Professor Dr. Geert Vanden Bossche: Impact of mass vaccination on the innate immune system and how to remedy
Dr. Geert Vanden Bossche: The impact of mass vaccination on the innate immune system and how to remedy
Dr. Geert Vanden Bossche has served in various roles at several vaccine companies throughout his career, including vaccine research and development. He joined the Bill & Melinda Gates Foundation’s Global Health Discovery team as Senior Program Officer and later worked as Senior Ebola Program Manager at the Global Alliance for Vaccines and Immunization (GAVI). In 2015, he questioned the safety of the Ebola vaccine used in trials by WHO in Guinea. Dr. Geert Vanden Bossche is currently conducting his own research on vaccines while also serving as a Biotech/Vaccine consultant.
This is an edited segment from the weekly live General Assembly on November 15, 2021.
[00:00:30] Shabnam Palesa Mohamed: It gives me great pleasure to introduce professor Geert Vanden Bossche.
[00:00:33] And he’ll be talking to us about the impact of a mass vaccination on the innate immune system and how to remedy it. Also, somebody very popular, certainly here in South Africa and around the world, for telling the truth, for having the courage to want to save lives and for doing so with a sense of honesty and passion. Professor Vanden Bossche you have 10 to 15 minutes, over to you.
[00:00:55] Dr. Geert Vanden Bossche: Okay. Thank you, Shabnam. And can everybody hear me? I think the best thing to do is first speak a few words and then I would like to propose that I share my screen for the PowerPoint slides.
[00:01:09] First of all, I would like to say that mainly I’ve been focusing a lot of on a immune escape and basically on one element of the pandemic that we have been tremendously underestimating, which is the impact in fact of immune pressure that we generate by mass vaccination, the impact of immune pressure on the capacity of the virus to evolve and and to escape from that immune response.
[00:01:34] But there is something I’m going to talk about today is something which is which is not very good news, either. Which is that this immune pressure that is basically put on the infectiousness of the virus by the vaccine anti bodies is also exerting a lot of pressure on our innate immune system.
[00:01:53] So that is the other thing. So we have been underestimating largely underestimating, the impact of widespread immune pressure first on the capacity of the virus to escape from the new response. And secondly, on the on the erosion of the, of the innate immune system, that’s what I’m going to talk about today.
[00:02:15] Unfortunately personally, I think it’s by far the most neglected and ignored aspects in the scientifical situation of this pandemic is innate the innate immunity.
[00:02:27] And I would just like to start out citing just one sentence from a paper that was written about innate antibodies, innate immunity in 2020.
[00:02:37] And when we talk about innate immunity, typically vaccinologists think about innate immune signaling, cascades, and cytokines and all this kind of stuff, which are in fact innate immune stimulators and innate modulators. We rarely hear about innate antibodies or innate cytolytic cells, for example.
[00:02:57] So for me that is really what the innate immune system is about the effector cells, but what was put in this paper, interestingly enough, is I just, as I’ve mentioned, since their initial discovery, early 1960, the innate antibodies were found in every vertebrate species investigate in mammals, in birds, in fish and reptiles.
[00:03:21] Nevertheless, innate antibodies have been regarded as contradicted with established immunological dogmas, but gradually received more attention in mainstream immunology.
[00:03:33] It’s really important to know that we need to focus on the this aspect. Since I’ve been doing this, I must say that I, I had already in all modesty some insight into the dynamics of this pandemic, but when you understand how the innate immune system is impacted.
[00:03:50] It just it just shed it shedding a lot of light on a number of that that that we don’t understand. Shabnam, if you will allow I would like maybe to share my screen in that way I could probably also, yeah, I think can, I don’t know where everybody can see my screen or.
[00:04:09] Yeah, so I, I forgot. Yeah. I think it’s a slides together in a hurry. And I forgot the type of it’s very important not only the impact of the mass vaccination on innate immune protection, but also how to remedy. What can we do about. I will not go very fast. There is a few slides that it will be new to everyone.
[00:04:27] And also for me, it’s the first time that I presented this kind of of very interesting things, I think. So, as I already mentioned when we talk about humoral and cellular effectors of the immune system, we know of course about the acquired antibodies and the T cells. And it’s very well known to everyone.
[00:04:45] What we know less well is the effect of the innate immune system, innate antibodies, and in T cells. And typically vaccinologist, and I’m a vaccinologist, don’t care too much about this because what we do is with the vaccines, we immediately use acquire antibodies and T cells. So we bypass in fact the innate immune system.
[00:05:06] Innate antibodies, there’s a lot of literature that I put also on my website for those who would like to to read those sources. I think it’s extremely interesting. And as I just mentioned, completely neglected field in immunology, and also certainly in in vaccinology. In fact, innate or low affinity antibodies that are polyreactive or poly- specific.
[00:05:28] So that means they can recognize a number of patterns that are shared by several different pathogens. It’s that they have not, they’re not antigen specific and they are also presemt in, in people, in individuals who are completely antigen inexperienced. So you don’t need to have seen one of the other antigen in order to mount this, or to have this, this antibodies.
[00:05:52] They are typically secreted by a short lived plasma cells. So the abbreviations in the next slide. By short-lived, if the plasma cells and to replace with aging, they’re replaced by long-lived plasma cells. And I don’t explain how this comes, because this is very important. This is about the training of the naked human system.
[00:06:12] They are what we call self directed and they are replaced with aging by ‘altered-self’ directed. So what does that mean? As a matter of fact the, during embryonic life, there is a lot of glycosylation taking place that is very important for embryonic development for maturation of proteins, et cetera.
[00:06:32] And so the newborn has a lot of innate antibodies that are in fact directed against some glycans, because remember when these cells that are heavily glycosylated are replaced, we knew you get, of course, a lot of I would say degree of uh, cells that’s start circulating and that is of course equipped or decorated with cell glycans.
[00:06:58] What to use is the wants to avoid of course, is that these cells components would be internalized vantage of presenting cells and presented to the to the classical immune system to be recognized as foreign. So the innate immune system and innate antibodies, what they are going to do is to clear to eliminate those cells or some flight components in a sense that the innate antibodies recognize cell glycans and provided they have in high concentration.
[00:07:27] They can also recognize glycans that have similarity with with the self, uh, glycans and they can simply eliminate that. First of all, yeah, this is a slide and I think Rob Verkerk is listening in that was from Rob an article that was recently published. This is just simply to demonstrate that the role of the innate immune response that we know that has been documented has been published typically responsible for asymptomatic infections.
[00:07:55] So you have to imagine, so these are, when you have a sufficient innate immune response, you have these two possibilities, but you don’t have to read briefly explain this. So we have to imagine innate antibodies, as I was saying, they can recognize cell glycans. They can also recognize the glycans that have similarity with cell glycans.
[00:08:16] Now, as a matter of fact, on SARS-CoV-2, we have a number of glycans that are self-like and also an influenza, for example, on RSV, on a number of these respiratory viruses called causing acute self-limiting infections. You have glycans that have a similarity with cell glycans and therefore can be recognized by innate antibodies.
[00:08:37] So either these guys come in and they were immediately recognized by the self directed innate antibodies, and they can be utilized to the same extent as, for example, a virus can be utilized by acquired antibodies, but if you have not and when that happens you, in fact, you prevent infection. So the virus is not even capable of entering the cell.
[00:09:00] In other cases, the virus will not be completely neutralized by this innate antibodies, but innate antibodies will bind and to make a mention that I have previously documented is also on my website, but I’m no not going to elaborate too much on this, but by a mechanism that is similar to the mechanism of the acquired immune system via antibodies that do not neutralize, so to say lifetime antibodies, but that can bind to the virus, can facilitate entry into denditric cells to then be recognized for example, by T cells. Here you have a similar mechanism where innate antibodies that recognize self like motifs on a number of viruses for example, can facilitate entry into a cell macrophages and can present patterns that self like motifs on those cells that they can get recognized by the cytolytic not T cells, but cytolytic NK cells. And when that happens, this is typically where we think that you may develop some very mild disease.
[00:10:04] You will also share a little bit of virus, but as innate immunity and T cells can react very fast. So this is typically is, are typically so to say the asymptomatic, asymptomatically infected people who may show a little bit of mild symptoms and will shed virus for, for just a few days at a pretty low concentration.
[00:10:23] But then of course thanks to the, uh, self-limiting NK cells [inaudible] virus will completely be eliminated. So important to, to realize already at the stage that we are talking about sterilizing immunity, we are talking about killing virus infected cells, or we are talking about neutralizing cells before they can even get into the cell.
[00:10:44] Okay. This is a slide with a little bit of texts. I think we should maybe just go through it.
[00:10:49] You mentioned innate anti cell antibodies are directed at glycan patterns on host cells. These glycan motifs share some similarities with glycan motifs on the surface of separate respiratory viruses. So on other coronaviruses and other than itself, for example, Corona viruses that cause common, cold so different from the SARS-CoV-1, SARS-CoV-2, those are fluid, for example, RSV all days or enveloped viruses that have glycan structures on the surface.
[00:11:17] So now provided there is sufficient capacity, sufficient concentration sufficient type that I would almost say of anti itself, antibodies soft environmental shift in the antigen environment of the newborn innate immune system. But does that mean a soft environmental shift? You go from cell to cell fly.
[00:11:36] So all of a sudden they don’t see the cells, the glycosylated structures have, for example cells that have been decomposed or that have been renewed but they know, see similar cell stretches or self-like structure on the surface of invaders, pathogens, viruses, for example. So that is a soft environmental shift in yet in gen environment that can still be recognized by these antibodies.
[00:12:01] So that is also the reason why you both mentioned respiratory virus can be neutralized or eliminated by this innate antibodies. It’s important that it’s at this point to emphasize once again, that these diseases there, or these pathogens costs harmless childhood infections. So they are a frequent in children, cause frequently infections, but mostly they cause asymptomatic to mild disease.
[00:12:30] So in other words it’s a childhood infection, but not a childhood disease because of the similarity of the glycans, with cell glycans, on the surface that can easily be taken care of by innate antibodies. And we know the innate antibodies newborns young people have have a lot of of those.
[00:12:48] So the insurance sufficient neutralizing capacity of the inmate and the self antibodies, as I was saying, if this capacity is not sufficient to directly utilize, it may be something vital clearance spine case. And that is an outcomes. Importantly, this is just in the acquired immune system.
[00:13:04] This phenomenon is going to lead to the induction of B memory cells or T memory cells. When this happens, when the neutralizing capacity of this antibody is not sufficient and the virus needs to be eliminated by the NK cells at that very moment. It’s like the new system is saying, wow, my-
[00:13:23] Did not sufficiently recognize the self-like pattern to neutralize it right away. I must do something to recognize it better. So that next time around I can eliminate it right away. And that is the training effect. So the fact that this virus or that virus gets eliminated by NK cells leads also to sensing its self sensing of progenitor B cells.
[00:13:54] These are the IGN secreting memory B cells that are going in fact to produce through plasma cells. Of course, and these are the lonely plasma cells, they’re going to produce innate antibodies of a higher affinity. So what does that mean have a higher affinity. That means that these antibodies, because of their higher affinity, they will now more readily recognize the cell fly because it’s not really itself.
[00:14:20] It’s cell fly. It’s similar to cell, but if the innate anybodies did not suffice to recognize efficiently this self-like switches of the virus, then this new antibodies they will know because they have higher affinity, they will now more readily recognize the self-like structure. And interestingly enough these cells do have memory.
[00:14:44] So it’s very interesting because here we are now dealing and most likely this is due but this is of course, a field of a very interesting research. It’s probably due to epigenetic changes that is training, that is what we call the training effect. The fact that the innate antibodies that are short-lived are now replaced by long-lived antibodies that have say memory and that have higher affinity.
[00:15:09] So there is a kind of near to of this whole thing that is more aimed at targeting the self-like structures. So this is the training, which is most likely induced by epigenetic changes. And of course it only occurs provided dividers does not break through the host innate immune system, because remember if the viral load for example is way too high, that the innate antibodies cannot deal with it, or when is very low.
[00:15:39] And for example in, in elderly, Then there is a high likelihood that his innate antibodies can barely do anything. They barely, they are not be the first line of defense. So to say the first line of immune defense is broken and then the virus goes immediately breaks through the innate immune system. In that scenario we have, of course you’re dealing with disease and we are dealing with induction of acquired immunity, but we don’t have a training effect.
[00:16:06] In any case of any capacity deficiency that is what I just said. For example, with aging, if there is insufficient antibodies or very important, we are going to come to this when the innate antibodies are suppressed and I will show what phenomenon leads to suppression of the innate antibodies, then a self-like virus for example SARS-CoV-2 or any of the others that I’ve mentioned can break through the innate immune defense.
[00:16:32] That is where you get natural disease. We are no longer talking about mild disease or asymptomatic disease. We’re really talking about moderate or even severe disease, and that can lead them to naturally acquire immunity. And that is the system of course, that we all know. This is to illustrate that sorry going too fast here.
[00:16:48] That lack of neutralization of the SARS-CoV-2 by self-directed antibodies. So that is the training phenomenon. Triggers and T help independent activation of this memory B cells. So that is the reason. This is not acquired immunity. This is in between. There is a memory. There is higher affinity. So there’s a kind of moderation but it’s T help independent in contrast to a generation of memory B cells and also a memory T cells in the acquired, according to the acquired immunity where you need a T help, this is a fee health independent phenomenon.
[00:17:24] So you have to imagine that if the title of the self-directed innate antibody is high, for example, in newborns, in young children, et cetera. And it decreases with age. So knowing the titer of this antibody is going to decrease when it’s there’s a certain level. The threshold I called the threshold of
[00:17:45] If there is fewer of the title is lower than this threshold, for example, then the innate antibodies can no longer contain the virus. And that is where it breaks through a DNA immunity. And that is where you typically get moderate or severe disease. So typically in older people, and that, of course we have seen is at the beginning of the pandemic or people with underlying diseases who have a very limited capacity, innate immune capacity, you will see that these people tend to develop a moderate or severe disease, but as a younger people, they will either neutralize the virus right way even without the shedding, without transmission, or they will aggregate the transmission and the infection via natural killer cells.
[00:18:33] And when this happens, you have the training effect. Okay. Important to note, severe disease almost is almost only the case in, in, in this scenario. We have, you have untrained, let’s say you start with untrained antibodies when you have live disease. So what it means as well is that if you now look at the number of individuals that happened naive and
[00:18:55] I mean,
[00:18:56] non-SARS-CoV-2 train innate antibodies at the beginning of the pandemic. It’s very high. Of course, when the pandemic evolves over time, you will see that more and more of the individuals will be confronted with the virus.
[00:19:11] Some of the figures I just mentioned, the virus will just break through and you will have disease and acquired immunity, but the large majority certainly at the beginning of the pandemic, we’re just developing asymptomatic infection. And a lot of them developed trained immunity, trained innate immunity.
[00:19:28] So what does that mean? The more you have people with trained immunity, the more easily you can of course eliminate the virus. And what we see is that if you look at public health, England, for example, data you have to look at this. At the start it is bar diagrams or by a bar graphs that they published in the reports over the last the last few weeks or the last few months, I should say. There you can see that over time, overtime,
[00:19:56] this, of course, all these people are all been vaccinated. Over time there is a very fast and a dramatic decrease in the infection rate in the non vaccinated. And that is a phenomenon that is typically due you to training, because these people come repeatedly contact with the virus. They start training, they have memory, they have antibodies are now very efficient, have high affinity and innate immunity.
[00:20:23] As we all know, acts very fast. Having such a reduction as you’ve seen the PhD data within one or two weeks, you will never ever see this with with acquired immunity. But so the important thing to know is that innate antibody. Can be suppressed by a specific antibody, specific antibodies.
[00:20:50] So when does that happen? I mentioned this several different time times in my articles. It’s really something very important to bear in mind when you go to an asymptomatic infection and especially those who did not neutralize the virus right away that needed to go through the NK cells.
[00:21:07] They have seen the antigens for a short while that they are innate immune system. They are serving their B cells not really thrive. So I’m not talking about innate immunity, acquired immunity and they develop anti spike antibodies that are short-lived. It’s a kind of a very superficial activation of the acquired immune system, but there is no memory.
[00:21:30] These antibodies have low affinity, but they do bind to the spike protein on the virus and by doing so, so these are the antigen spike specific disease. They can out-compete or compete at least with the innate antibodies, which are rebuilt the antigen specific, the poly specific reactive IgM antibodies.
[00:21:50] So due today’s phenomenon. The innate antibodies, can be out competed. Normally this takes only place for a short while. Why? Because there’s antigen specific. IgGs following asymptomatic infection use, or my alter disease usually lasts only for six to eight weeks after eight weeks.
[00:22:13] They are no longer detectable. So that means that that innate suppression normally lasts only for a few weeks. And then when these antibodies disappear, then of course you get back your full fledged innate immunity. So…
[00:22:28] Shabnam Palesa Mohamed: Professor, Professor Vanden Bossche is such a fascinating presentation. That’s why there’s a number of questions already for you in the chat. We are really interested in asking you through Tess, so if you don’t mind, what we’ll do is get a copy of your presentation that we’ll share with our affiliates, but we’d like to start with the Q&A section, if that’s okay?
[00:22:52] Dr. Geert Vanden Bossche: Yeah you can start with the Q and A, but this was just my observations but I can understand that that people, this is very new and I tried to simplify it to the extent possible. That’s why it’s taken me quite some time to do this, but please go ahead and I’m, I’m of course, happy to ask questions already.
[00:23:12] Shabnam Palesa Mohamed: Thank you very much. And I believe you’re joining our science and medical committee. So we’ll be in very good company with you sharing your knowledge and expertise. Professor Vanden Bossche a couple of weeks ago, you and I were having a conversation in which you said a very profound statement. I feel very concerned about Africa.
[00:23:30] We need to preserve people’s innate immunity on this continent and protect them from mass vaccination. Africa can cancel bold herd immunity. Whereas the Western world has completely destroyed that option because of mass vaccination of their population. Do you want to comment on that in the context of this very clear drive to erase innate immunity from science, health and medicine?
[00:23:55] Dr. Geert Vanden Bossche: Yeah. That one is a sort of say an easy one. As I just explained already, asymptomatic infection can suppress your innate antibodies. And I was just saying. Although asymptomatic infection is generating very lousy anti spike antibodies because they are short-lived.
[00:24:19] They have no memory. They are not really functional. They have not a high affinity, but nevertheless there, they can bind to the spike and that is already sufficient to suppress that. That was basically what I was showing in this slide, the suppression of the innate antibodies, due to for example immune pressure that exists following asymptomatic infection. Now to your question, this is very mild, because I was saying these antibodies, they are not doing a fantastic job in out competing innate antibodies because their affinity
[00:24:53] so it’s relatively low, but you can imagine, and that is one of the following slides that I wanted to show. If
[00:25:01] really prime your immune system you’re going to have of course, high affinity antibodies, and those are going to suppress in a much, much stronger way, the innate antibodies and that will have of course, several different consequences.
[00:25:20] But that is basically completely eroding the innate immune system in a sense that in those cases you will be all the time below the threshold of innate immunity. When you’re below the threshold will of innate immunity, it automatically means you can not have sterilizing immunity.
[00:25:40] It’s impossible. So you cannot prevent infection and you break through, you literally break through the innate immunity. So all what you then still have left of the vaccinal antibodies, which of course we know can not prevent infection. They cannot induce sterilized immunity. Depending on the strength of those antibodies,
[00:26:05] you will have maybe prevention of disease, but it’s no longer the case. The only guarantee that you still so to say have is that they prevent against severe disease. And we know that the virus, this is the whole story of the immune escape. That the virus is increasingly escaping from this normalizing antibodies.
[00:26:22] So when the time comes that you have more and more escape from these neutralizing antibodies. There is nothing much left really for the vaccines because the specific antibodies are no longer doing a good job. Their functionality has already tremendously decreased. Remember, initially we were promised is what they do is a herd immunity.
[00:26:46] Then it was it would reduce transmission that it was it will reduce disease. Nowadays, I put the bar as low as possible. Yeah, they still a bit use severe disease. That, that is problematic because you can no longer rely either on your innate antibodies that I was just saying, there is nothing that suppresses your innate antibodies more than
[00:27:08] antigen specific antibodies that have been primed. So that in other words, that interact with high affinity. So normally during a normal vaccination, there is no problem. I mean what would be the problem? You have high affinity antibodies, that’s fantastic. They have memory, they have high specificity.
[00:27:26] It’s only a problem when this antigen changes, when you have continuously new mutants because then the, this antigen specific antibodies don’t recognize very well, your dividers anymore. That is one thing. The other thing is that we are now dealing with a pandemic of a highly infectious variant. What does that mean?
[00:27:47] That means that people whether vaccinated or not vaccinated doesn’t matter are re-exposed all the time to this virus. All the time, twice a year, three times a year, 10 times a year. But every single time that your body, your immune system gets to see this damn virus, your immune systems will be boosted.
[00:28:06] So you have been primed by the vaccine. Every single time, your immune system sees a little bit of the virus or antigen, your specific antibodies and you will have basically permanent basis. So I just wanted to show here when you have the suppression of the innate antibodies, as I was saying you to, you too, the people had the asymptomatic infection. The problem is when people have asymptomatic infection, normally these antibodies specific antibodies disappear after six to eight weeks, but again, we are dealing with a highly infectious barrier. So that means that now the likelihood that somebody gets re-exposed to the virus before the short lived antibodies have disappeared increasingly high. So more and more people are now re-encountering the virus while still sitting on the short-lived antibodies because their reinfection took place within the next six or eight weeks after the first infection. So that is what in its own right already explains why we are now having a number of younger, sorry, of younger people who get infected, because that is the suppression for example, in young kids.
[00:29:22] So plenty of innate antibodies, they don’t care too much about the suppression. They still have plenty of antibodies, but here is the threshold, right? So you can see that for example, if people who are middle-aged for example, this mild relatively [inaudible] were still not talking about vaccinal antibodies. We’re talking about the shortening of the antibodies following asymptomatic infection, this suppression already suffices to make a number of younger people ill. That was not the case of beginning of the pandemic because we didn’t have this phenomenon. Now we do have this phenomenon.
[00:29:58] You see immediately a shift from A to B towards the younger ages. I would like to insist, so a number of younger people are now getting really the disease, even moderate disease, could even be severe, but still the vast majority of these younger people will recover from this disease without going to the hospital.
[00:30:18] The people who really get the severe disease, these are the people who get hospitalized, but probably had already some to a large extent underlying disease. Nevertheless, and this is really very important because that we all get killed with this bloody argument that still the rate of the vaccinated people is still hospitalized is still much lower than of the unvaccinated people.
[00:30:44] I will tell you the people that now go to the hospital, of the unvaccinated, and I’m not discriminating against the vaccinated or those who are not vaccinated that I really would do everything to help both parties, I would say. But primarily we are now seeing these people hospitalized and we are seeing some of those hospitalized that have been immune suppressed.
[00:31:06] So please remember that the people that non-vaccinated people that are now hospitalized are all people that have either underlying diseases, as was the case at the beginning of the pandemic, where we didn’t even have this phenomenon, but also people who are immune supressed. These people are immune suppressed. Their antibodies are to some extent out competed by spike-specific antibodies.
[00:31:35] So in other words, what we do stratification of the non-vaccinated people that are currently hospitalized, would we do stratification for underlying disease and immune suppression. We would simply see that the vast majority, the overwhelming majority of the people that are now hospitalized with severe disease are not the non-vaccinated, but the vaccinated people. That is very clear.
[00:32:03] There is a major confounder in this evaluation in a sense that we are not taking into account the non-vaccinated who need to rely on the innate immune system, if they have underlying disease or that very innate immune system. For sure they have a high likelihood to be hospitalized, but how can you compare all this, the hospitalized, the vaccine, the vaccinated versus unvaccinated without stratifying for underlying disease or immune suppression, which is the key element for the non-vaccinated to not only protect against disease, but even to protect against infection.
[00:32:42] As I was saying, this is inducing sterilizing immunity, I think that is very important, to understand. So competition with short lived specific antibodies, as I already mentioned are the reason for immune suppression, and cause of disease. So then you could say so yeah, you get the disease, but then you can develop in many cases spike-specific antibodies of high affinity.
[00:33:03] So that is what gets you acquired with immunity. And then, and these antibodies of course take care of the fibers that is when you’ll recover from a symptomatic disease when the virus has broken through your innate immune system. So in fact, the antibodies take care of it. That is where the idea came from.
[00:33:20] Well guys, instead of first separate from disease let’s vaccinate, so we can avoid disease and have these specific antibodies do immediately the job and we can simply bypass disease. And there is no problem because the viral transmission will diminish. When the virus transmission diminishes the antibodies titers will wane and viral transmission will diminish, because symptomatic infection, the um, the, uh, antibodies that are generated as a result of a symptomatic infection or have a broad spectrum of a broader spectrum than vaccinal antibodies. So to some extent they can indeed deal with variance. So when these viral transmission diminishes and the antibody titers way, and that innate immunity is restored.
[00:34:04] So what is the problem? The problem is if we can not control viral transmission or infection, then of course we have continuously the virus circulating and exerting this immune pressure. And that is a problem. So if we know, see what is the effect of vaccination? Then we see. So this was the effect let’s say of the short lived antibodies that are generated as a result of asymptomatic infection.
[00:34:33] And that could be present more or less in many variables on a permanent basis because they have continuously contact and they continuously re-exposed, but compare this to a vaccination where the anti-bodies, have much, much higher affinity, can readily out-compete these innate antibodies yet.
[00:34:51] They don’t. Yeah, they do. Yeah. But when you have a vaccine vaccinal antibodies, that then do this right away in people that have less innate antibody. So they have lower titer. They can even go below the threshold that is anti-self, antibodies can recognize self. Imagine when that happens, when these innate antibodies that are so important for homeostasis is there for clearing away self antigens that need to be eliminated from the circulation.
[00:35:24] If they can no longer do this, because they’re so big surplus to a level that is even underneath the threshold for recognition of the self antigens. By these innate antibodies, you can imagine what you get. These antigens have no longer going to be clear and could lead to autoimmune disease.
[00:35:43] So here, for example, When these antibodies, they are below the threshold of innate immunity. So here you break, the virus breaks through the innate immunity. Not only because remember these antibodies are not specific for SARS-CoV-2. This will also apply to other viruses with cell self-flying glycans on the surface, as I mentioned.
[00:36:07] So therefore, immune pressure by vaccinal antibodies, exceeds threshold for innate immune protection and therefore will prevent protection against severe or symptomatic infection by SARS-CoV-2 and other self like glycosylated viruses. As those that I previously mentioned in middle aged children.
[00:36:27] So this would be the middle aged children, and black here in black, in middle age, children that are. SARS-CoV-2 inexperienced. So they have very little or encounters with the virus. And of course, in older children in this older age group, the likelihood that you have more experienced individuals is of course higher.
[00:36:49] But they’re in this high affinity as specific antibodies, they can even suppress protection against free circulating cells, glycosylated cells in of course, people that have lower innate antibody titers, which are typically the case in the teenagers. So that leads to reactivity towards overload itself.
[00:37:09] That is the situation in SARS-CoV-2 untrained individuals. If we now look at the situation in the trained individuals, what is going to happen there? In trained individuals one has to imagine this, or people for example, older people who have much, much fewer innate antibodies. So if they have, so that, that means less it antibodies, it’s much more difficult for these people to recognize self-like glycans on the surface of of these viruses because there is they recognize it.
[00:37:46] Much more in a much more difficult way. So what they have to do that trained affected as the innate antibodies are so low. They can only compensate this by doing a training that basically leads to innate antibodies that have much higher affinity for the virus. So again, no innate antibodies, they go to the training system and this training will know, nevertheless, despite the low innate antibodies allow them to recognize these viruses simply because the change in affinity is much higher.
[00:38:24] So they go to a system that is much more auto self-directed it’s much more different from self. It has much higher affinity. This is the level of affinity, but nevertheless, the immune pressure by vaccinal antibodies. Of course, this is not only directed to SARS-CoV-2. There are also glycans on SARS-CoV-2.
[00:38:44] We do it on the other viruses that are much more different from the self glycans. And so even the vaccinal antibodies, the vaccinal antibodies can even out compete those. So the immune pressure by the vaccinal antibodies exceeds the thresholds again for innate immune protection and therefore prevent protection against SARS-CoV-2, but also against others viruses that will have glycosylated structures that are much more different from the cell life, because here the affinity is much, much higher following the training process, according to the or for the reason that I just explained.
[00:39:21] So this is going to happen now with middle aged adults, we will see middle aged adults, a number of diseases that are driven, that are triggered by viruses, enveloped viruses that have glycosylated structures that are very different from those on SARS-CoV-2 or other coronavirus influenza that are, for example, more typical for viruses like HIV, like EBV Epstein BARR, like cytomegalovirus, for example, and this high affinity and specific antibodies
[00:39:56] they can, even in people that have less trained antibodies, for example, younger people, they have less trained antibodies. They can even suppress any new recognition or free circulating altered self. If they go even below the threshold of recognizing altered self and they, by doing so, they infuse a kind of phenomenon of tolerance to all the self glycosylated cells that we see, for example, on certain cancer cells we all know there are certain types of cells or tumors that develop glycosylated stretches on their surface that are responsible for the immune subversion of the immune system.
[00:40:36] So in other words, this is in a summary. What we can expect to see is that because of this repeated viral exposure, We will have strong and sustained suppression of innate immune antibodies. It’s not like in a normal vaccination outside of a pandemic where the titers go down. No the titers will not go down because you get continuously due to the CELTA variant exposure and boosting of your vaccinal antibodies.
[00:41:02] So you will have a sustained suppression of that ‘naive’ innate antibodies, as I call this will lead to an increased incidents of its high to hit, but we will see, but I think we’ve already seen some of these cases where you’re you see increased incidents of disease or severe disease. And that depends, of course, on the antigen specific antibodies.
[00:41:21] You, you cannot no longer protect them against infection. So will you have disease, moderate disease or severe disease? This will, of course, depend on the vaccinal anti-bodies. When the vaccinal antibodies would still protect against disease. Okay. You cannot protect them against infection because you broke through the innate immune system that you can still protect them against disease.
[00:41:41] But right now we can add. Protect against severe disease, thanks to the vaccinal antibodies themselves. So incidents of disease will be increased not only SARS-CoV-2, but also other similarly glycosylated viruses all the coronavirus RSV, flu, for example, in middle aged children, depending on the presence of antigen specific antibodies, the increased incidents of autoreactive and towards autoreactivity towards self-like glycosylated cells in teens and teenagers who have lower, low innate antibodies, therefore this suppression by vaccinal antibodies can put innate antibodies down to a much lower level where they are no longer capable of recognizing.
[00:42:22] Self structure, some components that would, that need to be eliminated from the circulation in order to not induce or autoimmunity in the train for the training. People, I would say the, there is an increase in incidents of disease or severe disease again. So of course by SARS-CoV-2 and all that, but now different glycosylated viruses.
[00:42:43] I just mentioned that. In middle aged adults, depending on the presence. Again, antigen specific antibodies, some of these people will have antibodies acquired antibodies against the MB for example, against Epstein BARR. And will still be able to prevent disease, but those who don’t have those, they have, there has been latency for a wrong time and types have been declined.
[00:43:03] They are at the risk of developing severe disease. On the other hand, we will, it’s likely very likely that you’re going to see an increase incidents of tolerance towards ‘altered self’ glycosylated cells in young adults. Of course, the stronger the immune pressure, the higher the affinity of the vaccinal antibodies.
[00:43:20] For example, if we now start boosting these people, or when we start when people who got vaccinated get boosted naturally by the circulating viruses, we are just going to increase the affinity of the vaccinal antibodies. You can imagine that higher the affinity, the more we are going to out-compete the innate antibodies and the more the incidents of other acute respiratory diseases and self-glycan-specific autoimmune disease will extend to children of increasingly lower age for as far as the other respiratory disease are concerned and higher age for as far as the self-glycan-specific autoimmune disease is concerned. You see exactly the opposite for the trained people who got their innate immunity free, the more the incidents of chronic viral diseases, enveloped viruses, and all the glycan-specific tuber disease will extend to adults of increasingly higher and lower age respectively.
[00:44:13] So that means more increasingly higher age for viral diseases. So in older adults and a lower age, for those who develop are prone to develop tumor diseases, of course the aim of any vaccines and any other intervention. I know Dr. Cole has been talking about it, that dampens recognition of PAMPs, of the pathogen associated molecular patterns.
[00:44:37] For example, because this was on purpose done for the MRNA vaccines in order innocuously use a new response against the RNA, but what it does is that it dampens the recognition of the pathogen associated molecular patterns. And that of course, will enhance even enhance the immune suppression by the antigen specific antibodies.
[00:44:55] Shabnam Palesa Mohamed: I’m going to have to ask you to pause there. There’s so many questions for you and well deserved because you presented such complex information in ways that people can generally understand what it is that you’re trying to convey. And for us as the world council for health, it’s an absolutely invaluable contribution and service that you provided.
[00:45:16] So what we’d like to request those of you who have asked questions to professor Vanden Bossche, can you send them to him directly. So he just, so in case he doesn’t miss them in the general chat, but when you’re responding, can you go reply to everyone so everyone can see your response? If you can do that, absolutely brilliant.
[00:45:35] Dr. Geert Vanden Bossche: Well it will depend on how many questions there are, of course. But yeah, I can try.
[00:45:41] Shabnam Palesa Mohamed: As many as you can, if you can text your response to everyone, we would really appreciate that. Thank you very much, professor Vanden Bossche. Like I said, your service to science and health is invaluable.
[00:45:51] We appreciate you very much. World Council for Health and of course, affiliates around the world, professors Vanden Bossche is a one of six speakers or panelists at this time for humanity trailblazer town hall, hosted by Trial Site News in association with the World Council for Health this Saturday, the 20th 7:00 PM central African times. You can register on trialsitenews.com.
[00:46:14] He will also be at the African health summit this Thursday. More details on that soon. And of course, professor we’d love to host you as the World Council for Health in a one-on-one interview to give you the kind of space you need and deserves. It will try to find a spot in your diary. Thank you very much for contributing this evening