McCairnDojo.comPast episodes & related streams

Study Hall: Immunology of Long COVID with Akiko Iwasaki (Nov 10, 2022)

Hello, everybody. I'm still just trying to figure out how to do everything here. I'm sorry. I'm being such a dork.

I'm still trying to figure out how to get all this to work correctly.

It should be okay. But I still don't have that switching, because that won't switch.

I'm not using any inset anymore, and now that I'm switching that way... this...

...then I actually don't have that either.

But I can do this, right?

So today we're going to watch a video by Akiko Iwasaki, immunology of long COVID. I hope that this is going to work out all right here.

Just get this off.

Captain Kirk will keep coming in all the time if we don't put him away for now.

As I try to get this all going. Here we go. Welcome, everyone. We're pleased and honored to be hosting Dr. Akiko Iwasaki this evening and to have so many people in attendance. I'm Leslie Kremholtz. I'm the co-founder of Hugo Health Kindred. And for those of you that don't know, really quickly, Kindred's building a network of what we call data-enabled people who've been impacted by COVID and who want to contribute to research in partnership with leading scientists. I strongly encourage anyone who is not a member of Kindred to check us out. I have put a link to the website as well as information about the LISN study. If you're interested in joining LISN, you need to actually join Kindred first. The LISN study is being led by Dr. Akiko Iwasaki and Dr. Harlan Kremholtz. So I'm not going to take up another second of your time. I'm going to pass this right over to Akiko for introductions, kick off this very important presentation. And once again, just to say thank you so much for spending an hour of your evening with us. So Akiko. Thank you so much, Leslie. I'm delighted to be back on the town hall again with Kindred Hugo Health. And I'm also delighted to be sharing the stage with my colleagues, Ornali, Cesar, Harlan. So very happy to be here. All right. So I'm going to jump in to my talk. Okay. Hope you can see this. Okay. So what I wanted to do today was to give you an overview of our current understanding of long COVID, particularly immune responses in long COVID. And also, I'll spend some time at the end speculating on how vaccine-related long haul could occur based on some of the data that the Yale LISN study has already collected from many of you participating tonight. So before I go in to discuss long COVID, I just want to emphasize that COVID is not the only infection that results in post-infection, post-acute infection syndromes. And I was fortunate enough to co-author a review with Jan Ciotka and others on this topic, which is really important to keep in mind because it means that many other viral and non-viral infections can lead to prolonged symptoms, some of them leading for decades of disease and others kind of having an onset that is much later than what we're seeing with long COVID. Something that happens decades after the infection. So there is a lot of complexity into these post-acute infection syndromes. They haven't been really well studied. And that's something that we're going to change by studying these diseases at the molecular and immunological level to understand what might be going on. So the long COVID pathogenesis, there are multiple hypotheses that have been raised. I just want to go over the four major ones. There are many others that have been proposed. The first hypothesis is the viral reservoir of viral pathogen associated molecular patterns. And this is a hypothesis that says that even though the viruses are considered acute infection, it's possible that these viruses may remain in some form of replication capacity, may not be infectious particles, but they are remnants or they are parts of the virus that resist being removed. And that could be persisting in a person. And that could lead to recognition of these pathogen associated molecular patterns like RNA structures, or it could also lead to the expression and persistence of viral antigens that lead to chronic stimulation of lymphocytes. So that's one hypothesis. Another one is autoimmunity. Many infections precede the onset of multiple types of autoimmune diseases, multiple sclerosis and lupus and many others. So it's possible that the COVID infection can be leading to stimulation of bystander or molecular mimicry autoimmune responses, and that could be prolonged and leading to symptoms. The other possibility is this biosis of gut microbiome, or reactivation of latent viruses. So, all of us, many of us, most of us carry multiple different viruses, and many of these viruses don't cause any diseases but they remain in the host as a latent form. And these types of viruses can become reactivated upon immunological stimulation or immune suppression that may be caused by COVID, and that reactivation itself could trigger this virus to become activated, replicate, and then cause disease. The final possibility is tissue damage, and this is, you know, virus infection and or immune responses that are induced by the infection that can be triggering tissue damage that is hard to repair, like fibrosis, and that could be lingering or very difficult to restore in a long term, and could be leading to disease. And I'll give you examples of each of these hypotheses. So there are over 100 papers now, demonstrating some form of viral antigen or RNA that's present in people with COVID, months after the infection, and many of these virus antigens and RNA has been located in the gastrointestinal tract. So this may be a place of reservoir, or at least some antigen being remnant there. There was a very nice study by Jim Heath's group that demonstrated that EBV Epstein-Barr virus viremia at the time of COVID diagnosis is one of the four predictive factors for developing long COVID over the three months period that they were studying. So right away she's bringing up other viruses, right away she's bringing up coinfection, right away she's bringing up re-stimulation of dormant viruses, right away she's bringing up microbiome dysbiosis, right away she's bringing up the sustained viral protein reservoir. She's bringing up a lot of things that we know have existed before COVID, have manifested before COVID, have been brushed off as imagined before COVID. And so it cannot be underestimated how wicked of a thing this long COVID mythology is because again, even though our current speaker is being quite honest about it, she's not pointing out that this honesty is not reflected in the television, it's not reflected on the news, it's not understood by the average doctor. And it needs to be understood by the average doctor. She should spend most of her time explaining how this is not a new phenomenon. Anyway, I just wanted to make that point. So it's been reported in other studies also that EBV can reactivate and seems to be happening preferentially in people who develop long COVID. The other finding from the same paper demonstrated that lupus-related autoantibodies are elevated at the subclinical level in patients at the COVID acute phase, who then go on to develop long COVID, the second of the four predictive factors for developing long COVID. And then there is this tissue damage. So we, with Professor Michelle Monge's group at Stanford, demonstrated that even a mild respiratory only infection with SARS-CoV-2 in the mouse model can lead to significant damage in the brain for extended time period for over six weeks post infection. Whereas similar types of prolonged damage was not seen with mild influenza infection. So there's something about SARS-CoV-2 that may trigger this long term tissue damage, even if the infection itself is completely resolved. So we suspect that long COVID is a multiple diseases under one umbrella, and that there are multiple endotypes of diseases with different drivers, molecular drivers. And if we can subset long COVID into the right types of disease drivers and target the root cause of disease, that would be the best way to go forward with therapeutics. There's also the interesting paper where they train dogs to detect inactivated SARS-CoV-2 infected supernatant, and these dogs were able to identify in a blinded manner, 51% of the long COVID patients, their clothes, whereas 0% of the controls were identified by these dogs. This, to me, indicates that there are volatile organic compounds released by the people with long COVID and likely having to do with the virus infection itself. That's why I put that in the viral reservoir category. That's unfortunate. That seems like a very, very big jump there to assume that what the dogs are sensing in the clothes of long COVID patients is directly related to the virus would need a long viral syndrome from somebody else with a different cause to be put in there as a control group before you could ever make that statement. That seems a very irresponsible thing to say. She's essentially jumping to the conclusion that it works in one particular way. And then also very carefully not admitting that if it works that way, which is that it comes from a viral protein, it's number one, likely the protein that gets made the most during a viral infection, which is the spike protein, and therefore it is the protein that was present and is present after the transfection. So I'm already a little bit frustrated because we haven't talked about this at all in the paper, that the expression of protein of viral protein is driven by the transfection. And it is the protein that is expressed the highest of the highest levels, as far as all the monitoring that we're capable of doing genetically and otherwise of viral replication, it is the spike protein that has the most abundant sub genomic RNA. It is the spike protein that's only present in the transfection. And so, until she starts to become very specific about what she's comparing and very specific about what's present. It's sketchy to me, and that last statement is extremely sketchy to me. That's just me listening. Just listening. There's also papers from David Waltz group that demonstrated circulating spike protein in people with long coven. So this sort of reservoir antigen RNA, there's a lot of accumulating evidence for it, but that may not be the only root cause for long covered. So today I want to discuss our latest work on collaboration research that we, we've done with monsignor group, led by Dr. David Patrino, who is just an amazing human being and a great leader who is treating people with long coven thousands of people with long covered from the very beginning of the pandemic. And he his team listed here Jamie would lower topic of the name Dana McCarthy, and our team at Yale have collaborated to dissect the immunological phenotypes of people with long coven. And these are the co first authors of the paper, john Klein who led this study and currently working on the review. And so what's unfortunate about this is is that you're going to find very quickly that what we're going to look at is we're going to start out with the idea that this long spiral syndrome has been around for decades, but poorly understood. Now we have another example of it and we're going to study it as an island. And so I want you to see how how pigeonhole this investigation is from now on I'm just guessing what it's going to be but my guess is they're not going to compare it to chronic fatigue syndrome they're not going to compare it to the symptoms of anything else. They're not going to compare it to any other data sets that were produced before the pandemic on long viral syndromes, even though she started with an introduction, which made it seem like she understood that these things were likely to have a common mechanism. Are you starting to see how the bamboozlement works will give you money to study that. And even though you know it's related to these. I'm going to focus on that. And so, careful titration of money grant calls and careful encouragement and promotion of people who stick right to the science, the science that they're supposed to do the science that they were told and paid to measure, which in this case for all of these people is people with symptoms as defined by covert infection PCR positivity and certain symptoms. We're ever going to invest any time and looking at the manifestation of other long viral symptoms, long viral syndromes that existed before the pandemic to see if there are any clues as to a common mechanism because that is not the goal. We want to make COVID as novel as possible vision of this paper so we don't want it to be something that has a common is with anything in the past in our rings lab, who's using this rapid excess or audition profiling to look for antibodies against our own antigens auto antigens as well as viral antigens. Lou is a brilliant student in David von Dykes lab, who does machine learning on all the parameters that we've measured to try to predict which factors are most contributing to long COVID. Lou tirelessly looks at everyone's peripheral blood mononuclear cells, using real time flow cytometry to look at the cell types in the blood. Jeff and Sasha have been working very closely together to look at the patient data as well as antibody reactivity to extra SARS-CoV-2 antigens. So, this Mount Sinai Yale long COVID study is currently in med archive, anyone interested can read this, but just to briefly go over what we've done was to recruit participants from the Mount Sinai long COVID clinic, and to study a variety of electronic medical records from the quantum survey flow cytometry to look at cells that are in the blood. Human exoprotein, this is the REAP technology developed by Dr. Ring's lab to look at autoantibodies. SARS-CoV-2 antibody profiling, peptide display library to look at linear epitope mapping of antibodies from these patients, and used plasma proteomics to look at plasma factors that are distinct in long COVID patients. First, just briefly about the demographic nature of these participants, the long COVID patients listed always in purple have, most of them are between 30 to 60 years of age. There are some younger and some older, and similarly the convalescent control, these convalescent control groups were people who were infected around the same time as those people with long COVID, but have recovered from COVID. And their age group was similarly enriched in 30 to 60 years of age, some younger and some older. There is no significant difference in the age, and the sex is female dominant, this is seen over and over in every study on long COVID, there's definitely sex bias for female. Also, we focused on people who did not, who were not hospitalized. We wanted to focus on so called mild COVID that then turn into long COVID, because this is, we believe is a distinct disease from those people who were in the ICU and who were receiving drastic medical treatment versus people who were staying at home and, you know, fighting the virus infection, but then develop long COVID. So days from acute COVID in the convalescent control and the long COVID are again not significantly different. They were overall 400 days out from the original infection. So these are the first wave of COVID that hit New York City. And so we're looking at a much later time point than most studies that have been reported. And so we're also looking at a very specific clone. If there was a unique SARS virus, which hypothetically was released in Wuhan, Iran, Italy, Spain, and New York City in Washington, for example, that's one scenario. I think that my most parsimonious scenario is that of a virus already present in the background. And if it was necessary, perhaps a few seed cases, but that's it. So what she's speaking of here are specifically looking at those first cases in New York where hypothetically, and again, I've said this many times in terms of trying to explain how I'm sure that there was a virus and I'm sure that it exists. I'm not at all saying that there's no virus for all the people out there who are trying to twist me into saying that. But again, I am saying that the no virus argument holds a lot of water because of so many aspects of the real data in retrospect. So, I'm of the bent that in 2020 during the first part of the pandemic several different places in the United States and around the world had some cases of ARDS a unique lung disease possibly caused by an agent and RNA based agent virus or otherwise. So she's talking about the first cases in New York City. These are people with this long COVID and these symptoms. These people could have been exposed to the original pathogen the original agent. Presumably had amongst its expressed proteins, the original spike, which made it into patents which made it into the original formulation of Pfizer and Moderna exposure to that original spike, which I would argue did not travel beyond the release points. At least not very far, and not to very many people before it fizzled out and disappeared. Those places would have had these syndromes those places would have had these severe cases, those places could provide this data, she could be presenting genuine long viral syndromes caused by the agent. First, looking at the immune cells that are in the peripheral blood and looking at various different cell types what we noticed was that there is increase in non conventional monocytes. These monocytes are known to patrol the body for viral infections and other infections so that's elevated in long COVID. There was a reduction in dendritic cell subset, known as CDC ones, and these cells are critical in priming cytotoxic T cells and type one TH one cells, which are important to fighting the virus infection. They elevated activation of activated B cells, as well as double negative B cells. So these are the features that are were elevated in long COVID. So it again suggests that the B cells are being stimulated by something, whether it starts could be to or some other antigens. I also find myself wondering there was nothing no discussion here of whether these people had taken the transfection later, presumably they hadn't if this is from the first wave in New York. So it's a curious set of data. It's definitely a curious set of data I wonder for example how many of these people were ventilated. How many of these people had remdesivir. How many of these people were given other treatments but how many of them are ventilated is super important how many people are given other treatments like other vaccines is also important. So we're not looking at this from the. Let's get everything into the bucket and then see what we catch this is really already assuming that the syndrome that they have is caused by the virus cause called SARS-CoV-2. That's the assumption that they're making. And there is nothing in this data, nothing in these experiments that will prove that otherwise. Experiment here that's designed to show you that the SARS-CoV-2 virus is the result of this or causing this or making this happen. You should see that as being at least dubious. We don't know. In terms of the T cell subset. So here we're listing the CD4 T cells on the top and CD8 T cells on the bottom. There's really no need to go into the detail of these markers but suffice to say that the CD4 T cell and CD8 T cells there is a significant increase in the exhausted T cells. Exhausted T cells have been seen in chronic viral infections and cancer when the T cells are stimulated over and over seeing the same antigen and they basically go into this state of exhaustion where they are not no longer very functional. Okay, so here's the immunologist telling us that we've seen this in cancer. We've seen it in cancer treatment T cell exhaustion. I'm really curious as to how the CDC and the FDA get off saying that children can have a vaccination four times to something in their life. That my kids could in theory have a flu vaccine every year. That in theory, you need four DTAP shots before you're done. That in theory, we should have had four COVID vaccines by now because we would have taken a booster and then a bivalent. So here she is Yale HHMI master immunologist just telling you the truth, but then only selectively applying it to certain stories and certain ideas, but when it comes to transfection she doesn't have any opinion. When it comes to transfecting children of six months age and over, she doesn't have any opinion. Even though she's very well aware that overstimulation of T cells results in exhaustion, which is far from optimal. It's not really the best way to augment the immune system. She knows that. So what are we talking about here? How is it that we can talk about long COVID and the possible reasons why long COVID is occurring and then not realize that four shots is too many? And we only not give four shots of COVID, but we give four shots of a lot of things to our kids. Why? And so that is elevated in the long COVID patients. And interestingly, when PAY1 looked at the ability of these T cells to secrete cytokines. So cytokines are important factors that are released by T cells to communicate with other cell types throughout the body. What we saw was an elevated cytokine secretion or production from CD4 T cells from long COVID patients for IL-2, IL-4, IL-6. These are cytokines, IL-4 in particular are known as TH2 cytokines. And these cytokines are very important for fighting Hellman's infection, like these warm infections, but are not very effective in fighting virus infections. And we're seeing elevated levels of all these cytokines. In particular, the IL-4, IL-6 double positive T cells, T cells that secrete both of these cytokines, were pretty much only uniquely found in the long COVID patients. So this is interesting because the kind of T cell you want to fight a virus infection is known as type 1 or TH1 immunity. And we're not seeing that. We're seeing something that's diverting from that protective immune response against viruses. We then looked at antibody responses to SARS-CoV-2. Okay, here we already go to antibody responses. She just skipped over the best part that she was saying. And what she's saying is that it's not moving toward the type 1 protective response in T cells, but it's moving to something else. What's frustrating about that for me as a budding immunologist is that I understand the immunology system, the immunological system in our body as having two extremes. One is an elimination. That's a foreign toxin. And the other is a tolerance because that's a tasty food. And somewhere in between is where the immune system operates most of the time. And so if you're telling me that you're moving from a protective for an elimination response, you're moving toward a tolerance response. It's very easy. And I'm not really sure why in light of the data that's out there in light of the things that we understand about the immune system, people didn't say this a long time ago. That if the transfection or repeated transfection of people with the spike protein allows them to be repeatedly infected, then we are essentially creating tolerance in those people for viral infection. We are going to weaken them forever. Will it kill them? I don't know. But will it make them a constant carrier of viral viruses, a constantly higher viral load of anything that grows in them? Perhaps. We're dealing with a very, very dangerous situation here right now, ladies and gentlemen, because the the facts about how immunology works have been remained unchanged since the beginning of the pandemic. That's one of the reasons why I found myself on such solid footing in the end of 2020 when I decided, OK, I guess this summer and fall, I'm going to learn immunology. And in so doing, I got way ahead of the ball, way ahead of everybody, really, because they were playing the I've got immunity antibodies, right? I M M U N I T Y. That's what I got. I got bodies anti. And so that whole story blew up right away in the beginning for me. I didn't need to be I didn't need to be awakened for that part. And ever after that, you and I have been ahead of this. This is the reason why this is also so easy to understand. It's terrible and somehow comforting. We're not crazy. So what we noticed was that antibody against the spike protein or the S1 region of the spike protein or the receptor binding domain that actually binds to the target cells. They were elevated in the long covered patients over healthy controls or accomplishing controls. So the healthy controls, I forgot to mention, are people who've never been infected with covid, but live in the same area. And all of these people have gotten two doses of vaccines, so they should have equal levels of antibody. And yet what we're seeing is an elevated levels of anti spike antibody from long haulers. And I'll come back to the functionality of these antibodies later. We next looked at what are the most distinct factors that are found in long covered patients compared to non long covered patients or controls. And what we found was that the number one, the most significantly different factor we found in the plasma of long covered patients for the cortisol level. So cortisol is a very important hormone, it's known as stress hormone, but that is a. Where am I going to go with this one. Where am I going to go with this one. Come on you know you can say it, say it out loud before I say it. They don't have the measurements of these people's cortisol before long covered onset. So they're looking at people with long covered and people with our control groups and they're saying that they have more cortisol levels, but we don't know if they were already that way before they got infected. And if they were that could be the main variable. That your immune system is in a certain set state, if you're in this high cortisol level for a long period of time who knows bad boss bad marriage, terrible kids lost your job, I don't know. But you need to understand that this is a multivariate system. It is the interaction with your environment, which is everything outside of you. And your immune system, which is supposed to kind of be the gatekeeper between everything that's you and everything that's outside of you. And the thing that strikes me the most about this in the recent weeks is that injection intramuscularly is something that in all actuality, your body was never designed to deal with. Your body was not designed to deal with intramuscular injection. This is where intramuscular injection is used in nature. It is used in a lethal way. The things that are supposed to enter our body are supposed to pass through the air and through the lung blood barrier or they're supposed to pass through our gut and pass through the gut blood barrier. Everything is supposed to enter our body through intramuscular injection full stop. I'm off topic there sorry bit of a misnomer because it's needed for everyday physiological function, like how we nutrient handling glucose utilization wakefulness. Many different aspects of physiology is controlled by cortisol. And if you look at this panel. So what she's saying again is that if your cortisol level is that much higher than your average human, and you have long COVID. That's interesting. What she hasn't said is whether or not that cortisol was present before they developed long COVID and therefore can't say if it came first, and it's the chicken, or it came after and it's the egg. Or it's the egg that came first and the chicken that came but she doesn't know. And so again we're waving or hand waving we're looking at long COVID over here. And we're still not comparing it to any other long viral syndrome. We're not trying to see if it's the same we're not trying to find parallels with other treatments it's frustrating. The long COVID patients in purple. They had about half the level of cortisol, compared to the healthy control. And this is the most significant because they were uniformly lower than the control groups. Whereas other factors there is a huge variation. Some people have very high levels and low levels, but the cortisol level was the most tightly different distinct between these groups. The cortisol is secreted by the adrenal glands, and it performs very important function it's a diuronal hormone, which means it is the highest level right around the time you wake up, and then it level levels down during the during the day. And the wakefulness is controlled by cortisol. If you have very low cortisol it's very difficult to wake up and be motivated to start your day. And it's tightly regulated through this hypothalamic pituitary adrenal axis, the HPA axis. And so we wondered this low cortisol, whether it's low cortisol driving higher levels of this other hormones for them from the that's even worse. Usually when you have lower than so anyway I'm going to pause this for a second because I was a little lost there sorry about that in order to. Unless I was not listening well enough to her. It's lower cortisol which it doesn't change the interpretation right number one, let's go back to Katie's point, the low cortisol is easily something that the dogs could smell. That's, that's almost obvious. If they can't smell the low cortisol they can smell the baseline cortisol in the people that are awake. So, that's interesting. A low cortisol, changing the way that glucose is available. Changing your activation and general yeah wow alertness that's really extraordinary now. Now it makes more sense to me. Again, again, even more important now in my mind because low cortisol levels are things that are associated with certain long term psychological states whereas I think race cortisol. That's, that's, that's harder to sustain. This actually makes more sense for the argument that I was trying to make which is that we need to know whether these people already had this, you could almost see it as a type of depression. Before they got the long coded. And then this just took a deeper, or they were set up for that kind of thing that's that's important to know. Sorry about that screw up compensate for that low level so you make more and more cortisol. That is not what's happening with long coded patients, meaning that something upstream of adrenal gland potentially the pituitary glands, or the hypothalamus. There may be dysfunction up in the CNS region, and that's leading to this low lower levels of cortisol. It's important to note that the collection, and that's something I think that is present widely in the American population, a sort of imbalance in in these basic hormonal feedbacks. And that is due to malnutrition that's due to a lot of the chemicals were exposed to the toxins were exposed to the bad food, bad water. So, I get more and more skeptical as I'm, as I'm paying more and more attention to this again because she's presenting all the data in, in terms of long coven itself I think she's doing a fairly good job of trying to give it out there without explicitly saying that we don't really know what long code is and it's probably related to all these other things. I'm sure we would find a similar lowered cortisol in those other long viral syndromes and if we didn't, that would be a thing. I hope that point is clear. If we looked at a bunch of chronic fatigue syndrome people from 2020 and we found a low cortisol level. Wouldn't we want to think about that. Frustrating it's very frustrating. The plasma of the blood was around the same time in the all the three different groups, meaning that the changes in the cortisol level has nothing to do with the diurnal nature, or when we pick these blood samples from these patients. So, and then cortisol is number one, but there are other inflammatory factors, such as interleaking eight is a very well known chemokine that attracts neutrophils these are highly inflammatory cells. We also have many different chemokines again chemokines or these factors that recruit white blood cells to many different tissues, as well as some, some complement factors so there is definitely something inflammatory going on. So what's driving this and why the cortisol level is lower is currently unknown, we suspected something to do with the HPA access deficiency. Okay, so what about these other hypotheses. We didn't look at dysbiosis in this study, we probably should do this in the future, but we did look at reactivation of latent viruses. We did this in three different ways and found the same answer. So one way in which we did this was to look at the REAP score this is the rapid exoskeleton androgen profiling, which enables us to look at antibody reactivity to like thousands of different antigens, some of which were viral antigens. As I mentioned just a few slides ago, the antibody level against the spike receptor binding domain was elevated for long COVID patients. However, what was striking is that we also saw elevated antibody level. And I think that's a little curious again because if there is anything right about the story of the clone, it would be that they inserted. They inserted epitopes, which would allow the protein that contained those epitopes to virtually guarantee T cell activation and seroprevalence generation. Now there are a couple of different hypotheses I have for what they put in there, but one of them would be the obvious DC sign epitope that's contained in the diffuse document. Now DC sign was identified in the spike protein before the diffuse document was released. That's one of the reasons why I find the diffuse document to be a little too convenient because Jiki leaks or I think actually it was ducky and clucky and the chicken that identified DC sign and a specific or a non-specific T cell epitope, the exact same term that Herod von den Bosch has used in a interview with Brett Weinstein saying that the spike protein of SARS-CoV-2 had a non-specific T cell epitope in it. And that this would be a problem because T cells would be activated, but they wouldn't be activated in a specific way. This was something that Herod von den Bosch tried to explain several times. This would lead me to believe that this is evidence for it because the receptor binding domain, that part where DC sign is embedded around, where the spike protein is cut near the furan cleavage site, DC sign is just on that side of it. You can imagine a scenario where always everybody exposed to that spike and in this case that would have been the spike from Wuhan. The clone actually there would have had this problem or a propensity for this problem. I think long COVID could be tied to the DC sign sequence. And so I don't think that there are too many people now developing long COVID anymore as a result of an infection that they're getting now. However, people who have been infected by the original virus in 2020 may have developed a long syndrome because of the presence of that non-specific antigen epitope, whatever. That's my crazy idea. There's the Zoster virus. These are sort of mononucleosis and chickenpox viruses that most of us, before the vaccination for chickenpox, most of us carry these viruses inside of us without any symptom. But under certain stress, such as a COVID infection, some people are elevating this level of reactivation of these viruses. And what's intriguing is that this is a highly elevated in long COVID compared to the convalescent control or the healthy control. Antibodies to other viruses. You see it's zero prevalence they're looking at to other viruses. So the zero prevalence to flu is going down here. Zero prevalence for for NL 63. That's one of the and and and two to 90 the receptor binding domain antibodies go up as well. So I'm not really sure what to think about this, ladies and gentlemen, other than to say that the immune system is activated and they have a lot of zero prevalence that the controls don't. Again, leading me to believe that there was a a synthetically designed protein that your immune system couldn't ignore. It was designed to be unignorable. So your body had to respond. Why do I think this is a cool idea, because if you found such an epitope, then you could make a product that would always produce an output. In other words, every time I stick you with it, you're going to show an antibody boost. And so obviously my product works really well right. Most previously adjuvanted vaccines would not have that three, four dose effectiveness measured by a bump and zero prevalence, because that's not how immunity works. But if they had discovered some kind of nonspecific T cell activating epitope that they could insert in there so that any protein that they made via via transfection would be impossible for your body to ignore and would have to produce antibodies to Tata. Well, now they have something. I don't know maybe that's too complicated to be explaining like this people, how many people have latent viruses, there was no difference in these groups. So it's only the reactive. So reactivation dependent antibodies that are elevated. And there were some other differences like herpes simplex virus specific antibody was slightly lower than the controls. So I told you we did this three different why didn't you mention measured reactive antibody is through ceremony, which is a linear epitope mapping strategy very different from reap, but we found the same answer. So, this is the reap data for the GP 42 which is a glycoprotein glycoprotein on the surface of the BB. The IGG against this is elevated in long coded. And also, this middle panel is from the ceremony analysis. We found that only GP 42 yeah but look at the data guys. Look at the data above my head here. Look at how many of the long coded patients do not have this rise level of IGG targeting GP 42. How many of them don't have a raised elevation prepared to the healthy controls what in the hell are we talking about here. How can you tell the story if so many of these patients don't have the elevation that you want us to believe is responsible. Don't you find that a little annoying. And pinpoint the specific amino acid sequences within the GP 42 that the patients are reacting to. And we mapped that right here in this pink. So this particular set of amino acid is being recognized much higher in long coded patients competitive controls and GP 42 is a very important viral antigen that is required for entry into B cells. So, activated B cells, GP 42 reactive antibodies type two is like IL four or six secreting CD four T cells. They're coming together to tell us something. And indeed, when we look at the correlation between GP 23 or 42 specific antibody and IL four or six double positive CD four T so frequency. We see there is a linear correlation in long coded patients. Holy shit that these things. Ladies and gentlemen, if there's a linear correlation the R number. I'm crazy. I don't know. This is not a very impressive linear correlation. This is this is ridiculous. I'm not sure how this P number is generated that P value is extremely significant if you think of it that way but I don't see the correlation a linear correlation should be visible. I don't. I don't know I don't know I don't, I don't like this but you know that they're hunting for dancers, maybe linked to each other. And it's well known that EBV because they express this GP 42 blocks, the T cell activation through blocking of MHC class two, and they kind of divert these T cells into a th to IL four secreting cell type compared to th one. So, in our heads, we're kind of making some links in between these observations. I can get that one of this GP 42 blocks, the T cell activation through blocking of MHC class two, and the correlation between GP 23 or 42 specific antibody and IL four or six double positive city for T cell frequency. So there's a linear correlation in long COVID patients, meaning that these things may be linked to each other. And it's well known that EBV because they express this GP 42 blocks, the T cell activation through blocking of MHC class two. And they kind of divert these T cells into a th to IL four secreting. Okay, so let me just try to explain what she's trying to say here. There are two levels, two lineages of T cells, and depending on how they're activated, you can get one or the other th one tends to go toward B cell in any production I believe th two tends to go toward toward toward CDA positive cell formation. I'm not absolutely positive on that one. But the point is, she's suggesting that this EVB virus through the infection of B cells and the interaction with T cells, that it plays a role in governing whether or not T cells convert to th one or th two helper types, and that's very important because she sees a rise in IL four which is TL per two. Now again, you have to go back to the original data. What about all these people without that? What about all the people that don't have EVB? EVB is important to understand in the people that have it, but not important to understand in the people that don't. And if it interacts with the B and T cells and influences the way T cells can be activated in one pathway or another, then the presence of EVB is certainly very important in understanding how long COVID manifests in these two groups. And yet there's still only one group in this paper. I can't figure out how we can talk like this as this this is science we aren't even really getting down to one variable at a time here. It's shocking really that she tried to explain the entire thesis on what's going on when a significant portion of those people couldn't possibly fit that thesis, because they don't show the serial prevalence that you're using to generate this idea that antibodies to the EVB protein, reduce the interaction of the EVP protein with T cells, which means T cells convert on one path instead of the it's just, it is just wild mythology creation. As we listen. We're making the problem worse. Wow. Cell type compared to TH one. In our heads, we're kind of making some links in between these observations. What about auto immunity. Well, we found a lot of functional auto antibodies during severe acute COVID. When we look during the early phase of the pandemic, hospitalized patients and ICU patients had a lot of these auto antibodies that block the immune system itself, like type one interference specific antibodies, for example. So we were expecting to see a lot of auto antibodies. But we didn't. We did not see auto anybody significantly different in long COVID patients compared to controls. We did this in many different ways. This is the Joe Jacob's work with Aaron ring. And this is basically looking at different patients on the different columns and different roads indicate auto anybody presence against different energies. There really isn't a universal pattern or anything enriched that we can see in the long COVID patients compared to the controls and anybody reactivity per patient was not different. There's no difference in anybody reactivity number to long COVID propensity score. This is sort of the severity score that we calculated. So, all in all, we don't see a signature for auto antibodies against extra cellular antigens. It's possible though, that there are intracellular antigens that are being targeted by auto antibodies. And that's something that we need to separately examine. For machine learning algorithms that have been conducted by Rahul in David van Dyk's lab, we were able to separate long COVID versus non long long COVID participants just based on immunological phenotyping alone with 96% accuracy. And when they asked what are the factors contributing to this distinction of long COVID patients. They saw that auto anybody had very little predictive faculty ability. Whereas, antibody against the spike of SARS-CoV-2 had some predictive ability, but it was really the cytokines for cytometry and antibody against EBV and things like that that were able to distinguish people with long COVID versus those without. And when they looked at all the different parameters that we've included in the analysis and asked, what are the most significant and most differential factors that we see that are either lower in long COVID or higher in long COVID. We found that cortisol came out as the number one factor as a lowest factor in long COVID patients with the highest degree of specificity. But there were other things like the TCM, these are the central memory CD4 T cells that were also lower. And then CD8 T cells, for example, were also lower, but not as significant. What's higher in long COVID patients are these activated B cells, EBV reactive antibodies, and exhausted T cells. So this is starting to paint a picture of dysfunctional immune responses and reactivation of endogenous viruses that may be sort of distinguishing. It can get frustrating to listen to someone struggle like this to try to explain a obviously very heterogeneous phenomenon on a single cause, trying to find a single pattern. And the level of of insistence that there should be a single pattern to discover a single cure to to find or identify a single patentable drug. It's just it is it is making me breathless. Because, again, without trying to venture off into what previous long viral syndromes we know of, and what they can tell us about long COVID, we appear to be don't die on me. Where'd you go, girl? What just happened there? I lost one of my computers. The point being that I really think there's something disingenuous happening. And I think we've known this for a long time. It's one of the reasons why I've tried to stay away from talking about long COVID. Because it is a umbrella term. It is an unfairly broad classification of a previously existing set of syndromes that is now overlapping with some of the stuff that we're seeing here. That's really all we can say. And the idea that somehow or another we're going to spend millions of dollars trying to get at a solution to this very heterogeneous problem. By looking at a few people that were exposed to a viral clone or derivatives of it in early 2020. And that those data can somehow help us understand all the stuff that's happening now. When the original spike protein and its extremely dangerous designer protein sequences is not present anymore. This is just fear mongering. This is just sustaining smoke and mirrors that isn't worth sustaining unless you're going to start talking about where this likely came from. And that it is likely a combination of toxins, exposure, predisposition, and bad health. I doubt there are very many people that didn't get the original virus that are showing long COVID. I doubt that there are very many people that didn't get the original virus and were healthy and are showing long COVID. Anyone that was a super athlete and now has long COVID got the original virus in 2020. I'd put dollars on it like lots and lots of donuts and dollars on that. Long COVID in 2021 is from the injection. And the interaction with your immune system with your environment after the transfection there is no doubt in my mind. And so the trick is that because the protein that they put in the transfection will have the same bioactivity as the protein of the original virus, you can rest assured that there will be much overlap in the syndrome. I think that's a reasonable assumption to make regardless of how much you think the clone spread around the world and went for three years or three weeks. At least the biological factor for long COVID. So these are the key findings from this study. I didn't have even time to talk about patient-reported outcomes, but they alone were able to predict or identify COVID patients with 94% accuracy. So ask the patients in order to diagnose. Second, immunophenotyping reveal these distinct increases and decreases in different cell types, I guess notably the exhausted T cells being elevated. SARS-CoV-2 specific antibody response, particularly spike specific ones, were elevated. Evidence of herpes virus reactivation, EBV and VCV, were detected in a subset of patients. We did not see any significant increases in autoantibody to exocellular antivisions. And long COVID alone using machine learning can efficiently predict, sorry, immunological data alone can predict long COVID patients with very high accuracy. And the low cortisol level was the strongest predictor. Be careful with that number six. What she's saying is, is that machine learning could tell the difference between the two groups when given the data sets. It doesn't say that you can put your data into the long COVID and then it'll tell you if you're going to get long COVID because these people already had it. It's a bit like the dog being able to smell the difference. Who cares? But again, using machine learning gets you grants. Learning using machine learning fits the grant call, which probably said that we're looking for labs which can combine immunological bench work with machine learning to advance our understanding of long COVID. Here you see it. I want you to start to think more and more about the grant call that brought about the research that you're reading. What was the grant call that this research was answering? If you start to think about that, you can start to see where the conclusions come from. You can start to see where the figures come from. You can start to see where the experimental design comes from. This grant was not trying to find out about the causes of long viral syndromes. It was about long COVID. Even though the author knows that there's very likely to be a very strong mechanistic link between these and probably a lot of good data to be had by looking at them, the grant call didn't ask for that. So the figures don't reflect that even if there will be a sentence in the introduction. I think I can probably leave it here. I think this is kind of where I wanted it to be. I'm not going to listen to all the questions about long COVID because it will drive me nuts. So I'm going to show you a couple of slides looking at sex differences in long COVID. This is not even on the med archive yet. It's fresh off the press or whatever lab. And this is analysis that are done by Julio Silva and Takahashi. They took the same set of my long COVID data and started to look at sex differences. And what's striking about this analysis is that female and male patients suffer from distinct symptoms. There are some that are overlapping, but some that are very distinct. So females are indicated in blue and males are in pink. So please forget your stereotype. Basically, over here on the top, where the curves are overlapping with each other, there are sort of the common symptoms that is, you know, for example, sleep, disorientation, urinary issues, and ingestion. These are similarly reported for male and female patients, whereas there are some symptoms that are slightly higher in female over male, but they're not that separated. Whereas there are these sets of symptoms, at least in the my long COVID participants, were quite different. There were female dominant symptoms that included numbness, dizziness, and many other features that are listed here. And there was only one that was significantly male dominant, which is sexual dysfunction. And hair loss is the most significantly different reported symptoms that were predominantly female. And if you look at the symptom burden, there is overall higher symptom burden in the female. And then organ system involvement was also higher in the female participants. And what was another striking thing that we found was that in long haulers, especially in females. I already told you that long haulers have higher levels of anti-spike antibodies. But when you ask the question of are these antibodies functional in neutralizing the antibody, the answer is no, that these people with long COVID, even though they have elevated levels of anti-spike antibody, their functionality is quite low. So female and male, if you look at the long COVID compared to control, the steepness of the curve indicates how potent the antibody is against neutralizing the virus. And you see that there is a lot lower slope for the female and male participants. I'm not sure what this means. I don't really get that. If you have antibodies to the spike, but they don't neutralize it. I don't know what that means. Then they're not very specific for it. I think that means they're not very specific for it. So then calling them spike antibodies is actually kind of a misnomer. You see where we're going. It's not really right. If you use the spike protein to pull down antibodies and antibodies come down, it doesn't necessarily mean that those antibodies were produced by your immune system to target that spike. So I don't even know what she's talking about here. I'm sorry to say, but I assume it's some kind of bench in vitro measurement, which you can quantify the binding or quantify the relative affinity for the antibodies. And somehow the affinity is lower. They're not as strong binding that makes her argument even weaker that she understands what those antibodies are doing and why they're there. If for example, there is overlap between GP 42 antibodies and the spike protein. Then GP 42 antibodies being elevated in the long COVID will also then be show up in this as elevated spike. I mean, God dang it. The female long COVID patients have the lowest level of potency with respect to neutralizing antibodies compared to male patients. So even though the elevating levels of I would have to look up what a relative potency is. I don't know what it means or what these antibodies are not very functional. So the antibodies aren't very functional, then you need to talk about why virus or antigen remaining in these people, but these are pure speculation at this time. And people with high disease burden tended to have lower levels of antibody potency compared to those with moderate levels or the organ system involvement. Again, it's consistent with the notion that if you have very high potency antibodies, you're slightly better off with the symptom burden. So based on these hypotheses on data, we hypothesize that the original four different pathways to long COVID. It's unlikely, or at least for the exercise antibodies. We don't see much correlation of auto antibodies for long COVID. And we also think that with the increased levels of antibody with decreased level of potency in long COVID, it's possible that it supports this viral reservoir hypothesis. And we also found EBV and VZV reactivation that is much more prevalent in long COVID patients. So, and then tissue damage we did not look at we just looked at the blood from participants so we don't know the tissue level analysis yet. So this is sort of like what we're seeing overall. It's still a very, very early phase. This is a sort of hypothesis generated in long COVID. It's possible that it supports this viral reservoir hypothesis. And we also found that the original four different pathways to long COVID. It's unlikely, or at least for the exercise antibodies. We don't see much correlation of auto antibodies for long COVID. And we also think that with the increased levels of antibody with decreased level of potency in long COVID, it's possible that it supports this viral reservoir hypothesis. And we also found EBV and VZV reactivation that is much more prevalent in long COVID patients. So, and then tissue damage we did not look at we just looked at the blood from participants so we don't know the tissue level analysis yet. So this is sort of like what we're seeing overall. It's still a very, very early phase. This is a sort of hypothesis generating research, we don't, we need to do a lot more work to understand this better, but at least we're seeing some hypothesis that's more likely or less likely. Yeah, what I wanted to do for the remaining, hopefully five minutes or so. I don't know if I can do it so quickly but I wanted to share with you a, again, unpublished data on post vaccine long haul. So, this is all based on Yale Listen study that many of you are participating. And this was done by Bornelli, who is on the panel tonight, so any specific question you can address to her. But she asked the question, how do symptoms and demographics compare between long COVID and post vaccine long haul. And because the Yale Listen study already has many participants who have either long COVID alone, the purple is the PASC control, not control, PASC participants, and green bars indicate vaccine adverse events. The grays are people with both who have both long COVID and vaccine, post vaccine long haul. And here's the demographics. There seems to be again dominant female over male, the numbers of participants reporting these symptoms in our study. And then, total number of participants in these three groups is 206, 135, and 108. We would love to increase these numbers by recruiting more people into the study. This is already revealing something very important, so I encourage, for those of you who are not on the listen yet, please get on to this study. It's, you basically join through Kindred online. And Leslie can help you if you have any problems getting on. And the mean age, again, it's very similar, much younger than what you would see for severe COVID but typical of long COVID. And Ali wanted to compare the health status of people with PASC versus vaccine adverse event versus both. And these are your data, people who reporting for health, fair, good, very good, excellent, do not know. The percentages are very similar. Overall, in the three groups, and also another survey, thank you, boss. Again, very similar pattern, we're seeing there's nothing significantly different in the three groups. This is based on a questionnaire that we have on, you know, listen. It asks you, have you ever been told by a doctor before COVID, so before January 2020, that you have any of the following diseases, and there are two questions here. But essentially, if you look at the bars, there are strikingly similar percentages of people reporting allergies or arthritis, asthma, whatever, whatever diseases you look at, they're very, very similar. There may be. I've come to understand allergies as possibly generated by vaccination, and possibly generated by adjuvant exposure I am. And so people with allergies could be people that are mildly damaged by vaccination. People with auto immunity could be mildly damaged by back anyone who is mildly damaged by a previous childhood vaccination could be potentially vulnerable to long COVID. Do you see where I'm going with this guys. Do you see why we need to understand what's going on here with the original shots that some of us got more of than others. I'm begging you to open your mind wide enough to see how far I've come from being a guy who gave his kids, all of his shots, all of their shots in 2022 to being a guy who will never give another shot to his kids again. Not until this is all sorted out not until these people are out of a job not until this illusion is broken. Some differences and some of these psychiatric diseases but these numbers are just very low we can't really make any conclusions from this. We need more people to participate so we can understand the differences, if there is any. Let me just explain to you how another. Oh, I thought I didn't do it. Let me just explain to you how I think allergies work allergies work. Pretty simply, your immune system gets activated by an attack, an assault, a virus. You get measles. If during your measles exposure your measles sickness you're also exposed to a chemical, there is a possibility that during your immune activated state you will develop an allergic reaction to that chemical and go on your life having allergies to that chemical as a result of exposure during immune activation. What I would like to suggest is that unlike immune activation during an infection, which is natural controlled and governed by the symphony of your immune system interacting with its environment. The immune activation that occurs during adjuvant exposure I am intramuscularly is non natural activation is unnatural opening of that window, and the propensity to generate auto immunity or allergic reactions to things that would otherwise be inert to your body is greater. Therefore, as we've increased the number of childhood vaccinations we've increased the number of allergies and our kids, full stop. You do the math. Lee have you ever been told by a doctor that you have any of the following. And there are two sets of questions. And, of course, the most different answers turned out to be pask itself. So people with pask or people who have both, obviously they have the highest level of answered yes, compared to vaccine adverse events. Whereas reverse is true people who have vaccine adverse events or reporting. Obviously, these two last groups, but the past people, there's nothing. So this is sort of an internal control the surveys working very well. But if you look across the other things they were just very little difference. The only significance that we saw is migraines and neurological conditions that are slightly different between these groups. But again, we need a lot more. Holy crap really understand, you know how sick. Did you see what's different migraine and neurological conditions and who's it raised in it's raised in the vaccine adverse events people. I don't know if that's significant differences. But overall again, incredibly similar right. This is a question about all that you believe that is said, had as a result of pask or vaccine adverse events. And this is a patient's own assessment of what symptoms may be attributable to long coven post vaccine long haul. It's very similar there are some things that are slightly different and brain fog memory issues, difficulty speaking and so on. But overall, very similar. Now, I mentioned over and over, we need more people, so that we can really look at this in a larger population but so far. Surveys are showing us that these three groups are very strikingly similar. So currently there's this remarkable overlap in symptoms and sex ratio for long coven and age group. So based on this, what we hypothesize is that there must be a significant overlap in the drivers of these diseases. For instance, it's possible that the vaccine stimulation of innate immune responses could be similar between the acute coven infection and vaccine and what's trigger downstream is similar. And we know for both of these that there is inflammation activation on RNA sensor stimulation. These are two key innate recognition pathways that are triggered by vaccine and virus. So that could be the commonality, and this should result in acute, you know, within, within hours or days. I'm going to lose the script, I'm going to pause here, where is this vaccine stimulation and I'm going to reflect on the response, there's also one thing that overlaps between coven infection and vaccination, which is the spike. So it's possible that these surveys are showing us that these three groups are very strikingly similar. So I'm going to pause here, I'm going to lose the script, and I'm going to reflect on the recurring feeling I have of impending doom. So based on this, what we hypothesize is that that's Walensky from the winter of 2021 when she went into the winter of 2021 in October she saw, she had a feeling of impending doom. And then she also started crying on the news, there must be a significant overlap in the drivers of these diseases. For instance, it's possible that the vaccine stimulation of innate immune responses could be similar between the acute coven infection and vaccine and what's trigger downstream is similar. And we know for both of these that there is inflammation activation on RNA sensor stimulation these are two key innate recognition pathways that are triggered by vaccine and virus. So, so here we have some pretty big honesty here vaccine stimulation of adaptive response leads to immune immediate damage spike. So why not do for then right for would be great. Do I have that up. I have that up. Sure I do right here check this out. Got this website here from the Canadian public health services I was looking at vaccines and it says vaccines are complex biological products designed to induce a protective immune response effectively and safely. Minimal vaccine is safe with minimal adverse effects effective in providing lifelong protection against disease after a single dose kit can be administered at birth, inexpensive stable during shipment and storage and easy to administer. Some vaccines come closer to fulfilling these criteria than others well you don't say. I guess the Canadians didn't get around to changing their definition of vaccine on their main website yet. These don't exactly meet those criteria at all really do they, they don't provide immunity, it's definitely not lifelong, certainly not single dose they're not inexpensive or stable during shipment. Holy crap. Has it ever occurred to you that intramuscular injection of pharmaceutical products is an unnatural way of exposing your body to anything, and that your immune system is in no way shape or form adapted to intramuscular introduction of antigen. It never dawned on me until this year. Until late 2022 it never really dawned on me. That injecting stuff in my kids might not be smart. That's how much of a biologist I am how smart I am. So that could be the commonality, and this should result in acute, you know, within, within hours or days symptoms, whereas vaccine stimulation of adaptive immune response there's also one thing that overlaps between COVID infection and vaccination, which is the spike. So, it's possible that anti spike antibodies that form, you know, is causing immune complexes that may be leading to vascular activation microclots or other issues. Now, whatever hypothesis here is absolutely speculative. There's no evidence for this so please take this with a huge grain of salt, but based on the symptom data and demographic data. These are the kinds of things that we're starting to think about because we're starting to think about antibodies or T cells that attack spike expressing host cells endothelium. Gee, I wonder when Jay first started thinking about endothelial cells expressing spike protein and getting attacked by the immune system, leading to auto immunity. I wonder when I first started talking about the mimicry in the spike protein maybe that was when I heard from Dolores Cahill in 2020. Weird right. Wow. That the molecular mimicry of the spike protein could cause antibodies and could cause auto immunity that that spike expressing cells will be attacked. Wow weird right. I remember that we were talking about this for almost a year and a half before we're launching this talk, say that now we're starting to think about this, the Yale immunologist is now just starting to think about this. When I started thinking about it as soon as they said they were going to transfect us. That's when I started yelling about it in the halls of the University of Pittsburgh School of Medicine to other faculty members who use transfection every day. What in the world are you thinking? You know that they're going to eventually want to transfect your kids to this protein. Will you do that? Well, it's not transfection Jay. I'm sure it's a little more complicated than that. No, it's really not. I think it's better if we don't let her go on any longer. And instead, we try to cut back over here and let it play for just a second longer and we'll, we'll leave this as it is. There is also anti-spike antibodies or T cells that could attack spike expressing host cells. It could be endothelium, it could be epithelium. Epithelium is definitely a target of virus infection. The vaccine can be taken up by different cell types and express the spike protein. So again, there may be some overlap on the vulnerable cell types. There may also be antibodies that target auto antigen that is similarly induced by spike in the virus, similarly for T cells. It's hard to believe they threw, sorry, that's the camera. They threw Dolores Cahill out on the street for saying that there was molecular mimicry, molecular epitopes in the spike protein that were dangerously close to human epitopes. They made fun of, of people like Mike Eden for saying that there was an overlap with synxatin as a possible molecular mimicry problem here. Now she's allowed to say it. The Yale immunologist is allowed to say that all of this stuff is possible when two and a half years ago we couldn't say it. Ladies and gentlemen, we are in year four. You are finally seeing the culmination of all of this work. You are finally seeing me and others being vindicated here. Quite frankly, I think that Kevin McCairn was also saying that molecular mimicry was a problem for these cells. These, this, this spike protein. She's not saying anything about amyloidosis here. She's not saying anything about prionogenic protein attributes. But if she's already admitting this stuff, and we already know that those motifs are present in the original spike, how long will it be? You've got to wake up and apologize to everyone. You've got to wake up and apologize to yourself and to everyone and then get on the horse and start learning this biology so that you can explain it. Start learning this stuff so you can talk over these people so that when your friends and family bring this stuff up, you can counter it. Or you can send them to my stream, I guess, and we can figure it out that way. Ladies and gentlemen, this has been GigaOhm Biological, a study hour, an open study session. Let's try this and see if this works. Does that work? Can you see that on the screen? Look at that. A little lower third there for you. This has been fun. I knew that I was going to get this upset. Hopefully, I don't know, hopefully this was useful for you. I'm not saying again that these long viral syndromes aren't present. Not at all. Just saying that it's a much more complex picture that we can understand if we start to step back a little bit and look at vaccines, look at vaccine damage, look at previous vaccine damage, look at previous sub crisis level vaccine damage, including allergy generation, for example, and you can start to get a better picture of what's actually going on behind the scenes because all of our health care system, ladies and gentlemen, is precedented on the pretense that vaccines and immunizations do nothing. They don't contribute anything bad to the health of the children that get them. Even if they get 30 of them before they're 12, they don't get any bad side effects from repeated exposure to adjuvants. And that misunderstanding needs to be cleared up once and for all, so that we look back on this time in history and shake our heads, knowing that we did the right thing when we still could. Thank you very much for joining me. I will see you again tomorrow for another show. We're going to do this as often as possible. I'm not, I'm just getting started, I assure you, just getting started. I haven't even put in the ears on yet.