaxxers. I know people don’t consider me as an anti-vaxxer. I know that some anti-vaxxers highly appreciate me and other people who are trying to, who are driven by by a passion for the truth and finding out how we can solve this problem. So it’s about people, really. I mean, it’s not about certain groups that are putting forward certain ideas and or pretty extreme. And I think many anti-vaxxers have also learned a lot since we have been sharing a number of our insights. So, yeah, so it’s like

Speaker3: [00:13:54] If I could chime in on this, Philip. Sure. Go ahead, Rob. So I share your perspective, particularly the the wish that we didn’t find ourselves separating into these antagonistic groups. I think it’s highly counterproductive. Personally, I find the term anti-vaxxer pejorative. It’s a very simple label that the media likes to use to discount people. It’s it’s grossly oversimplifies what’s a complex landscape. Yeah, Deborah just posts pro-choice, not anti-vax. That I think that this term is is a derisive pejorative that is applied and it’s part of a. Some types of conversation. That’s that’s the thing that I found most troublesome about this whole environment. We’re Gerda and I are trying to talk science. We’re trying to make sense out of a very complex landscape in terms of the viral evolution and and the interaction of that with vaccines and with vaccine policy. And the press always loves to label things and to separate everybody into opposing camps and set us off against each other. I guess because it it promotes clicks and sells whatever it is that they’re selling, but it doesn’t make for good science.

Speaker3: [00:15:23] And then then they introduce these terms like anti-vaxxer and try to. Yes, exactly, Maria. They try to put us in a box to suit their narrative, and they reinforce it through a variety of of interesting tools like these fact checkers. But it’s A. And using these terms is destructive. It it destroys our ability to communicate complex ideas and to try to resolve them in in a scientific fashion, which requires, as you know, Philip requires that we be allowed to have open and constructive dialogue. So I just want to get that in about this whole pigeonholing of people as anti-vaxxers. I, I work with some of the people that are have been labeled anti-vaxxer have been named on the Dirty Dozen list by the president of the United States. I find them very reasonable, intelligent people that are trying to make sense out of complex information, just the same as the rest of us are. So in in some. I’m not. I’m not asking you, Philip, but I really wish we could stop using this term. I think it is counterproductive.

Speaker1: [00:16:39] Absolutely. I use the term specifically because there is so much confusion, and this is the perception that is being put across in the media that when you question the narrative, it means that you’re against vaccines. And it’s very, very important for us all to realize that science is science. It doesn’t really matter opinions. We’re just trying to get to what the bottom of the science is. And so with that in mind, I wanted to go back to Gert and I remember speaking to you in March, and at that time you were very concerned about the mass vaccinations. Before we go into you explaining some of the concepts, I just wanted to feel out what you thought about where we are now. Is it what you expected?

Speaker2: [00:17:34] Yeah, well, honestly, yes, it’s what I expected, of course, it’s always very, very difficult to predict exactly when what is going to happen, but that we would have massive surges of the infection rates, especially especially in the in those countries that had a very aggressive mass vaccination strategy, like in Israel, like in the UK, like in the United States, et cetera. So I think we are seeing this already. But unfortunately, I must say that for me, according to my insights and my predictions, this is not at all the end and that what I predicted a huge surge when the vaccine or the virus would become really more resistant to the vaccines. I’m afraid that this is still something we have not seen yet in a very pronounced way. We are seeing essentially the consequences of the virus becoming more infectious. We still have a kind of disconnect between the mutations that enable virus to escape from neutralizing antibodies and the mutations that enable the virus to become more infectious. So we we see that increasingly in strains that are already dominant, like the delta and more infectious. We see increasingly a number of mutations taking place that also enable escape from neutralizing neutralizing antibodies.

Speaker2: [00:19:22] And that is really this was the prediction. The worst case that I’m really afraid is still to come unless I insist because I don’t want to be fear mongering or whatever unless we we intervene, and that is something we can discuss later on. But yes, I think the that we would drive the virus more infectious or propagation of more infectious strains or more infectious variants. I think that has clearly happened and is still going on. And every second day we are dealing with new variants, of course, those that are most infectious right now, the Delta are still still dominant. But and also that I think I also predicted that first we would it would primarily affect the vulnerable people, the elderly, but then the virus would come back and hit also increasingly younger age groups, which is what we are seeing right now. So it’s, I think, pretty much in line with indeed what I predicted, as I was saying, it’s difficult to say this is going to happen the next month or before the end of the year. But all in all, it’s yeah, this is the picture that I was expecting.

Speaker1: [00:20:44] So, Robert, when when you look at this in Israel and I’ve picked a six month timeline, and if you can see in the in the middle here, this is probably where we thought everything was one. And there were some days where there were no severe patients, no deaths. And suddenly you see this. We’ve had three million booster doses given in Israel and you have a flattening, but it hasn’t disappeared. Any thoughts? Robert, as to what is happening here?

Speaker3: [00:21:18] So that that is Israeli data is fascinating, but it needs to be reviewed and considered carefully, there are some confounding variables within that. One of them that is often not recognized is that we think of the Israeli population is fairly uniform in their vaccine uptake, but that’s not true. Uh, there is the fundamentalist religious community, which is generally skewed older and which is very vaccine gently put, hesitant resistant might be a better term. And so we have, yes, very high vaccine uptake. But then we have these populations within buried within that larger population that are older and relatively unvaccinated. So when we see these presentations of the incidence rate, morbidity and mortality in the vaccinated versus the unvaccinated cohorts in Israel, we have to be cautious in that comparison because in general, the vaccinated cohort skew younger and and the unvaccinated cohorts skew older. And within this religious community environment, that is very close. So virus can spread well. But there’s no question that the Israeli data, I think, are not only concerning to me, I think they’re highly concerning to the U.S. government right now. I think that forgive the slaying. I think their pants are on fire at the moment over this, and they don’t quite know what to think about it and a lot of us. One of the things that’s fascinating about the Israeli data set is not only is it all Pfizer, but it was administered in a relatively compressed timeline. So there was those that took up vaccine. They took it up within a very short period because generally the Israeli people are very compliant with government directives.

Speaker3: [00:23:31] So you have a single vaccine product administered to the majority of the population over a very short period of time. So it’s almost the ideal laboratory for looking for what Gert has been warning us about. And so what we do seem to see is is signs that the durability of the product is relatively poor. And so we had this period where suddenly there was an awareness that the Delta strain was moving aggressively into that population as. That population was moving into this six month plus post, jab to window, and then you saw the thing take off now. What’s sustaining it in the face of multiple subsequent boosters is kind of fascinating. And there’s a whole train of thought that we have because the data are suggesting that the vaccinated have relatively less morbidity and mortality. The mortality question is kind of complex also, but let’s say they generally are less sick. There’s less morbidity in the vaccinated that do become infected, and the data are showing that that protection from infection replication and spread from the vaccinated is now down in the high thirties to maybe 50 percent protection. So in really leaky vaccine now in terms of protection against infection. What I’m particularly intrigued by is there the distribution of the data in terms of viral load in the vaccinated cohorts? To my eye, it looks like it’s a little bit skewed to higher levels of replication relative to the unvaccinated. If that was true, that would be a potential sign of some vaccine enhancement of replication or other other kinds of signs.

Speaker3: [00:25:44] But in terms of this phenotype that the vaccinated show less disease in general, if you think that through. What you’ve got a situation in which the vaccinated, this is going to be a little bit of a mind bender for people, the vaccinated are actually at higher risk for becoming super spreaders because they’re replicating virus at at the same or higher levels as the unvaccinated, but they feel better. So that means they’re more likely to be out in the community. And we’re in an environment now where both vaccinated and unvaccinated are at risk of infection because the ability of the vaccine to protect against Delta is relatively modest. So. So that’s if you think that through you’ve got a situation where you have people that are feeling relatively good moving out in the community, highly infectious, infected and producing virus at high titers, in nose and in oropharynx, and that that could well account for some of this surge. Now, whether the the additional jabs are are really causing plateau, there’s some alternative interpretations that look at the mortality associated with this, and it’s important to look at all cause mortality. And because there’s so much contamination in the data, I don’t know how else to put it. Ambiguity. So there is in my mind, there’s still an unresolved question of whether, even with the additional jabs, we aren’t seeing some vaccine enhanced replication at a minimum. Yeah.

Speaker1: [00:27:45] Then there’s yeah, go ahead before you move on with that. I wanted to quickly ask, does that seem to make sense that the vaccinated could in fact, in fact be almost super spreaders? Would that would that fit what we’re seeing?

Speaker2: [00:28:02] So my understanding of this whole thing is is the following, and you can check this in countries where you have high vaccine coverage rates. So high rates of vaccination, like U.K., like Israel, like the 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 this U.S., U.K., Israel, for example, with other European countries, you will see that that plateau is much, much higher. So we know that and maybe I’ll have an opportunity to explain this to your audience, Philip. The effect of mass vaccination that indeed in vaccinated people, they exert a lot of immune pressure on the virus. And this is in fact an ideal breeding ground for more infectious strains. So the more you vaccinate, the more you’re going to see that you’ll not succeed in bringing down the infectious pressure. However, however, if you still have a substantial proportion of the population that is not vaccinated, you will see that these people will of course, get infected. But what will happen is that a lot of them still 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 are going to reduce infectious pressure and those who get the disease, they will build, of course, lifelong, well, maybe not lifelong, but at least a long list immunity and also contribute to diminishing the infectious pressure.

Speaker2: [00:29:59] So you will see that. Yeah, so that is important. You will see that in those countries where there is still a substantial amount of non-vaccinated people who can get asymptomatic 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 still see some substantial waves every time you get unvaccinated. People get a 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 is going to disappear. So in other words, what I am expecting in Israel to see is that this movement of waves will come down, will come 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 substantial amount of non-vaccinated people. Again, the average level of infectious pressure is still way, way above what we had like a year ago. And you will still see some movement because there is still unvaccinated that can get a disease once they get infected, for example. Asymptomatically, I call them the vacuum cleaners. They will eliminate a lot of virus from the population.

Speaker2: [00:31:32] Those who get get the symptoms, they will mount long, lift immunity and also contribute to reduction of the infectious pressure. So they are the wave will stop again. You will have diminished infection pressure, but then there is still other unvaccinated that can get the disease, et cetera. 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. For example, countries like Germany, like my country, for example, et cetera. It will become as high as in the countries that have now already high vaccine coverage rates like us, like the UK. And then we are just waiting for the huge wave. And that is my prediction, and that is what I interpret when I see this death in Israel, where you see there is no big waves anymore, but the plateau is very, very high, right? And what what else do you expect? You have almost vaccinated all people, and we know that the vaccinated people are not going to contribute to diminishment of the infectious pressure. The only people can do this or the or the non-vaccinated right and the fewer don’t vaccinated, if you were, the less impact you have of the average infection rate. So this is my prediction. People can follow this, right?

Speaker3: [00:32:59] Can I come in? Can I go ahead? So I’m going to try to paraphrase what Gert just said in a really simple way, OK? The issue now. The truth is that it’s the vaccinated that are creating the risk and not the unvaccinated. The unvaccinated are, as he says, serving as virus sinks. For the most part, unless they are in those high risk groups, the probability of them having significant disease and death is Manute, particularly if one administers anti-inflammatory drugs early. And and the real risk here in this whole equation is not being generated by the unvaccinated that then develop broad based natural immunity to multiple antigens and epitopes that is 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 are driving through selective pressure evolution to escape those key epitopes that are present on those primarily on the receptor binding domain. Am I understand you correctly?

Speaker2: [00:34:16] Yeah, there is one thing, Robert, that and I’m sure you are getting this right, but I want to emphasize this because this is so important. Again, as as I’m saying all the time, we should not stigmatize people. We should not blame. The vaccine is as individuals and therefore, Philip, it may be good just you in a few seconds, maybe to put up the slide, because that will clarify because it’s not because somebody is vaccinated and is exerting an immune pressure that this, this person, this individual 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 I want to convey. It is not a problem of individuals being vaccinated. We know all, Robert, you confirm 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 would not have done any harm in terms of evolutionary escape, et cetera. So the problem are not the individuals who are vaccinated, and we will come later to that. The problem is the mass vaccination is 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 and become dominant and.

Speaker2: [00:36:03] And of course, this population can no longer reduce the infectious pressure. So well, yeah, maybe in this light. I just wanted to make very clear that in this whole thing of immune escape. So first of all, people, typically the fact checkers, they are saying, Well, you guys, you are talking nonsense because the vaccination is not driving mutations or mutants. Nobody ever said this. Nobody ever said, Of course you have mutants. You always. Yeah, yeah. But this is I think it’s so important that we we explain to people where the confusion comes from, and there is no other way to do this than with this light to give a little bit of clarification on what exactly is the problem. So I’m showing two situations to individuals. If you like one who is vaccinated and the other is not vaccinated, and I’m trying to keep this very, very simple. And as we were saying, you always have a proportion of mutants. I call them here, for example, more infectious variants and you have, let’s say, and I’m simplifying, I know there is many variants, et cetera. So I only take one variant and you have the bigger, the bigger, bulkier here or so to say the original strain. So let’s say we have one hundred viral particles, right? And the ratio is eight 80 wildfires. So the the one strain and 20 variants, so it is a ratio of one to five one variant and four for one lineages.

Speaker2: [00:37:55] So one in five for the variants. So what happens when this inoculum will be put on a vaccinated person versus an unvaccinated? Well, the vaccinated. Of course, if it’s vaccinated, will have antibodies against the spike protein, and therefore there will be a selection of this of these different viruses. Because when I I’m representing this by a small hole only. In fact, the smaller bowls and these are the variants will pass through that hole. So that means there is a resistance. The resistance is the smaller hole, which is in fact the immunity against the S, the spike protein. And if that resistance exists, well, there is only those viruses that can overcome this resistance by passing through this small hole that will be selected so we can, for example, from the one hundred particles we can through the selection, reduce them, let’s say, to 10. So we have a reduction of ten times, ten 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 one that managed to pass through this small hole. So now exactly the same situation with an own vaccinated and unvaccinated person. And so let’s assume we have the same level of reduction from the one hundred particles we are going to go down to 10 particles.

Speaker2: [00:39:34] 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 one strain coming in that the vast majority of the people were protected through innate 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 of one to 10, let’s say the same. What is the difference? Well, the difference is know that the innate antibodies they do not they are not selective. They do not. They do not discriminate against the more infectious particles or or 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 one hundred particles, I’m going to end up again within particles, my factor reduction of thin, but I’m going to have the same ratio one to four that I had at the beginning one variant for four original particles. So the thing that I have here. Well, there are two variants and eight wild type viruses. So the intersect, I’m still having 10 infectious virus particles, but the difference is in the individual who got vaccinated, I will have 10 particles of the same nature, all more infectious, whereas in the what? That did not get vaccinated and that did not put this immune selection pressure on the virus.

Speaker2: [00:41:26] I have 10 particles, two of which are the variant and eight of which are the wild strain, exactly the same ratio as I had at the beginning. So now? What does that mean, immune selection if there is only one individual who in a whole population who does this? I mean, there is no problem because these these variants will never, ever be able to dominate in the population. So the problem is, if I know going to mass vaccinate, then I do have a problem and I’m giving the example of a population being twenty five percent vaccinated. So twenty five percent means that one in four people, one in four people will fit into this scenario with a smaller hole, and seventy five percent will fit into this scenario, where the hole is much larger and there is no selection, no immune selection against the protein. So you see here these are twenty five percent one with the smaller and three with a large hole. So in that situation, I will now compare, let’s say, to a situation where I go to seventy five percent of vaccinated people. So now that means that three out of four people or in the scenario where immune selection pressure is exerted against the S protein and only one in four twenty five percent fits into this scenario.

Speaker2: [00:43:06] Ok, so what is going to happen if I know make the calculation? How many infectious, more infectious particles do I have in total? So here you will see. I have one two three four four variants out of seven in total, whereas here with the seventy five percent vaccination rate, I have one two three four variants out of a total of five five viruses in total. So you see the concentration that is taking place four out of seven is something like 60 percent. Four out of five is 80 percent. So you can imagine the more I vaccinate, the more I have this selection and I will end up basically with only more infectious variants. So when that happens, this election, this reduction doesn’t take place anymore here. I had a reduction. Why did I have a reduction? Because I had the selection factors I had a selection factor against s. But if all of them order any more infectious, I am not going to have a selection anymore, so I’m not going to reduce the infectious pressure anymore. That was my comment on the Israeli curve, where the more you have vaccinated, you have this high plateau, you will not be able to bring it down anymore. So the interesting thing is, the interesting thing is if you look at the non-vaccinated, I don’t know if can you still put up the slide just for a second? Yeah, you will have here.

Speaker2: [00:44:50] So that also works the other way around. So how can I go from seventy five to twenty five? Well, the only way to do this is to bring in not vaccinated people, right? I mean, I cannot make the vaccination undone, but I can bring in new unvaccinated people. That’s why I’m saying I posted something. You know, the baby boom. That’s what we need. But it’s very interesting when, for example, in the U.K., in the UK, the UM, the lockdown measures were lifted in July. What did we have? Well, you know, people were again mixing. There were still there was still a fair amount of non-vaccinated people and people had close contact again. So you bring now these people again in contact with the fully vaccinated people. What you will have because here you have no selection. You will have a kind of dilution, a dilution of the infectious pressure because the competitive advantage that exists here, that that the more infectious variant has here, the more infectious variants has a tremendous competitive advantage will be weakened. It will be mitigated when you have more non vaccinated people when you intensify these contacts. Of course, if everybody gets vaccinated, you won’t have this anymore. And that is the next slide where I show this curve of the infection rates in the U.K. for, for example.

Speaker2: [00:46:23] So that is what I mean. So this is the peak. Nobody could explain this. Boris Johnson was just, you know, he he was just gambling. He was just trying, you know, something, why was he trying something? Because he was saying, Well, you know, for the first time in the. Pandemic, we see a disconnect between the number of cases and the number of deaths, so let’s take advantage of this disconnect. We have a high number of cases. Nevertheless, let’s lift the lockdown measures and what happens and here Boris Johnson was very proud. Within the next two weeks, we saw a quite substantial decrease because, of course, I mean, we had no closer contact, still a number of non-vaccinated people. And this is despite the fact that mass vaccination, of course, continued during this time. Right. And so this is the kind of examples that I’m asking people, Well, how do we explain this within within 14 days, within two weeks? I mean, this has nothing to do really with vaccination. This has to do with the contacts and with closer contacts with non-vaccinated. And I call them really the vacuum cleaners because they will reduce the infectious pressure without without putting pressure on the infectiousness of the virus because it’s not selective. It’s the the innate antibodies that, well, the more infectious variants as the less infectious variants. The binding mechanism is completely it’s completely different. It’s through multivalent binding and that has been destroyed.

Speaker1: [00:47:58] But what I want is that Robert. So as an independent, I want you to try and see if you can take that and see how would you put that across? Does that? Yeah.

Speaker2: [00:48:13] How does that make sense race? How does he translate this in English? Yes, that’s the question.

Speaker3: [00:48:21] Well, so one conclusion is that I’m reminded of the statement. Hate the game, not the player that it’s it’s not the individual. It’s the policy. And it’s the if I’m understanding correctly, the policy of of universal mass vaccination is our problem here. As he emphasized, it’s not targeting any individual because of what they have or have not elected to do that. So how do I explain it to the average person I try to? The problem I face here in the United States is that a large fraction of the population is unfamiliar with Darwinian selection. So that’s the starting point is, I can’t even really have a conversation about selective pressure with many people. And I’ve and so you have to kind of have that understanding before you can go further. In terms of how do I explain what Gert has just shared, the 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. Now I have it’s going to take me a while to think about how do I simplify that into a tweet and walk people through this? The the I like, I like the idea. So basically, what he’s saying is that the unvaccinated service sort of a dampening function, a sponge in the in the distribution of the virus mutants and because they have a more diverse immune response. And so they’re not going to be selecting for a specific variant. I think that’s the key in what he’s saying with his metaphor of a thin channel is is if I’m understanding him right? What he’s really focusing on is not just that there’s an immune response, but that there’s a very selective immune response that is going to result in a particular set of phenotypes that are able to circumvent that.

Speaker3: [00:50:42] I’m often given this challenge, as he did, that I find frustrating and perplexing that that this that will why isn’t the unvaccinated the ones that are selecting for the mutants? And and it’s hard to express the idea that the diversity of immune response and the diversity of each of us in terms of our MHC molecules makes it so that, I guess, in his model. In in the unvaccinated population that hasn’t been driven to this common endpoint in terms of their education, their B and T responses, they’re there. They have a wide diversity of of how they are responding to the virus. And so instead of really one narrow poor, it’s as if he has a metaphor of a large poor. I guess it would be more like that. It’s has a lot of pause that that the selection is on a lot of different proteins and a lot of different epitopes. And so the virus doesn’t converge. This is one of the things that I’ve learned. I think from him is is the idea that this mass vaccination is going to be driving to a common adapted final endpoint. And I think this is the one that he’s warning us about the explosion from and my understanding you correctly, Gert.

Speaker2: [00:52:20] Yeah, yeah. And we wanted we

Speaker3: [00:52:23] Will see convergent convergent evolution towards some final endpoint.

Speaker2: [00:52:28] Of course. Of course, that is make

Speaker1: [00:52:30] An important point here is that based on the research that I’ve been doing as well, one of the difficulties is that this virus is largely benign in the sense that if you take a neonate or a young child that they get infected with it, they don’t get severe disease. And so the the question is about when somebody gets infected. The huge problem seems to be about the interferon response and the virus is able to block that. Now, in somebody who is vaccinated, what was interesting is it finds that they produce a weak IGA response. So they do produce some antibodies secretory IGA against the virus, but it’s not enough to stop the replication of the virus. And additionally, it will be targeted to the wild type of the original virus, and therefore you will only end up with replication of a virus that can evade that weak IGA response. And so you’re right, it does select and this is, I think that I saw a very interesting paper that was shared. We’re in a prison population. They had a huge outbreak of COVID 19 when the majority of the prisoners were vaccinated. And that suggests that, yes, somebody ended up selecting or a few of them selecting a virus that could evade the antibodies. And then you end up with spread of a mutated virus that will be able to infect everybody, both the vaccinated and the unvaccinated.

Speaker2: [00:54:10] Mm-hmm. I think the the.

Speaker3: [00:54:14] Go ahead. I was going to say has made the point that we under this type of scheme using Merck’s disease as the metaphor that we’re and this is one of the things that he and I had disagreed with previously. But now I’m coming to his point of view, I think, is that the risk is that we’re not only generating escape mutants, we’re generating mutants that are more highly replication, competent, more highly infectious and and potentially more pathogenic. I think 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 ability to replicate and infect is shifting and that’s creating more risk in these younger cohorts. Do I understand that correctly in your thinking?

Speaker2: [00:55:15] Well, my my opinion is slightly different in a sense that I think we need to distinguish really between infectiousness and virulence when when we are talking here about immune selection pressure very, very clearly because we are, you know, these are is based vaccines. And so the immune pressure is against, of course, the the protein and immune pressure is suboptimal, as you were pointing out, because otherwise we could really have sterilizing immunity, which we don’t have certainly impossible if we vaccinate in the midst of a pandemic. So we put suboptimal immune pressure on the spike protein, and the spike protein is, of course, responsible for the infectiousness. So in other words, we put suboptimal immune pressure on viral infectiousness, right? So now the question of the virulence for me is is is different because there is no I don’t know, I’m not. Aware of any pressure that is exerted on the vital pathogenicity, the the the virulence, and if we would have seen such spectacular mutations, I mean it would have been published, it would have been shared. So far, there is none of this. So then because this is the thing nobody really can explain, how does it come then that all of a sudden our younger people, younger age groups or getting the disease or becoming susceptible because the virulence is not changing? And there my explanation is that we do have because of the circulation of more infectious strains we do have on average and we see it on the curves.

Speaker2: [00:56:54] Again, look at the curve in Israel. On average, we have a higher we have higher infection rates, right? We have higher infection rates. So the likelihood that somebody get exposed shortly after the first infection becomes higher and higher. So the likelihood that somebody becomes now exposed again to the virus just a few weeks after he or she has been exposed for the first time becomes higher because of the high infectious pressure and that there is a few very interesting publications that show that people like youngsters, young people who the first time around were not showing any symptoms that they develop as antibodies that are short-lived and these antibodies that are short lived, that do not induce B cell memory. So they are not really primed but is 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 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, right? 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 reinfected within a short time frame after this first infection, while sitting while still sitting on short lived antibodies that are not sufficient really to neutralize.

Speaker2: [00:58:38] But that can that can suppress the innate antibodies and that they do not neutralize. I mean, why is very clear this asymptomatically infected people, they eliminate the virus. They have already eliminated the virus before the short lived antibodies start to peak right. So the short left antibodies have no no function at all in the elimination of the virus, it’s completely. So why are they there? I mean, when such things happen, we cannot afford to leave any stone unturned. And this is a very interesting trick of the of the virus because by doing this, it can take another path out of these reservoirs. Right of this of these young people, you will see the more the virus becomes infectious, the more we we we will go down with the age groups that become susceptible. And that is my fear. The more we vaccinate, the more infectious, the higher the infectiousness of the dominant circulating virus, and the more we will go down in the age range of age groups that become susceptible to the virus. So it’s not for me, it’s not a matter of intrinsic virulence mutations. It is 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.

Speaker1: [01:00:08] Can I can I point out something that I think is important when we reflect on how the virus works with children? One of the the issues that have been having is that we’ve we’ve stopped doing autopsies. We’ve stopped studying the details. And when you have a virus, the Delta variant is producing, I think, a thousand 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 getting affected, affected now is because they are know, 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 with with COVID 19, which was a cytokine storm. And we seem to be missing doing these critical things. I just wanted to ask Robert his thought. No. One topic keeps on popping up all the time, which is E.D. and any any thoughts with regards to what? What would you say about that? Well, probably first define it.

Speaker3: [01:01:28] Yeah, so so you just asked you, just you, you. 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 in bridging that to the cytokine storm viral pathology. And then you introduce the thread of antibody dependent enhancement. So the I caution with the primary viral infection, the viremia phase that that one is only your language suggested that you were focused mostly on the pulmonary track. And so just just to to hammer the point home, this thing goes everywhere. I have friends that are our primate virologists that have been doing detailed autopsies, and they’re seeing that this pathogen pathogen. I have an echo, 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, so there is that I just caution focusing too much on the respiratory tract when we have what appears to be spike mediated effects on coagulation, on endothelial damage, on renal disease, on lung, yes, but on a variety of other tissues, including the reproductive tract. So that’s that’s and if we’re having higher viral loads because we have selected mutations that enable higher levels of viremia, that totally makes sense to me that we’ll see more of a primary viral pathology in all these tissues then in terms of the cytokine storm. Uh, I the cytokine storm thesis seems to be less of an issue, except in those that have the pre-existing conditions.

Speaker3: [01:03:47] It’s like they don’t move into that second phase. We clearly have a two phase disease and that second phase that I’m told with Delta now, instead of starting at about day seven after infection, it’s more pushed up towards day five when it does occur. And I’m perplexed as to why the vaccine should be dampening that, that that the phenotype that is less severe disease and death associated with the vaccinated I’m that’s for me, is troubling how to make sense of that because what’s killing us is that hyperinflammatory response. And so why an antigen specific vaccine would be dampening the reactive, hyper inflammatory response in patients that have just as much viral load, if not higher IgM. It doesn’t make sense to me. I’m looking forward to reading that manuscript and in an upcoming issue of Cell, I’m sure, but I haven’t seen it yet. So there’s that then the antibody dependent enhancement. So I got the. The FDA specifically called out antibody dependent enhancement in its various communications as a risk that was uncharacterized in unknown still at the time that they issued the license, which are the emergency use authorization. It still remains unresolved to what extent it occurs. Gert will probably tell you, and I can share with you that that in the case of, say, dengue virus, which the classic example of antibody enhancement one has the greatest risk during the waning phase of the immune response, there’s because the slope 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.

Speaker3: [01:05:51] And so it’s it’s that waning phase window that seems to be the setup for ADI. Here’s the rub. And and this has been pointed out to me multiple times by others is that even though the FDA’s use the term and all the prior literature on coronavirus vaccine development use, the term aid is the risk. In fact, this virus is not replicating in macrophage and monocytes. So that data, those data are not there. And and so for the purest antibody dependent enhancement is defined as facilitation of uptake through FC receptors into monocyte derived populations like macrophage. And so that you get this explosive replication in cells that otherwise don’t have the right receptor. So then they say, No, you can’t call this ad., Robert, you’ve been fact checked. You’re wrong. So that’s I think that’s a little bit of nomenclature thing. Tomato, tomato. I prefer to use the term vaccine enhanced infection or replication or disease because it’s a broader category. 80 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 otherwise aren’t being used? Notice I’m saying the same thing, but with different words.

Speaker3: [01:07:29] I mean, the presumption is aid has to occur through FC receptors. Well, FC receptors aren’t the only way to pick the lock 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 the key question in my mind, people say, Well, we’re not seeing enhanced disease post-vaccination, we’re seeing attenuated disease. I say, yeah, but the disease is the inflammatory response to the viremia. It’s not the viremia itself, generally speaking, right? That’s what we just established earlier when you were talking about the hyperinflammatory 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 the kind of the proximal thing we could look at is what are the viral loads now? Do we have decent tools for looking at viral loads? Well, actually, if we look ourselves in the face, the answer’s no. As Cory Mullis, prior to his untimely death, like to point out, PCR is not a quantitative assay. And so we’re and we’re not having people do classical virology like Gert and his veterinary colleagues do. Where you’re actually looking at virus titers and culturing them in cells and and micro titer plates, we’re relying on the surrogate assays of what is the cycle? No, as an indirect quote, an indirect measure of viral load.

Speaker3: [01:09:26] So if you if you were able to detect virus after a much lower number of PCR cycles, well, that’s suggestive that there’s more nucleic acid there. And so we use that as a crude surrogate for viral load. So that’s the problem in my mind is we’re not asking ourselves the question and we’re not we haven’t really taken up the task of looking at it rigorously. We’re we’re kind of a skeptic could say that we’re avoiding the question studiously. But but that’s why I’m I’m very. Eager to see from my Israeli colleagues. Data, even if it’s PCR threshold number where they pass 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, three weeks when you have peak three or even three months versus six to eight months and look at at load then. And I think that would be the indicator of whether or not we’re having vaccine enhanced replication. But right now, I 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. Nobody wants to fund them. And so it’s we’re in a world where it’s knowable but unknown. That’s that’s my sense about the whole vaccine enhanced replication disease, a spectrum of things.

Speaker1: [01:11:26] So it brings us to a very important phase of our discussion. Do you guys understand how the regulators think, can you have 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 would start would probably go. You want to start with that girl?

Speaker2: [01:11:54] Well, I mean, I would be saying is that, yeah, I would, as I’m trying to do since the the beginning of this year is. Trying to explain what what the impact is of mass vaccination and making it clear to them because I think even the regulators, the regulators, they 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 has repercussions on the evolutionary dynamics of the virus. And those influences and interactions are having an impact on the effectiveness of the vaccines, et cetera, and we see 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 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 as in terms of viral infectious infectiousness. And that is something that is completely completely absent in their reasoning.

Speaker2: [01:13:55] 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 like a regulatory authority to say, Well, guys, sorry, but we we first have to dive in our books and in a number of publications and listen to a number of experts who can explain as those dynamics before we can reasonably make an assessment of of a dossier. So yeah, I mean, it’s and I think I think one of these regulators, I happen to know pretty well one of these regulators who left FDA. And I think this is kind of like, you know, this uncertainty and anxiousness of not knowing and not understanding what is going to happen. Because if you understand these things, we are all scientists. If you understand you can act in good faith and you know, these are the risks and these are the the advantages or disadvantages. But if the beast is unknown and you do something at such a large scale, an authorization at a large scale and you go into children, something we really do right away with vaccines, right? Then it becomes really something that is it looks very, very scary to people. And I think personally, we are going to see other folks leaving. Right. That’s that’s what I think.

Speaker1: [01:15:33] And your thoughts, Robert, what what would you what would they be thinking? What if you were in the room? What what would you be thinking and doing?

Speaker3: [01:15:45] So there’s let me I’m 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 that Gert is giving the benefit of the doubt too much, and I can’t speak for the European Medicines Agency or the individual regulatory authorities in Europe and how they think, what I can speak to, what I see in the United States. Your question infers that if you’re talking about regulatory authorities, I infer you’re talking about FDA. So FDA operates based on checklists, and they are they are kind of rigid in that way. They have it’s like a punch list, like you’re going to go shopping and you have to get this thing in that thing and the other thing and they all have to be done or the list that your spouse gives you on the weekend of chores. So that’s kind of how FDA approaches that they’re not a whole lot of thinking. They don’t set policy. So your question is really kind of a policy question, but it presumes that policy decisions are happening at the FDA level. They’re not at the FDA level. 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 is is in that regulatory space, 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 licensor.

Speaker3: [01:17:41] Your letter in that they flat out at the FDA state that the existing database structure that exists within the United States, so that’s theirs, be safe. And the databases from the Medicare, Medicaid and VA and army medical system, et cetera. They’re not sufficient. They’re not structured in such 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 and why did we see the two two of the top regulators in the vaccine branch resign over the issue of the third jab the boosters? The reason is because the FDA is no longer independent from the policymaking apparatus, which exists in their executive branch. So it’s it’s the White House that’s setting the policy. Which is to say, because Tony Fauci is appointed basically the czar of of this disease. It’s it’s mostly comes down to Dr. Fauci’s personal perspective. And then then you flow. And we 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 the data on behalf of the FDA.

Speaker3: [01:19:38] This is the Verbeek panel, and they made it clear unambiguous decision that despite the lack of sufficient data to make a go decision in terms of safety and 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 showing and some American data showing that the vaccine durability was so poor. So these people are now at higher risk and they were already at higher risk, and now their vaccine protection is dropping. And so they said, OK, in the balance, we should go ahead with that. But then you had the director of the CDC, the I’m sorry, the FDA, Janet Woodcock, step in and say, Well, that’s all fine and dandy, but I’m going to add 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. Ok, if you’re fifty five or forty five or whatever, that’s your risk stratification. It does. There aren’t data saying that if you’re a grocery clerk, you have a much higher probability of death and hospitalization if you’re twenty five than somebody who isn’t a grocery clerk. So they made that political decision because they want to impose universal mandates. So then it gets tossed over to this is just let’s understand how the U.S.

Speaker3: [01:21:17] works, then it gets tossed at the CDC. And the CDC independent panel called the ACIP evaluate the same data, and they say, no, we reject this added third group that the director of the FDA has added in. That’s all those with public contact. We reject that logic. There’s no data to support that assertion. And we just think you should go ahead with the same recommendation. The Verbeek gave and then we had within two days, the director of the CDC overruled that. And went back to the same policy that Janet Woodcock, the director of the FDA, had rolled out, which is basically coming from Tony Fauci, as I explained. So that’s how things are working here. Now there’s other wrinkles to this. We’re we’re we’re in a situation where we we’re operating in a way that is independent of science. It’s the science no longer matters, really. It’s it’s public policy by fiat. And in in the case of the CDC in particular, I think it’s important to understand that CDC is a classic case of a regulatory group. In a sense, they’re not really regulatory, they’re policy advisory, and 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 with the CDC that they have a dual function, they are explicitly tasked with vaccine advocacy.

Speaker3: [01:23:07] 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 is an intrinsic conflict of interest within the CDC in that it is funded largely to promote vaccines, but has also the underfunded mission of evaluating their safety. So that’s that’s the situation in the states. Now you ask the I parse that part out. What would I say? I’ve been given this question, you know, assume that President Biden calls you up. That’s not going to happen and says, Dear Robert, what should we do? Oh no, we’ve got a problem. You know, red lights are flashing. I’m so concerned about what you’re saying on Twitter. I have to call you up and get your advice. Yeah. So but that hypothetical was presented to me and Peter Navarro. And so we did come up with a set of policy statements. And published them in The Washington Times, and they amount to four key policy items, and they’re very, very informed by Gertz thinking, frankly, when I finally got my head around wrapped around mostly around what Gert has been trying to teach us. I realized that we had a big problem and we had to change course. So my what I’ve advocated and I advocated, by the way, with Cardinal Turkson at the Vatican two weeks ago, I was granted an audience that indicated in Portugal, I advocated in Italy, and I have abdicated here in the United States through those op eds with Peter Navarro is a four point strategy.

Speaker3: [01:25:00] No. One. Reserve our vaccine for the elders and the morbidly obese and the high risk population and make it available globally, it’s it’s right now we’re overusing vaccine in the western world. We’re basically being vaccine pigs. I’m sorry, that’s a little blunt, but we are hoarding the resources in the West unnecessarily. We’re actually, as Gert 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 to populations in less economically advantaged countries that don’t have the capital to buy. It’s not just buying the freezers, it’s the cold chain is enormously expensive and difficult. So we’re we’re hoarding vaccine and it’s the elders in those other countries that represent the memory that represent the wisdom and knowledge of each of those countries, villages, townships, etc. And it’s it’s a huge I don’t know how else to say it crime that we’re not providing vaccine coverage for those people that need it just as much as the elders do in England and the U.K.. I’m sorry and the EU and the United States and Israel, for example. So. Spread it out. Use it where it’s really needed. Don’t hoard it, don’t use it as an economic weapon, which is happening. And number two, make early interventions of widely available the the the agents that are out there, including the monoclonal antibodies, are very effective when administered early and aggressively, and a number of those agents are considered controversial.

Speaker3: [01:26:58] And yet they are being used widely, often in emerging economies that are having better outcomes in terms of morbidity and mortality than we are in the West, certainly than we are in the United States. The most recent example being Uttar Pradesh, with their wide use of ivermectin in India and suddenly collapsing just abruptly strike, strikingly collapsing the incidence rate of death and disease from COVID in Uttar Pradesh. We saw it before some fantastic examples in Peru, and that was kind of a challenge challenge experiment where they deployed ivermectin and then they changed policy and didn’t deploy it and the the morbidity and mortality shot up. So it’s that we have a number of agents, not the least of which is vitamin D. That makes a big difference in the morbidity and mortality, so make those available early. Number three, I believe that rapid test kits that are biased towards false positives because any test will have a bias. And so acknowledging that 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 that people have a good idea that they don’t have respiratory syncytial virus like was what was ripping up the pediatric population earlier this year, and everybody thought it was SARS-CoV-2 as RSV.

Speaker3: [01:28:41] You know, they can differentiate between that or the flu or whatever rhinovirus. So make test kits available third. Last point, I really think that we need to address the fear. I think there’s been way, way, way too much fear promoted. And as Gert has kindly 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. In fact, what you will get for most of us is broad based, long lasting immunity, as Gert 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 my the four policy points that Peter Navarro and I have come up with. And of course, after we published it in The Washington Times so that everybody in D.C. 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 trying to influence policy, but it’s I feel like it’s a labor of Sisyphus. So there’s there’s my analysis of your question.

Speaker1: [01:30:13] Wonderful. Any anything else you would add to that, Gert, because that’s quite a comprehensive viewpoint that that Robert has just done.

Speaker2: [01:30:21] Well, for me, I think that the most important thing to do if there is one thing that I really need to point out is to reduce these infectious pressure. And that is for me, something nobody. 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. I mean, it’s not like this virus is going to say all of a sudden, well enough is enough. I I’m going to insert a number of mutations that are going to diminish my, my, my, my infectiousness. And as I was saying for me, this is really a huge threat to those, all those who were previously naturally protected. We have seen young people, all these younger age groups. I would say below below sixty five, et cetera, having almost no problem whatsoever when the pandemic started and. Now we see increasingly also younger age groups that that get a 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, again, we have to stop these mass vaccination the worst thing ever. The worst thing ever that we do is to vaccinate younger age groups. As I try to explain, this is the buffer, the younger age groups you bring them in, for example, non-vaccinated you, you’re going to see a diminishment in the infectious pressure. They are the vacuum cleaners. And even if they get a disease, I mean, most of them resist relatively well to severe disease because of their younger age, because of their still fairly high rate of innate antibodies.

Speaker2: [01:32:18] And all those, I mean vaccinologist know very little about innate antibodies, but go on my website and look at the publications. I mean, it’s really fascinating. So if if we if we start vaccinating these people, they lose this potential, I showed you when people get vaccinated, they are going to breed. In fact, those infectious, more infectious strains and through a new selection pressure, there is no longer this elimination. We lose completely this buffer that people get the disease, they build long lift immunity. So this is really our hope for herd immunity. I mean, nobody talks anymore about herd immunity. What is the objective still of the mass vaccination campaign? Can anybody tell me what the objective? I mean, if there is no, there is no objective. Well, then there is also no strategy, of course, and there is no strategy. There is only tactics, right? I mean, there is like, you know, everybody is doing something, but there is no common objective and every country is doing its their own thing. So so this is really a disaster because the only way to solve this still, I mean, we don’t change virology, we don’t change immunology. It’s still the interplay between the virus and the immune system. It’s still herd immunity. So how where are we going to get herd immunity from? Certainly, not. Certainly not from the vaccination and even less when we do mass vaccination.

Speaker2: [01:33:44] So how can we if we could reduce this infectious pressure, we could save back to our kids, to our children, to the younger age groups, et cetera. Go out and do your thing. Because this was like then at the beginning of the pandemic where we had the one strain with a much lower intrinsic infectiousness and nothing was happening with its age groups, right? I mean, yeah, of course, there’s always people who have an innate immune defect, et cetera. But largely speaking, it was we didn’t see these incidences, no higher rates of morbidity, et cetera, in younger age groups. So we need to bring down to breed to stop mass vaccination, of course, because we are just starting all this, all this potential to build herd immunity. We are just converting this into the opposite, you know, people who cannot contribute anymore to herd immunity. And it’s not only from a public health standpoint, 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 no high pressure from the population on driving mutants that escape neutralizing antibodies. These are molecular epidemiologists who are describing this. Of course, they are not saying that this is due to mass vaccination, the immune pressure, but they are clearly pointing out that there is a fast mounting immune pressure and that drives increasingly mutations that escape from neutralization antibodies. And I mean, so, so so this is evolving, right? This is evolving.

Speaker2: [01:35:31] So that means that one day and we know already that some of these resistant variants are circulating it just that they have not necessarily become the more dominant strain or the more infectious ones. But I mean, we are that is what what we are going to end up with. I mean, let’s not be naive is with resistance, right? And then 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? What about tomorrow? What about three months from now? There is this limitation. We know that this protection is limited and we have already seen how it has been evolving. Initially, there was an impact on transmission certainly was right. Then there’s this impact was lost, but there was still an impact on, of course, disease prevention of disease. Now it’s only severe. So all this rhetoric and the narrative that is changing about the claims regarding the vaccine is just merely reflecting the evolutionary dynamics of the virus during this during this pandemic. So we need to bring down this infectious pressure and the only way it can be done, I mean, whether you like to talk about ivermectin or not. Frankly speaking, I don’t care, but we can only do this with antiviral chemoprophylaxis. I mean, how else are you going to do this and stopping, of course, mass vaccination? And what I would say, what is very important as well, according to my humble opinion and my humble interpretation of the data.

Speaker2: [01:37:11] We also need to avoid overcrowding. Personally, I think that the infectious strains that started circulating in the population even long before mass vaccination was started was due to a large extent in certain areas to really overcrowding. Because when you have overcrowding, you have a high infectious pressure. Of course, it’s almost per definition. So the likelihood that somebody who gets asymptomatically infected gets reinfected during the time where she or he is still sitting on antibodies is very, very high. So what does that mean? Immune pressure, of course. Immune pressure on its 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 only do we cannot do it with the vaccines, you say in all the countries where we have this high vaccination rates. That is where we have the high infection rates, right? I mean, what else are this is this is so for me, this is a complete, complete no-brainer, right? I mean, this is this is just simply simply common sense and it could be done. That is that is my frustration. Of course, it could be done. But if we continue with the mass vaccination, I mean, nature will win. We will end this. We will end this, of course, 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, let’s say, the ratio of mutants shed by vaccines versus the original strains to see whether there was a shift towards more mutants shed by vaccines compared to non vaccines.

Speaker2: [01:39:08] But then all of a sudden was said, Well, you know, if you are vaccinated, we don’t do the sequencing anymore. We close this chapter. We don’t do this anymore. So that was not the criterion. Now my next criterion for demonstrating the the detrimental impact really of continuing this mass vaccination would be to compare the ratio of severe disease and death in the vaccinated versus the non-vaccinated. And so the percentage, of course, the ratio right and we see already in some countries that in terms of the percentage the in the vaccine is, there is more case fatalities than in the new vaccine. But again, again, again, Robert, these these figures, these numbers we will never have, these numbers are not easily made available. Try to find them, try to find them. And if it takes still another month or two or three months for us to find them by that time, we won’t even have a control group any longer because, you know, everybody will be vaccinated and there is no there is no control group. So there is there is no means objective means for us to to to really prove that this is a dramatic evolution and we could prove it. But the tools are not made available or this data are simply not not not not shared. It makes it. Yeah, it makes it very, very dramatic, I think.

Speaker1: [01:40:41] I know Robert wanted to say something.

Speaker3: [01:40:44] Yeah, a couple of things. Actually, Gert, I think I call this the ghost in the data. We’re getting the Echo again in the UK databases and Scottish databases. There there is this persistent odd signal in the vaccine recipients of lower incidence. Relatively speaking, after you adjust for the you’ve got to adjust for the confounders of the percent vaccinated versus the unvaccinated, et cetera. But there’s this persistent signal in the UK data that there seems to be an excess in deaths in the vaccinated and yet a relative deficit in severe disease in the vaccinated. So it’s it’s as if it’s somehow protecting from severe disease, but is there is some increased incidence in mortality compared to the unvaccinated after you do the corrections and it’s paradoxical. So that may be the the sign that you’re looking for. There’s I’d like to before you close out, Philip, there’s a couple of things I’d like to mention that are a little bit worrying at me. So back in the day, I was more like Gert in doing primary vaccinology, and I remember very well the whole discussion about defective interfering particles, which of these viruses that aren’t truly infectious but still have the protein coats and other characteristics. The problem with those and I suspect that that we’re going to be seeing a lot more of this in these high viral load situations is immune complex disease.

Speaker3: [01:42:34] And Philip, I know you, you get credit in my book for being out front with recognizing the autoimmune risks. And clearly those are manifest, for instance, with the platelets and the thrombotic thrombocytopenia disease. So but I think that we’re going to probably see with these higher viral loads, more immune complex disease to other things that that Gert kind of almost touched on, but not quite. We have this issue of original antigenic sin. And he speaks about the pre-existing antibodies. But what we have with vaccine that is no longer a virus strain matched very well is that we’re we’re generating memory populations that are going to be reactive to developing antibodies, in particular against epitopes on a strain that is going to no longer really be circulating so much anymore. And what happens then, is you get when you get encountered a new strain, you’re predisposed to generating antibodies that are mismatched. So that’s the short version of original antigenic sin. The other problem that I’m worried about with this, you know, vaccinate every in a number of months, is it every six months or whatever is high, his own tolerance. And I’m sure Gert is very familiar with the controversies about overly frequently vaccinating for influenza. So this this idea that and I think it reflects the overall approach of the naive policymakers that more is better, you know, and I call it give a three year old a hammer and everything’s a nail.

Speaker3: [01:44:28] I think that we are overlooking the risk that over vaccinating can actually result in his own tolerance. This we know this is a standard practice for those who have children with allergies, for instance, and you know that your allergist will administer multiple doses of an antigen in order to elicit immune suppression. I fear that we’re at risk and there is some data that’s consistent with that that if we take this kind of a policy of over vaccinating and that includes there’s data supporting two jabs after natural infection can actually reduce your T cell responses. So I these are the things that that are worrying me. In addition to Gertz brilliant insights is is that as we look forward in vaccine policy, there’s the assumption that more is better. That’s not true with vaccines. And there are these other complicating factors as we drive towards higher replicating virus because of our policies more viral load. I suspect we’re going to see more immune complex disease, and that may be part of what’s contributing to the enhanced disease or or pathogenicity and some of these younger populations. So that’s that’s kind of my closing on riff on on following on Gertz comments a moment ago for me.

Speaker2: [01:46:03] But I don’t I don’t know whether you still I would promise that I would take just one minute, but if you could please put up my last slide because I think this is something that people are very concerned about is the current discrimination between the vaccines and the non-vaccinated. And I think that is what what what really bothers people. And I would really appreciate if I could just spend one minute on a handwritten slide just showing. I hope people can see this, but just showing what kind of of of complete scientific nonsense this is so compared compared to just two curves on the on the left hand. You see, I think these are not vaccinated and the right, the right care for the vaccinated. So I will explain. So this is a kind of representation of the viral shedding, you could say of one person over time. Or you could also say each part of the curve, each point of the curve as a different individual. So from this, you would conclude, and it’s not necessarily that it could be the other way around, but let’s even assume worst case scenario that the unvaccinated would on average, and this is the line that you see going through these all these peaks that this average would be higher than in the in the vaccinated, which is not necessarily the case. You would see that even then, even then, for one individual or for a whole population of different individuals, there are always points that are lower than the points on the curve of the vaccinated.

Speaker2: [01:47:58] So we know that the viral shedding come on. These are the basics of virology, whether you’re vaccinated or non vaccinated. If there is, if the vaccination is not blocking transmission, the shedding one person, for example, will be very different on the time of exposure to viral load. The inoculum at what time are you measuring the shedding and also the duration? There is so many parameters that define this right? And that or maybe that is shedding over time is not the same or that if you take several different people at the same moment in time, even if they’re all vaccinated or they are all non vaccinated, it will be very, very, very different. So the question really is not how much is somebody shedding and is the vaccine is shedding more or is the non-vaccinated shedding more? So this is what what drives right now kind of discrimination primarily against the unvaccinated. And this is completely scientifically a complete a complete nonsense. I think if you are, whether you’re vaccinated or you’re not vaccinated, what you need to care about is your susceptibility. What can I do to protect myself? We know, for example, that somebody who is vaccinated, who got two shots is better protected for a two shot vaccine than somebody who got one shot.

Speaker2: [01:49:25] We know that somebody who is young, who is in good health has a very good innate immunity, et cetera, is better protected as a non-vaccinated these type of things. So that is what we should. Here about and we should really please get rid of this unjustifiable discrimination between vaccines and non-vaccinated non-vaccinated discriminate vaccines and vice versa. We should not forget, for example, that in a vaccinated population, the non-vaccinated will, of course, also shed plenty of more infectious strains. That is the strain that is circulating. So how how else, what else could the non-vaccinated said? So this is completely, completely irrelevant. What is relevant is how can we protect ourselves based on an individual basis, our personal protection? And how can we increase protection from a public public health viewpoint? So that was what I was saying before is to diminish. See how we can diminish this, this infectious pressure. I absolutely wanted to to add this because this is something many people are worried about and there is a lot of discrimination going on that is even fostered by all these policies around vaccination mandates and all these ridiculous, ridiculous stuff, which has no scientific basis whatsoever. I think and hope Robert will to some extent agree with me.

Speaker1: [01:51:00] Yeah, I think I strongly

Speaker3: [01:51:02] Agree that the policies are are irrational, and I think they reflect a certain amount of frantic activity on the part of the public policymakers. I think they’re at a loss of what to do. And let’s get back to the give the three year old a hammer and everything is a nail. They think that that by doing this, they’re showing that they’re doing something, but it’s it’s incredibly divisive and I’m really grateful to hear you make this point.

Speaker1: [01:51:40] Wonderful. Listen, this has been truly a fascinating discussion. We’ve we’ve been here almost two hours, you know, guys, and we could probably continue, but I think it’s probably about time to wrap up. Listen, I truly appreciate you guys. I learn so much by listening to you all and just do a little bit of housekeeping before we wrap up next week. Hopefully, I’ll be doing a talk with some people from Pakistan looking at some of the challenges that are there in other countries with COVID 19. And in the week after that, we should be having our conference on Innovative Epidemiological Solutions, which fits quite rightly and quite closely with what you guys have been saying as well. And finally, I probably want to quickly share to listeners that we’ve started a COVID 19 Foundation 360 course because I get the impression that in effect, this is not going away quickly. And the more that people understand, the more that we will be able to grasp everything. So this is a course that will be focused really on trying to share a lot of the learning that I’ve had over the past 18 months, not just from research, but from listening to people, boosting your knowledge, empowering yourself, making you feel safer through knowledge and through understanding. So that’s essentially where we are now, and I just wanted to again quickly thank our wonderful guests. If it’s not too difficult, I suspect that we will probably need to try and do this again because I think that the insights that you guys have put out so far have been quite remarkable. And in the future, maybe some months down the line to see where we are would be quite insightful. So thank you very much, gentlemen. I’m sure our listeners enjoyed you have a wonderful evening or afternoon wherever you are.

Speaker2: [01:53:46] Thanks, Philip, and thanks for facilitating this discussion and for sharing the signs. Because Robert will confirm this. People are in desperate need for this information because in contrast to previous time, people feel like they need no to do their own research for reasons that are very obvious, right? So thanks for four for playing a really crucial role in facilitating and contributing to this and have a nice weekend too.

Speaker1: [01:54:15] Great. Thanks. Thanks, Joe. How about?

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