Alright folks, we're going to get right into it because I've got a bro waiting on the line and I've been less than professional in trying to get organised this morning. I blame, I blame the kids, it wasn't me Governor. Alright, so let me do this, always remember we're dealing with covert moral bio-enhancement and many, many other forms of psychological warfare. Let me bring Mary onto the screen and do this and let me, maybe I can unmute Mary. Come on, I don't know why Zoom has become very, very, am I missing something here?
Mary, can you hear me? Yes, I unmuted myself. Perfect. How are you? Pleasure to meet you face to face at last. Yes. Yes, so I titled the stream discussions with basically a professional virologist so I think we're very, very fortunate to have you here speaking with us. So I know you've been waiting, so without further ado. Thanks for having me on, I appreciate it. Maybe you could tell us a little bit about yourself without maybe doxing too much. Sure. So I did my undergraduate training in chemistry and jumped over to the biology side after taking an immunology course in college, went on to do a PhD in microbiology immunology at Wake Forest and studied molecular virology for my thesis there, so my specific training was in virology and studied several virus families throughout my research including eryxoviruses which are mesos and lumps and influenza viruses and microstock and did some work on rotoviruses as well and currently in a small company now.
Okay, so we can dispense with the obvious question which is do you think viruses are real? Let's not go there. No, I don't want to, I'm fed up with those people, they take up an inordinate amount of energy and time and it's a nonsense machine and what I found is they don't spend this time themselves to dig deep so they're willing to listen to a few videos and take somebody's word at face value without doing the critical thinking themselves is what I've found because it's all there. Yeah, it's a degree from YouTube right and they think they're ready to rock and roll and you know the really nice thing here is that, and I do say this time and time again, you can read all the papers you want but unless you've got bench experience, like detailed bench experience, you're always going to be lagging and perhaps misfiring with respect to the targets that you want to hit and so for people that are listening just in the previous days, I don't think we need to go through the basics of virology as we have an expert here, I want to sort of try and push the envelope a little bit and one of the things that's been a topic of contentious discussion I would say is quasi-species swarms and let's say their stability and adaptability and please I'm here to listen to you about that.
Okay, yeah, if you mind I can share my screen with a little schematic that helps that explanation here. Do you mind? Yeah, just give me, you have to enable it. The viruses are super cool to study and I'd be happy to touch on, you know, I've given you a slide deck on basic fundamentals of virology. I mean I have it to hand if you want to. If you think that'd be useful for your audience but I can quickly just review basics on that and then get into the life cycle of the virus and then how quasi-species swarms exist from that. Well, can I just ask a simple question which is quasi-species swarms just from my perspective seems, well, how solid of a theory is it when, you know, if you look at the literature there's a sort of understanding that there was variance anyway just because of genetic drift and, you know, point mutations, etc. Is it radically different to what the virology I learned when I was at university and grad school? I'm not quite exactly sure what your question is but the genetic drift that you mentioned arises because of the quasi-species nature of viruses and it has to be a dominant mutation over successive repeated passages and it's going to show you a little scheme to explain that. I think the screen should be working. Okay, cool. All right, I'm going to share just some slides here. It was my perspective on the irrefutable evidence of viruses and here's some really cool images I took since viruses are so cool. Oh, these are yours? Yeah. On the left is a cryo-EM picture of rotavirus. So it's got this beautiful icosahedral protein capsid. You know, viruses can have a membrane outer layer or a protein outer layer where the viruses have a protein and it has a very awesome geometric shape to it and what I did was applied some software to this and sort of cut through slices and saw what the inside looks like based on some modeling, yes. But the interesting thing about rotaviruses is they can replicate without the entire cell. So if you throw in salts, nucleic acids, it will pump out genetic material. Not a whole virion because you don't have enough acids to form a protein but it will start pumping out the stuff and what we saw here is a cross section of those rotaviruses and this is just an artistic point of view but the less dense features in blue are probably RNA and RNA is forming a very complex structure of what I call dancing stars here. But the core of this particle changes dramatically under replication and it gets very dense in the center and there's a lot of changes that you can see. But anyway, let me fast forward through these a little bit so I'm going to be jumping through and cover. I'm going to come back to life cycle in a minute because that's important to understand but the irrefutable evidence of viruses as I put it, we can directly see them on electron microscopy. We have animal models where we give the animals the virus and they can have symptoms. They don't have to have symptoms but you can recover virus back out from the animals or they can transmit it to other animals through cages. They have a direct effect on tissue culture. Part of the new virus crowds gets hung up on the cytopathic effect. Not all viruses even cause that effect. So you now worked with a virus that was really optimized at a steady state, pumped out tons of virus but didn't induce host cell death or even cytokines. So it had that optimal steady state level not to set off alarm bells in the cell but also able to produce a lot of new particles. That's a concerning one to me. That one is non-pathogenic. And then we can detect the virus material by several methods and then obviously we have specific immune responses to foreign sequences. And the most interesting part is the co-evolution of viruses with Bukaryotes and you can see a complex interplay between the host response and then virus antagonism where the virus actually antagonizes directly. It can degrade proteins. It can stop signaling pathways. They do all kinds of stuff. I was just going to... I don't want to shoot off at a tangent but there's been... I see a lot of chatter about SARS ability to co-transfect with bacteria. How much of an issue is that? Is it a real issue or just... So you say co-transfect so you mean infecting the same exact cell or... My understanding is they're able to infect the bacteria a bit like a phage. Oh yeah, sure, viruses do that. That was at the beginning part of the rest of the interview. How much of that impacts the quasi-species? Because that's a radically different replication environment compared to obviously human cells. Is that what's driving much of the difference? A couple of notes there. So a really interesting thing is that DNA viruses can infect a wide range of organisms whereas RNA viruses only infect eukaryotes. So that can tell us something about virus evolution and the last universal cell that are incestuous that loop up sequences. So it's really interesting to go down that path. But the state of the quasi-species is mostly dependent on the fidelity of the polymerase combined with recruiting activity. So I'll talk about that in a minute, but let me just flip through these intro. So I isolate virus in the lab on a daily. We can isolate virus, you guys. So you can do it through sucrose to sucrose gradient or sucrose cushion through ultracitrification. And if the virus is less dense it forms sort of a layer that you fractionate out of the sucrose column or if it's more dense and you're just putting it over one single concentration of sucrose pellets to the bottom and you have a white pellet which you can re-spin tighter and quantify the virus right out of that. So here's a good example. You got a question on that? Well, the comeback from no virus, I don't want to do too much no virus nonsense into this, but their argument is that because of the similarity in size with intracellular vesicles that you can't tell the difference. Except you can. You can do specific staining and molecular biology techniques to differentiate between the two. You can actually take control. You can take normal cells versus infected cells. You do the same procedure to both. So you have your control non-infected sample and you don't generate a distinct milky white layer where the virus would be. And there's no effect once you take that inoculum and reapply it to cells or reapply it into him. So So this is more electron microscopy. So this is transmission electron microscopy of pox virus families. What I'm showing here is various members of the pox virus family. These are distinct viruses within the same family. They cause similar symptoms in the host. Here we have canary pox on the left, small pox, which is human variola virus in the middle. And then on the right is my lab works with an attenuated vaccinia virus that's thought to originated from cows, but that's up for debate. So you'll see the distinct hourglass shape in the middle, which is inflated gas and material. And then there's a couple of membranes around that. And then it's got a surface collective proteins on the top. So we can see similar morphology within the same family of distinct sequences. Inclusion bodies are another fun thing. This is a Lassa virus inclusion body here within a cell, sort of a virus factory. I'm just moving quickly through this part because this is not the question, which you might discuss. So we can also detect virus material through PCR sequencing. A lot of people have a little bit of problem with the sequencing methods, but these are just tools that we have available to take a look. We use the tools. All techniques have limitations, right? But the layered evidence creates a very clear picture. Yeah. I always try to hammer to people that, yeah, when you're working at these scales, there's always sort of fuzzy boundaries. But once you start getting convergent lines of different techniques pointing to the same thing, at some point there has to be a working framework of which you can sort of push from. I guess the question I want to get to is, what do you think to the current PCR primers that they're using for detection with SARS? Well, I never went back and vetted that. I still have those question marks in my mind. But PCR is a highly specific process. And the spike protein in particular is very divergent from human seasonal strains. So it's not going to cross-react. It's very divergent from Oc43 or the other ones. All I can say is PCR is highly specific. You're not going to get much cross-reactivity there. Depending on the gene. Now, if you look at a highly conserved gene and the primers are targeting the polymerase, which is the most conserved region of viruses generally, well, yeah, you're probably going to pick up a few within the same family, but not crossing over to influenza or anything like that. The protein is a more definitive readout. We can do Western blots. These are immunostaining techniques where we have virus infected samples. We run assays. So we separate the proteins on a gel heater and then we probe them with antibodies. You have to remember antibodies are highly specific to their target. Sometimes it's cross-reactivity. That's why we do controls. Cells only don't show any bands. Infected cells do. And this is actually a picture of spike like the protein here. And then you can do immunofluorescence using a similar technique and as well as specific staining of those electron micrographs. So you can do immunoglobulin labeling on your electron micrograph for the specific surface virus like a protein. Well, the state of... I keep bringing them up, but they're even convinced that antibodies are not a thing. No, that's where it spirals out then. So I was like, well, what do you think about the immune system? What's the immune system? Just go read Janeway. Get your textbook out and do a little background reading. That's what I repeatedly say. My understanding... Well, I've seen electron micrographs of antibodies and just the fact that we can see the structure without sort of arguing about epitope specificity. It matched theory very, very well. You see short and long chain components. I've used antibodies successfully all through my career. And when you hit it, it's tough to hit it sometimes, but it's a very, very reliable signal in most cases. But my thing was just protein, intracellular proteins and neurotransmitters, things like that, not virology. Yeah. Antibodies are... Not only are they part of our immune system and they're used in molecular biology techniques, but we often use them in immunology as well to do specific cell depletion so we can administer antibodies and deplete CD8 T cells and then study what the lack of CD8 T cells does to define correlates of protection and such. Of course, we can see cytopathic effect, not cell death, cell rounding, or cell-cell fusion, syncytia formation on the far right here. This picture I took in grad school. I have a hyperfusogenic virus on the right-hand side. Then you got the plaque assays. So they get bent out of shape. Anything you can call cell death, whatever. So actually, a traditional plaque assay looks like this where you have a patch that's where the cells have lifted off the dish where you see a cytopathic effect of cells. But you can take the same sample, the same virus sample, and do immunostain and specifically detect for the surface glycoproteins. And actually, in my lab, we do plaque assays with this extra step to just, it ensures that you're not misreading your hole on the plate on the left side. Right. That's another. My understanding as well is that sort of modern techniques, there are culture methods that the medium doesn't even have antibiotic in, which is one of the arguments that they come up with, right? Oh, is it? I had not heard that one. Yeah. Yeah. It's best practice not to use antibiotics in cell culture. That's the best practice a lot of labs do to prevent bacterial infection, contamination, actually, in the lab. But antibiotics don't have much to do with the virus infection, so. But that's their whole, it's a big pillar of the no virus argument. I've never heard that. That sounds strange. Let's not even go there. It doesn't even make sense. These are my super cool pictures of rotavirus. So on the bottom, you can see that if you look really closely, you can see the dark lines coming out of the cell, and then the center of the virus gets really dense there. But we can also do models of infection. So we can take inoculum and put it in animals. And they actually did a human challenge experiment for SARS-CoV-2, right? Yeah. And only half the people were able to be infected with a controlled dose administered intranasally. Only half the people became infected, which I found really interesting as well. That's a reflection just of people's innate immune status, right? And well, they're into the play of genes and environment, I would argue. People thinking it's like a machine need to disabuse themselves of this notion. Biology is far more, how would you say, slippery. It's always multi-factorial. So it's never just one thing. It's your overall health. It could be a cross-immunity that you did have from seasonal circulating strains that prevented infection. There's a ton of different things you can factor in. But what we can do is we can put virus in and then get virus out of animals. And we can show on the right-hand side, these are just H&E stained slides of lungs. So after influenza infection, you see tissue damage in the lungs. Only infected animals, not control animals. And then, of course, we have our immune responses, two viruses. Both inadaptive immune responses are critical. Coronaviruses have been endemic in humans for a long time. And then sometimes we can have spillover events. And that's when we may see a little blip of higher mortality at the onset of a spillover event. And then this is probably one of your favorite pictures here with the signaling cascades here, Kevin. This is critical. So viruses dump their genetic material inside the cell and begin replicating. Well, the cell is primed and has a bunch of alarm bells that detect apparent virus replication and other virus products. They set off the alarm bells and that's what they type one interferon pathway. And that is put your cells in an antiviral state and viruses can come in here. This is actually a picture for SARS-CoV-2 in red is how that virus inhibits these innate pathways. So there's genetic inhibits, induction as well as signaling of neurons. So, all right, I'm going to get out of that screen and move on. Viruses are real. Yes. I'm just, once they're industrialized and used as tools, it's hard to sort of argue against their existence. But I guess we should push into the idea of the quasi species swarm and address questions that have been raised by Jonathan and his premise is that the only way for anything approaching a pandemic signal to be achieved is through the mass use of clones derived through plasmid replication in expression systems, bacteria, I presume. Do you have any thoughts on that or? I think I'm confused exactly what the crux of his argument is. And I actually thought it was the opposite. I thought he was trying to say we could never produce a bio-weapon from the cDNA clone. I don't know. It's hard for me to address. But let me start with the basics and let me move forward from the beginning. So I'm going to share my screen one more time and just quickly step through the life cycle. I hope this is not too boring. No, no, no. I love this stuff. I'm always happy to do streams when there's someone else talking. All right. So I've got an example of the virus life cycle here. It's really critical that we understand this because a lot of misconceptions come up about how phenotypic changes can occur in such a short timeframe sort of thing. So you've got to realize that the genome of viruses and especially RNA virus is extremely small. Coronavirus is one of the largest RNA genomes. But if we take a look at the life cycle, there's a few steps involved. You have entry. You have after entry and release of the genome into the cytoplasm, you have replication. So once the genome is deposited, it gets transcribed into the negative sense and the positive sense genomic material. The positive goes into the new virus particle. Nothing else goes into the new virus particle other than the fully genomic RNA that's been coded with the nucleocapsid protein. As part of the life cycle, obviously you got to produce proteins. So from the negative sense genomic template, you get these subgenomes. And then from there, the proteins are transcribed and sometimes even as a polyprotein. And when you start to dig into the mechanisms of transcription and translation of these viruses, they're really crafty and there's a lot of neat things they can do. There's slippery CISAP consequences. There's sometimes the polymerase can jump over and do a continuous sequence for whatever purpose. There's all kinds of cool things. So once you produce the subgenomic RNA, you get a translation of the proteins. The structural proteins are included in new virus particles, but a bunch of other proteins are produced from the open reading frames, a lot of non-structural proteins that have various functions and are not incorporated into the virus particle. Yeah, so my view has been, it's a one-dimensional view to think that everything is sort of geared towards the complete genome and packaging. When we know that some of the non-structural proteins aid in the disease process and, you know, I sort of focus on amyloidogenic sequences that we know will, well, it'll impact cell function such that it will allow, or in my mind, it would provide evolutionary advantage to getting out these complete virions, right? So you... Yeah, you can't leave anything out. The accessory proteins are, that's what they're called, accessory proteins are very important in our sort of cycle and have a number of function and are often multifunctional in a number of ways. How much of the sort of non-structural proteins are being sort of spit out by themselves to sort of, well, spit out is in one way because, you know, we're sort of dealing where we have these filopodia and infected cells often seem to pierce neighboring cells. And my, yeah, I've just, I want someone to sort of quantify for me how much the, yeah, maybe I'm asking too much, but how much are the... Yeah, I don't have an answer for you. I don't know the relative quantities of each of these proteins. But from an evolutionary perspective, does it make sense to sort of flood the environment with these non-structural proteins, the accessory proteins, to soften up the environment in a way to, you know... It depends. It depends on how many molecules are necessary to carry out their associated function. You know, if they can achieve aggregation of the type 1 interferon response with a small number of molecules that have basically shut down the signaling pathway, you don't need a lot around. And that contributes to disease pathogenesis in that way. If you're not even able to establish an antiviral state in your cell, the virus could spread, right? And it's going to contribute to viremia and progression of disease and overreaction of the host immunity and that sort of thing. But typically, you know, I have studied more in my time than I have in a negative sense, RNA viruses. And they typically put the glycoproteins, the surface protein, up front. And they have a tier transcription mechanism where the first gene gets transcribed the most and the last gene the least. And it's because of a fall-off rate of the polymerase and an increasing fall-off rate at each junction site, right? So their genome is designed to have that structural protein up front. And then they produce the most of that protein. So I don't know about the relative quantities. That's an interesting question though. But if we, so if we look back at the virus replication, you start off with this genomic RNA, shown here in blue, and you get the RNA-dependent RNA polymerase to transcribe this. So that is a unique enzyme to, it's not found in eukaryote, you know, DNA transcription, not RNA transcription in our cells. But that polymerase has varying degrees of fidelity to replicate that genome. And they're generally thought of as low fidelity. And I think some people get confused. That doesn't mean that every output genome is a bunch of garbage. It just means the amount of changes, I guess, changes in genome would be more than what we traditionally see with cellular organs. That's right. You know, I'm in two minds about the fidelity issue, because, you know, there's work that just shows that SARS has this exonuclease proofreading. Which is a separate function and then RNA-dependent RNA. Yeah, so it's almost got like two self-checking mechanisms. And, you know, this, this in my mind is a a priori hypothesis as to why the swarm would remain stable over longer periods, particularly if, you know, the molecular techniques are there to tweak the proofreading, right? Right. They've done those experiments. It's, you know, they've mapped it down to four amino acids. It's the DEDD domain. It's highly conserved, a bunch of exonucleases. But if you mutate areas of the exonuclease, you get a high number of virus mutations and non-viable genomes out. So that's experimentally how they approach that. So the nature of the swarm is going to be dependent on both the level of RNA-dependent RNA polymerase fidelity, as well as the exonuclease proofreading activity combined. Could you envision a way in which they could increase the, the ability to proofread synthetically through gain of function?
That's possible. You just have to make the mutations and do the readouts, do the sequencing readouts, and look at the swarm. So if we move into the swarms here, let me share another figure. I like to see images that helps me learn. So this is out of a virus quasi-species evolution paper. So my training is not particularly in virus evolution. That is an entire field of its own. And has entire journals attributed to purely virus evolution. I studied more interaction with the host cell. I'm not so detailed here, but it's really interesting. So if you look at the far left here, what we have is each number and line representing an output genome from a single infection. The discontinuous lines represent genomes that have accumulated mutations that make them non-viable upon the next infection. And all the symbols and colors here are various changes, either in the nucleotide or amino acid sequence, however you want to look at it. So if you think about this first set, the only virus genomes within this swarm that make it to the second set are the ones with continuous lines. And here, if you look at the entire group of this 27 genome sequences, that represents the swarm of quasi-species from an output infection. If you were to sequence this, the consensus sequence, which is the frequency of nucleotide or amino acid at each position remains the same. So they get a consensus sequence from all of these. What is the most common nucleic acid at each site? Here, over passage of the virus or reinfection of the virus, the consensus sequence is actually staying the same, even though we get all these scattered mutations throughout. So in the end here, over on the right-hand side, even though we've gone through many individual sequence and mutant swarms, here you have ultimately the same consensus sequence in the end for this example. Just a quick question. Could it not be argued, though, that the consensus sequence is an artificial construct in order to sort of simplify our ability to work with the virus itself? I guess the question is, how often are you seeing amino acid dropouts and changes in all the readouts? And is it 5%, 10% that they have to make a decision about what the... You have a position that says, okay, in 5% we see a change at this point. I don't know what the exact percentage is. That's a good question.
I would think it would have to occur in a majority of the sequences, sequence samples, individual samples. That's a good question. But here it's just showing you each round of infection, you get a different individual changes, some creating non-viable genomes. Many of the genomes are still viable, even though they contain certain changes. And in the end over this set of infections or passages, whatever you want to think about it, you have the same consensus sequence that you started with. I wouldn't say consensus sequence is an artifact. It's just that it's a consensus of what you've got. You have to look at it some way. We can't take individual one out of here and say it's representative of the whole thing. We take the most frequent... Yeah, it's like... ...glaucoma acid or amyloid at each position. Any population metric is going to sort of smear your data to give the mean, right? But I guess the take home from this is that there's still functionally recognized virions of the same clade and presumably having the same functionality, or that functionality being able to persist across multiple generations. Right. That's not always the case. Sometimes a selective pressure is applied to such that the consensus sequence does change over time. And that's what's shown by this example. Here, there's only viable genome shown. And what the authors of the paper are trying to demonstrate is then sequence number eight here, you see this star show up. And this star has conferred some fitness advantage to that particular genome. And it gets repeated and amplified over repeated infections and cycles such that you end up in the end with a consensus change in that position.
That's conferred a functional phenotype, phenotypic advantage to the virus. i.e. a fearing cleavage site. Sure. Yeah. That's really where this pivots is back to, you know, so if we look at the SARS-2 genome and say, oh, what's really different about this and what stands out? And I know you and your audience know this well, but it is that insertion of the few amino acids that was not in a prior study of the virus. And so that's kind of the prior related viruses. Well, I mean, the most disturbing aspect about all that is that, you know, they recognized a change in the length of the genome of SARS-CoV-2 relative to other beta coronaviruses. You know, obviously there being more in the environment, but the exact length of that increase was directly responsible for the fearing cleavage site and the HIV-like variable loops on the sort of tip of the receptor. And in my mind, in my mind and, you know, trying to sort of argue forward is that that is the fundamental signature to say that they did gain a function. And it's like you say, if it confers a advantage, the swarm will pick it up and the swarm will carry it. Right. It will be maintained within the swarm if it offers the fitness advantage. And, you know, I've checked the literature and the fearing cleavage site is still there in Omicron. And so, you know, it would seem to be holding with the theory as you've laid it out. I'm less sure about the variable loops themselves. Do you have any information on those? Are they – I presume the length of the genome hasn't changed, so I have to make the presumption that the variable loops are still operational at some level. I'm not as familiar with that concept. Are you talking about within spike protein? Yeah, yeah, yeah. I'm more familiar with the sort of mechanism of fusion of these black approaches. I don't know much about the loops. I can't really comment on that. You can educate me. Well, you know, I've done a bunch of streams with Charles Wixie. Are you familiar with Charles? No, I don't get out too much. So Charles is a marine long-serving – or was a long-serving marine WMD expert and, you know, has – and it doesn't have a PhD, but is a voracious reader and is very, very good at condensing down this information into a digestible format.
What's the art of its own? Yes, yeah. I'm old and lazy. I don't want to read any more papers. I've done my discipline.
What does he say about the variable loops? Well, so this – well, it comes back to that Pradhan paper, which was jumped on so aggressively at the start of the pandemic, right? So the uncanny similarity between SARS-CoV-2 and HIV. And that was, you know, immediately censored. And we know through the email foyers that, you know, the networks that were involved in narrative control deliberately set out to stifle any of that discussion. Now, the interesting – facts, I guess, if we can take them as solid facts – is that the loops are associated with different strains of HIV. And the even – well, perhaps darker aspect to this insertion is that when you look at the HIV literature with respect to them trying to make vaccines and so reactive epitopes and I guess – I don't know if they – well, the point being that those segments are always removed from any vaccine candidate. And also, as just an add-on to that, the Furing-Cleavage site, they knew should never be included in a vaccine candidate. Yeah. Many vaccine candidates did retain the Furing-Cleavage site, depending on which one you're talking about. But back to, you know, similar sequences with HIV, how I looked at this – and I think I vetted it a long time ago, and so it's vaguely in my memory – and what I found is there are either very short amino acid stretches, which can be easily conserved across virus families, or in the case of this Furing-Cleavage site, it's found in multiple species because it is very efficient. Cleavage, you know, it exists, and there's been some confusion about a Moderna pack containing these few amino acids. Well, so what? You know, they're making claims surrounding a Furing-Cleavage site. People use Furing-Cleavage sites in molecular biology all the time. I believe one of my patents has a Furing-Cleavage site on it, too. It doesn't mean anything. It means it can be cleaved. That's it. Now, as far as these HIV domains, I believe they were based on confirmation. Is that correct? Rather than sequence, was it based on the structure of the protein? I want to say it was homology at the amino acid level rather than nucleotide, but there's two groups, one being the Indian group, the other being the Paris-Ligue Montagnier, who came to the conclusion that their placement seemed, it was too functionally adaptive to be their argument, to be just fragments finding them, for example, you know, not randomly, but... Yeah, but based on that argument, the virus could have gained those function either through gain of function insertions or serial passage with right selective pressure or in circulation for a longer period of time. It also has the potential to gain fitness advantages. So what I was trying to say is a lot of times there are many conserved sequences, as long as they're short amino acid stretches that can be found all across nature, across different virus families, especially with these glycoproteins. And there's a few classes of the glycoproteins, but they've optimized fusion to get into the cell. So yeah, they're going to have some similar sequences and similar conformation. That's how I view it. I still don't believe there's any HIV component to this virus at all. That's my personal... Yeah, like so you're the viral expert, but I've been convinced by the HIV arguments. Well, but also the loops are unusually long compared to natural viruses in the same family. Well, they're not in related viruses. And the sequences have been patented as well. You can't patent the sequences, is another misconception. You can patent claims using the sequence. You can never patent sequences that occur in nature, right? So if you look at the patents, they're all using a sequence for a prophylactic treatment. That's how legal intellectual property works. You have to make a specific claim, and the claim cannot be to patent a sequence. The claim is to use a sequence as for something, it could even be a tool in molecular biology, it could be a method, it could be a treatment. After three years of doing this, I'm just firmly in the camp that it does look synthetic. It looks very much part of a larger campaign, pushing the globe in a dystopian, technocratic future. And this, I would lay a lot of my chips on that this was a tool that they've used to begin that process of leading the herd, for want of a better expression, into an environment in which they wish to increase surveillance. And the way they do that is via the medical system. And one thing that I argue on my stream a lot is that last century's Bolshevism failed because of, it was too divisive with respect to the population, working class versus the bourgeoisie, and so it was doomed to failure in that respect. But I would, again, put forward the premise that they've learned, right? Those people didn't go away. They've learned, and what they've come to understand is, what does everyone have and need in common? And that's medical care for your life. And so those systems become ripe for weaponization. And I think that's what we're seeing right now. They keep pushing into the conversation, the idea of vaccine passports to track people's movements, et cetera. And I'm of the opinion that we should be doing everything that we can to push back against these ideas and maintaining a posture of, well, sovereignty for the individual. Amen, brother. When tyranny becomes law, rebellion becomes duty. Amen, brother. When tyranny becomes law, rebellion becomes duty. Do not comply.
If we go back to where you started your sentences there, I do agree that there was some sort of gain of function, research that took place that led to the outbreak of SARS-2. I don't, honestly, I've looked at a lot of different papers, Jan's paper, and different ones about, oh, it could have been this, could have been that, or it's right, T.G., where it doesn't really matter how it came to be. It's here now. And it has been exploited for authoritarian policy. But there's a lot of evidence that points, so we just hinged off the fear and cleavage site. Well, everybody is familiar with the diffuse document, right? And if you take a look at that document, I've highlighted here exactly, exactly spelled out what SARS-2 is. We will introduce appropriate human-specific cleavage sites and evaluate growth potential. Now here it's just in cells, but they're already talking about, we're going to do research. We're going to make recombinant viruses. We're going to introduce human cleavage sites into the virus and see what happens. So they're already doing that. They're spelling out, they're doing that. Although this application was not funded, Peter Bassack's R01 was funded that was very similar to the strategy. I have to tell people all the time, when people are submitting grants, you're always ahead of what you've put in that. Yeah. It's just excellent. We've already done Ames 1 and 2. So we have, you can make the presumption that those experiments were in full flow. Absolutely. I'm agnostic as to the, was it Wuhan or was it seeded? To me, it doesn't make any difference. What it tells me is that we're suddenly being forced to dance to the tune of people who have intentions for us that are less than, certainly not benign anyway, let's put it that way. So I guess it sort of begs the question with how much, is it possible just from a single experiment in your mind to have a global pandemic? Or if you take Jonathan's argument, that you must have a lot of purified clone that has your adaptive traits in it, and you release at multiple points, sort of simultaneously. I suppose you could go about it either way, but they're not, we don't know, and the former is certainly possible. You can have one laboratory experiment where you've inserted an optimized cleavage site, or you don't even have to do it in a cloning mechanism. You can take a predecessor virus, sincerely passage it through animals to apply the selective pressure. Those animals can have human ACE2 receptor. They have those animals, they're mentioned in both the proposals that I just talked about. So if they took some predecessors, repeatedly passage it through the animals, there's going to gain advantages that allow the virus to use the ACE2 receptor and get into cells more efficiently. Either way, you can have a small amount of inoculum, potentially. In fact, the laboratory personnel, human error is rampant in laboratories. So in high containment, there's a lot of human error, as well as equipment malfunction. If the hoods aren't flowing right, if the air circulation handling is off, if you're not doing the incineration of your biocontainment properly, if the animal waste is going a certain place, who the hell knows? I don't know, but you can have that single source, and let's just say a laboratory personnel wasn't being careful. They didn't think what they were doing was serious, and they become infected themselves with the virus. They're the index patient, and once they transmit it to another person, and it has that fitness advantage in it, it's going to remain dominant over the course of repeated passages. So it can come from a lab. You don't have to generate giant quantities of the virus, as long as the features contained within the virus allow the fitness advantage. This is why I deliberately stick with lab origin. I don't like the push to say leak. I think that's a rhetorical trap that we could get into. Someone's want to ask you a question. Can you ask what she thinks about the preprint shown that SARS-CoV-2 can enter the nucleus through the furin cleavage site? I have not seen that paper. That doesn't sound right at all. The furin site allows for the fusion peptide to be exposed, and the fusion peptide is primarily functioning the cell surface, from my understanding. I haven't seen the preprint. That sounds interesting. I'll just read that abstract to you. So SARS-CoV-2, despite protein, appears to be a major pathogenic factor that contributes to unique pathogenesis of cells. Although the S protein is a surface transmembrane, type 1 glycoprotein is being predicted to be translocated into the nucleus due to the novel nuclear localization signal PRRARSV, which is absent from the S protein of other coronaviruses. Indeed, S proteins translate into the nucleus in SARS-CoV-2 infected cells. To our surprise, SMRNAs also translocate into the nucleus. SMRNA co-localizes with S protein, aiding the nuclear translocation of SMRNA. While nuclear translocation of nuclear protein has been shown in many coronaviruses, the nuclear translocation of both SMRNA and S protein reveals a novel pathogenic feature of SARS-CoV-2. If that made sense to you. I was reading quick. Yeah, that's interesting. I thought that the virus was contained to sort of the very nuclear space and didn't go deep within the nucleus as part of this replication life cycle. We have seen in the lab spike the protein at least localized to surrounding the nuclear area, but not a complete overlay. It's like, you know, around, there's a nucleus, it's around. I didn't look at RNA or anything, but my question would be how do they know that's contributing to any pathogenic feature? Well, I guess the presumption would be that any cytotoxic epitopes are going to just be causing problems in such a complex region of the cell. But if it's, yeah, I guess the bigger question would be is if it's integrating into the genome such that you were able to push out spike protein. And so I had a discussion, I don't know if you know, Walter Chesna, and we were, he brought up a paper that was looking at long COVID patients, and they were able to find a signal for spike protein, but no nucleocapsid protein.
That's interesting. So I'm just wondering if there is a functional integration that could potentially, you know, I was struggling to sort of... That's a rare event. If it were to happen, you know, you have to first transcribe RNA into DNA first, which is a rare event.
Isn't it? Well, one mechanism is through sort of line one elements. Yeah, those are also very rare. They're not rare in existence, they're rare in expression.
So they're there all the time, but they're rarely expressed. But it's possible, but I just say it, I believe it to be rare. Well, I guess where the rubber meets the road is where the clinical picture emerges. When I was young and I started my career, I was taken under the wing of a surgeon, and his words to me were, you know, you couldn't do a lot of theory, but in my field, which was clinically focused, he said, you've got to understand the patients and the presentation all the time. That must be your baseline before running off into theory where you're abstracting out data and hypotheses.
And, you know, if it's a solid finding that long COVID patients are spitting out spike protein over the long term, which that paper seemed to show, I'm inclined to believe it's perhaps less rare than... Well, you don't know, you just don't, you have to test it. You don't know if it's genome integration in particular. What if one of the sub genomic fragments is retained at a higher rate in the cells and continuing transcription of certain fragments? I don't know. You think of all kinds of mechanisms. It could be integration. There's one way that can happen.
Yeah. And, you know, it comes down as well to, well, if we're in a situation where part of the replication cycle is this front-loading of, you know, the non-structural protein or, sorry, yeah, non-structural proteins, accessory proteins. And I just wonder if they flood enough through a system that they can... and the RNA is being packaged up as well, sort of equivalent of like the vaccine almost, that you're getting smaller sub RNA sequences pushed out to, again, soften up the organism for infection. And, you know, all I think now is, well, if that's a if that's a mechanism, then these are mechanisms that can be leveraged and weaponized. And you know, I wonder how much goes on behind non-public science where they've really got a handle on those mechanisms that perhaps we're scared. I don't think there's any kind of handle on that at all. There's so much we don't know. And so if you talk about pathology and clinical disease, you can't take something like, you know, spike being near the nucleus or spiking RNA in the nucleus and translate that across without doing a lot of technical experience. There's so many things that contribute to pathology. Maybe it contributes in some way, but pathology is dependent on so many different factors. Like you were saying at the beginning, the health post and everything else comes into play. You can't nitpick one particular thing and say, oh, that that's making it. And then the toxic mechanisms of spike are so many that that's a whole beast of its own. And I can't particularly imagine primarily those toxic effects being within the cell, but rather what I've seen is a spike interacting with ACE2 or the angiotic pathway. It's interacting with other receptors, causing dysfunctional signaling in various sites and surrounding endothelial cell death. You can have fragments of spike protein that can undergo amyloidogenesis and that sort of thing. Everything is so multifactorial. You have to try to keep everything context of the whole picture and not pick out one thing here or one thing there. Well, you know, I have a hobby horse around amyloid and pre-inergic mechanisms because that's my sort of background. But, you know, my concern had always been that those mechanisms, the protein misfolding ones, are at another conceptual level that most people are going to find difficult to grasp, right? Even, look, trying to keep up to date with literature just around viral reproduction and interactions as whole particles is, well, you make PhDs out of it and you make whole careers out of that factor. And we know that they were looking to weaponize prions for quite some time. But the problem was that you could take the scrapie protein and aerosolize it in a room and you'd get an effect that way. But its ability to infect across individuals was limited. Whereas, you know, as the theoretical, well, not theoretical, but the science moved on, and particularly in my field, it was, oh, it's the virus themselves, viruses themselves, able to cause protein misfolding. And, you know, herpes was the primary suspect in my field. But, you know, you can take a look at the spike protein of SARS and you can run it through computational algorithms to see that there are a whole bunch of amyloidogenic sequences in it. Now, they're similar to OC43 and other beta coronaviruses. But the issue is, is that we've imbued it with this furin cleavage site, allowing it to have access to far more tissues and be far more permissible than the, you know, the mother nature's version. And… And it's not just that cleavage site, but also use of ACE2 receptors. Both of those factor in as the circulating strains enter through a different mechanism. But speaking of, have you seen this association of OC43 and 229E with multiple sclerosis? Yeah. Yeah. So that's an old paper from 2000. And the neuroinvasive nature of coronaviruses was known for some time. And like I say, you know, when this started, I, you know, I had a vague, you know, understanding and recollection just from SARS. But again, my, and the problem is in academia, is once a sort of hypothesis takes hold, that's where the crowd aggregates, because that's where the money becomes available. And, you know, I just wonder how much of a blind spot we've developed for, you know, what we would consider relatively mild pathogens. But if we're, if we're not understanding fully the host viral interactions, and especially this more fundamental, because you don't need the whole virion, right? If it's spitting out these toxic epitopes, even a sort of partial reads, then you're, well, it's, it's ripe for weaponization, right? In a way that most people just are not going to be able to grasp. And that's, that's what you want. You would, you would aim for that type of subterfuge in a, in a, in an agent that you wanted to cause mass disruption with, right? So what's interesting about that is, so nobody can escape the virus, really. So I think back to that. So design is some weapon in that sense. Nobody's safe, even the creators, right? Well, so does that make sense? Yeah, so this gets into the, well, so this is something that Charles has brought up, that they, they did have therapeutics available, right, the peptide fusion inhibitors. And this was, this was even discussed in the early discussion. How effective those are? But they, they have them. It's a possibility, like preventively treat themselves. Right. And if you, if you're able to do that, you're able to, well, shut down the, shut down the space of therapeutics, which they did do, which could have helped. Again, what they've done is seed massively into the population. And quite nefariously, when they know that there, you know, there are discussions, you know, you can watch the conferences where they say, oh, we would, we would never put furin cleavage sites into a vaccine. Right. And this, this to me just keeps nudging the needle over into the more, yeah, just darker, darker side of, you know, the analysis of, of what's going on. And, you know, we can, we can look at the epidemiological data and we can see that there's been a ramp up of diseases that you would, could predict from first principles, were these deeper mechanisms coming into play. And we see them at the neurological level, Alzheimer's, but not in everyone. Not, not in everyone. And again, you know, not everyone gets cancer in their lifetime. Not everyone gets dementia. I mean, you have to die of something, but again, it's, and so to just pull it back to diseases that we've seen increase massively is cancer. And all, all chronic type diseases that again, have a long lead time that they'll say, oh, it's non-SARS related. And these are, these are classified as excess death unrelated to SARS-CoV-2. Well, they don't know that I would argue. No. Because we, we, they're not, I don't think they're taking into account these, these disease mechanisms as catalysts to push people into a disease state. And it would be great if everyone was, you know, as God intended and perfectly healthy human beings for, you know, the length of their time on this, on this earth. But that's not the case, right? I have a little different point of view, maybe on this. I think the goal here was to seize on some outbreak and coronaviruses were the perfect example of an endemic virus that you cannot eradicate, eradicate because of the continual mutation. You can't use vaccines to stop it, or it's, it's gonna, it's gonna go and become endemic in the population. And so, you know, you can track and trace it forever and implement your lockdown and whatever next authoritarian policy you want, anytime you want. The next wave is coming, no matter what.
I think that was the goal is to unlock the spring trap of authoritarian policy. I really think some of these side effects of SARS-CoV-2, you know, we, we do see that they're retained within the seasonal strains and, and other coronaviruses. They're just a consequence of utilization of that pathogen and they don't care. They don't care, right? They care. But it hurts their story when it's mapped back to the spike protein, the toxic fats that are in long COVID, the amyloid fibrils or other, other things mapping back to spike. Well, not just spike. I mean, there are the multiple toxic epitopes through the genome of the pathogen. And once, you know, I've sort of made a conscious decision to focus on furin being injected into the swarm to increase the tropism, increase, increase the chronic disease. Chronic disease means people have to, will seek medical help. It could be. It's hard to say. It's, it seems speculative, but we've seen, you know, their plans before and utilizing other things than a pandemic outbreak to deploy their, you know, strategies of policy and potential for global governance. I think this is just one more tool in their kit. I've got to ask you this question before I forget. So when you, when you read the sort of virology and the pandemic literature, they're always like, oh, the next pandemic's coming around the corner. It seems embedded into every, you know, the beginning, right? Where does, where does that come from? At what point in your graduate training is, is, and what examples are given for them to be able to say this, this is coming and we, we nailed on sure that it, that it is when. That's an interesting question. So in my training, it was really super detailed on the molecular virology. And I didn't, I didn't really have that exposure during my initial virology training. It was, oh, look how cool viruses are, viruses can do that. And, and this or that, and I think over time, you know, people try to find value in their research. And instead of just, let's look at the basic science of what's happening with the host pathogen interaction. They say, what is the, the application to public health here? And of course, there's disease states of viruses and that's an obvious one, but there's also potential for, that's debatable whether, whether pandemics are even a potential reality, because if you go into it, with the viruses that have high brutality, die out very quickly and they're not going to be highly transmissible. So high lethality and high transmissibility essentially don't coexist in viruses. So typically the outbreak response world, which I've been very deeply embedded into and learning about over the past four or five years, comes from spillover events and, and they're, they're viruses like chikungunya or, you know, Ebola viruses or these other viruses that when they cross over into humans, they have a rather high mortality. But what ends up happening is they're, they're not highly transmissible and they don't spread widely throughout the population.
So we can argue whether a pandemic is even possible in nature or not. I think it, it could be possible under the right engineered circumstances and that's when we get the big scary, oh, bio warfare, but it's my personal opinion that we're too stupid. We don't know enough to design that correctly, to be quite honest. I think they did their best to make a very highly transmissible virus and it's got these great, let's go on the coronavirus family. It's got these neurotrophic factors or whatever else, disease states and there's going to be fallout in the long-term disease state as well. But again, I think it's the automatic immediate lockdown, lockstep response that that's been laid out in past documents. I'm sure your readers are familiar with. One health doctrine, it looks like it was being, the groundwork was being laid over many, many decades. And again, I just, I try to put it in these, in this context that people have to wrap their minds around that these events were poised, as you said, to be leveraged. And they've gone all in so much that they're taking a swipe at your children too in this, you know, fifth generation hybrid warfare that they've, and they're making a calculation about how much collateral damage that they can seed into a population. And this is, you know, I'm very, bye-bye to this YouTube channel, but I'm, you know, I'm concerned when they're bringing in gene transfection technologies into young children as, quote unquote, medical countermeasure for, you know, potentially... It's insane. It's insane. So I've got a small group called Ethical Science Council, and we haven't become very popular, but we've been educating on this for years now, and how children are not at risk of severe disease from coronavirus infection, and the risk of unknown vaccine technologies is certainly over time, has shown to not benefit children in any way, and is significantly harming children in more ways than we probably don't even see. So, you know, we have all kinds of pamphlets. I've read the clinical trials myself. There's really interesting things about after the first dose immunization, there is a negative 30% efficacy in both zero to two and two to four-year-olds. That was repeated in both age groups, so that means they were 30% more likely to be infected than the control group, and then there's also the vaccine. And the widespread bio-distribution of the technology is a huge problem. And so we can think about all of the sort of multivalent vaccines that they're developing, wanting to do COVID flu combos and put, you know, I'm sure they're thinking up 20 different messenger RNAs to put in there now. It's going to pump all through your body. Insanity. It just sounds horrible. Yeah. And then on top of that, they're further developing the RNA technology to be self-amplifying. So there's BioNTech themselves are working on the self-amplifying RNA, which is beast compared to the mRNA they're using now. And on a work which is granted to UTMB for studying a self-amplifying vaccine as well. Yeah. The bars of the prison seem very, very, very obvious. And, you know, this is why I'm infuriated. It's like, how should we say, I'm a tad aggressive with the no-virus individuals, because they get the medical tyranny part of it. Right. They come in and just start spinning the nonsense machine. And if you don't understand the weapons that are being deployed against you, there's no way that you're going to be able to circumvent them in any... The opposition would want you to think there's not viruses, because you cannot understand it to be able to counteract it. Right. Yeah. And so there's no scrutiny on the DoD programs that have been, I would say, central to bringing us to this point. Now, you know, it would be naive to think these are state actors themselves. I think, you know, I would postulate that what you're dealing with is super powerful transnational organizations that are in a position to be able to leverage the technology infrastructure of a state to push... Private-public partnerships. Yeah. And... You would believe the masses of money that are in the pandemic response.
All the web, the Wellcome Trust, CEPI, Florida, all of them. And why are they so desperate to immunize, you know, sub-Saharan Africa that's not experienced any sort of disease from COVID, desperate to get vaccines everywhere? That's what set the alarm bell off. And me, it wasn't even... I wasn't glued into the toxic effects of spike right away. But it was, you must do this. You must take them. So immediately I'm just... I swim upstream and I was like, no, no, I don't have to. Well, let me question why you're pushing it so hard, right? And for me, well, I have a good friend who speaks about sort of HIV origins and he makes a very sort of compelling case that, you know, it could have emerged from, you know, the use of primate vaccine, it could have emerged from, you know, the use of primate products for polio vaccines and all the...
All the... Well, the... The contaminants of the monkey cell culture and the production of vaccines. And the military side clued in on that very, very quickly. And like I say, if you wanted a sort of fingerprint of the modern infrastructure, you can go back to the 50s, 60s, 70s when they started doing this research and they started to find, you know, these unwanted effects when they've gone and mass distributed in Africa, you know, polio vaccines. And just as a sort of a side, what they... Koprowski, I don't know if I get the names right, had a chimpanzee colony in Africa. In Africa. And they made their vaccine and then basically were... They were getting maxillofacial cancers exploding. And they realized that, oh, we've got something here that is a... Oops, what's this? That's how much of science works. Because there's so much we don't know. We're really in the infancy of understanding immunology as well as virology. There's probably a bajillion viruses we don't know about floating around there that, you know, and only a very small subset of them are pathogenic. So we focus on which ones are causing pathogenicity, but it's much more complex than we realize. And a man's ego takes a hold and thinks that they're masters of the universe. And in the end, nature wins. Well, I would say that there's a select group that think they're masters of us and are doing everything humanly possible to... The motto I live by, live free or die. That's why I love the US man. It's so... It's just ingrained there. I love it. Hang on. Someone's sending me... This is who tells us the history of HIV. And, you know, I didn't know any of this stuff until recently. Let me share my screen. Actually, I don't know how you are for time. I could pull Nick in and, you know, he's a fascinating individual to talk to. Just about... I'll just let you know when I have to jump off, maybe 15 minutes or so. Okay. I didn't have too much else to talk about anyway, so that sounds fun. All right. Let me...
I did want to tell your audience that while we're all hyper-focused on SARS-CoV-2 and origin, and was it this or how was it cloned, they're behind the scenes doing a lot of other things. And the next wave is going to slap us in the face here with digitalization and digital currency and all health and financials being streamlined in that way. And we really need to because that is more of a control mechanism than vaccines or an outbreak ever could be. Yeah. And like I say, in my mind, that's, you know, I put it in warfare terms, but they've used this to push us in that direction. And it's starkly obvious when you see all these things being played out. Now, the problem is that it's starkly obvious, but they're able to inject into the public narrative, the goddamn nonsense machine. Again, you know, the people who will the people who will sort of be curious enough and maybe suspicious enough to say, hey, hang on a minute. What are you going to tell me? I'm eating bugs. And that they just latch, they'll latch on to the more lurid explanations. Because in a sense, they're more easy to understand. And then the it takes those people out. But at the same time, their noise and racket shuts down argument and data that could be used. Yeah, effectively. Let me let me try and pull Nick in just to Well, he can say he can cross examine you better than me around this. Just don't be too tough. Nice. He's a sweetheart. How often do you do your show? Pretty much every day. Yeah, I try to but you know, I take a sort of I have to make it sort of entertaining. Right. And so and so it's a lot of it is culture ball stuff as well. And, you know, well, to be careful not to get on to the sensationalism train, you know, spirals out quickly. Yeah, with the science, I've tried to be very constrained. And, you know, the hang on, let me just get the invite sent to this. Do this. Do this. Let's see if Nick jumps in. But, you know, I've I found that the censorship was already in place. It wasn't something that they, they slowly dialed up. It was there right at the beginning of this, this outbreak. And, you know, I was, I said, I tried to do a sort of professional approach, which was tried to warn people about the it's not a respiratory pathogen, as they're trying to tell you. It's a more complex disease. It targets the brain. And then I got shut down really, really hard. And then, you know, I just, well, you know, you see all the stupid memes behind me, and went on this sort of mimetic warfare path of warfare path of trying to upset the apple cart, in a way. And the, you know, it's, it's been somewhat successful, I'm able to, you know, reach a sort of solid audience every day. But, you know, there's only, you know, with respect to like the, you know, detailed mechanisms of virology and stuff, there's only so much I can do. I could speak about the neuroscience. And actually, there's a, you know, a constant stream of papers, which are exploring that, which is great, because people are taking interest in this sort of niche neuroscience field of neurodegenerative diseases, and also these chronic conditions like ME and CFS. And I'm great. It's wonderful. There's the interest, but there's also the human impact of that. And, you know, the, well, there was a question I saw sort of scroll back in the chat earlier, which was... Yeah, I was, I was censored, I was, I'm not on a lot of social media, and I was on LinkedIn, I was censored very early on, just raising basic questions. I wasn't even attacking too much, you know, is this response proportional to the threat, you know? And of course, I argued against their high mortality estimates were totally bogus, and all that other stuff. So I was kicked off of there early on, and that was coming out about the censorship. And I will say even, you know, just the general public who's not put into a lot of this, I try to engage people wherever I go. And I think that's important for all of us to do, you know, at your son's sports game, or, you know, the grocery store line, I engage people all the time. And, you know, just ask questions, get a little critical thinking, you know, tell the attendant, be happy to see her smile again one day when she decides to take off her mask, or whatever else. But even, you know, the general public is starting to wake up about the massive level of censorship. And they know that something's off, even if you don't know the details. But I don't know if Nick can hear us or not, but you're muted, Nick. Indeed, I just didn't want to interrupt. Okay, so Nick, meet Mary, Mary, meet Nick. Good to meet you. So you've got a pro virologist to hand Nick. What questions would you want to ask? Nick, who are you? Yeah, that's a good one. Whilst you two get to know each other, I'm just I'm gonna take a little wee break. Just bear with me one sec. Pop off down the loo. Okay. Hi, Mary. I'm an anonymous investigator. So I don't have an academic or institutional affiliation anymore. I was with a major university on the west coast, in the space of herpes research, in essentially a hybrid biology epidemiology. Yeah, so that's that was that's my academic connection in the background. I didn't like the structure of information and narratives. And I'm a bit of, you know, I poked the bear. So I decided to take it. Well, and it was a great experience. It was good to, you know, wet my chops on lab science and epidemiology and data sets and structures and pathology and really sort of round out a lot of that. But regardless, what I went back to, and probably what upset the apple cart was taking material from some lettered scientists who were whistleblowers who came across material about a program called the special virus cancer program, which ran from the 1960s to the 1970s. And it appeared when you actually peel back the onion and open up the papers, that this was an intersection of genuine, you know, some some projects were genuine cancer research, and others were clearly what we now call gain of function, they were pushing the envelope to create new chimeras, they were practicing attenuation, they were, you know, I just heard this litany of the practices and techniques coming out of your mouth for the last hour. So I went and gathered these arguments. One was from a dermatologist at UCLA, the other was from an HIV witness expert. One was from a pathologist, and his brother, the pathologist, you know, had fantastic baseline data about the activities in these projects, how it's related specifically to HIV, then a couple of people in that group got killed. So that's kind of why that whistleblower experience didn't really come forward. And it was before the era of the internet, that was all in the late 80s. A couple more people contributed to the discussion and the arguments. And one of them that was kind of a hit or miss was Ed Hooper wrote the river. And he was firmly convinced with Bill Hamilton, who was the evolutionary biologist who passed away in I think 2000, that the the oral polio vaccine, as Kevin was mentioning earlier, was most likely the heart of HIV in human beings. What Hooper never it's that I could find would really engage on seriously was all of the time in between that 1957 to 1960 campaign, which resulted in, you know, novel and unexpected cancers, there was definitely I would I don't know if you'd call it an epidemic, but there was the emergence of cancers, new presentations and in populations and demographics that hadn't had it before, all matching the footprint of where people had received this OPV product. And then there were many, many years, obviously, before we all came to understand HIV or AIDS or grid or whatever, whatever we came to learn it to be what I'd like to share with you right now is a little cameo from the middle of that era. If you need like a break, Mary flight, a drink or something. No, no, I know she's she's she's about done. I wasn't going to go into any discussion here because I heard I heard it's fascinating. Thank you. OK, so this is this is the work that was occurring in that in that midpoint. And it had a name called medical primatology. And you can see right here, there's a great number of examinations of the C type viruses which cause a variety of leukemias, solid tumors, sarcomas, transferring them back and forth between species and certainly a sharing of those findings. They went into the cycle of attenuation, recombination and then studying the chimeras. Now, Robert Gallo, who you recognize as the, quote unquote, co-discoverer of HIV, was in this track. He was in this research track from the very beginning since 1962. And he then emerges as the discoverer of HIV. They were making HIVs. The SIV was a contaminant problem. I've seen anecdotal data on it dating back into the 50s. Ever since we've had imported primates from around the world, we bring all of the endemic challenges, all of the contamination problems. Well, isn't the semi-inhuman virus now the model to study in primates, so that particular chimera? Yes, yes, yes. Another example. SIV, CPZ. Yeah, from a variety of SIVs. But so that's that's what Kevin and I have examined and explored. And I don't have the lab credentials that you bring to the discussion, but I will drop in the chat. I've got a timeline and it has some good artifacts. It has one of the major documents from this era. It's one of the annual progress reports where they speak in very clear terms about each project, the materials, the objectives, their progress. You know, you know, you'll recognize the landscape. But then all of this activity, this is probably the most germane to the current era. All of these teams, all of these new sort of hybrid functions of stepping just over the line between microbiology into biowarfare integrated into the NIH in 1978. They didn't come up with any major cure for cancer or major steps forward in treatments or therapies, but all of this activity and the recombinant DNA technology, which was the title of this this school of thought at the time, became a department at the NIH and continued. And that's where it seems that it branched out and became, you know, as you mentioned, private public partnerships. We've seen it permeate out into academia and into the nonprofits. And it allows, I think, the DOD to sidestep the global conventions and offshore. You know, they use a puppet, a puppet sort of a hand in glove as they will outsource these projects into the private world with companies like Merck. So anyway, I'll share that information. It was a pleasure to meet you. Thanks for entertaining my scary hypothesis here. That's interesting. I will want to note, just having had specific training in virology, that this is how we're taught to study viruses, to take their genomes, mutate the genome, sweep genes around, swap them around, switch them around, see what happens. And that's how we have learned to do basic science and research function of the virus proteins. So, you know, when the outside looks in and say, oh my God, they're creating all these mutants. Well, we've been doing that for years. That's how we study gene function. But as you say, it starts to enter a gray area when there actually is a phenotypic output or a pathological response to that. I mean, I have a question about that. So, how do we realistically contain this work? We're going to draw the line in a sea of gray. I don't know. I don't know. Because it seems to me, any effective pushback, particularly if it's their tactic is to use medicalization and disease threat, it seems to me that we have to sort of neuter these mechanisms that you're talking about. The techniques. That does upset virologists because that's how they've learned to do the research and they go through and make the changes and see what happens. But there has to be some line drawn. So, you know, the problem we had was that they did draw a line in, well, 2012, 2014 when they did the flu experiments, right, and Erasmus. And there was a lot of hoo-ha and discussion back then about what they should and shouldn't do. They introduce a moratorium and then we see this massive amplification into these, you know, eco-health, meta-biota-like organizations, which are then, they give themselves a lick of green paint to sound all eco-friendly, but they're the sharp edge of a very, very long sword being wielded by these defense entities. If you had a magic wand, how would you do it? How would you bring it under control? That's a really tough question. You know, maybe we shouldn't study viruses through mutational analysis at all, and we can use other approaches and it will limit our understanding in certain ways. I don't know what the right answer is. I don't have the right answer, but you can also study, you know, I was showing the different pox viruses before, you know, and not all of them have the same disease state. So, if you really wanted to look at something, you could look at various forms of the virus and then which ones were causing disease, and then map it back that way without having to do the mutational analysis. I always thought it was really weird when I was in my training, like, why are we swapping the genes around? It just seems kind of stupid, and it's only going in cell culture and doing this or that, but in reality, it has real impacts when there's negligence on biotainment, right? And so, you know, real impacts when there's negligence on biotainment, right? And I didn't bring that up before, but these people who want to deny the ability of cDNA clone to be a bio warfare weapon, how do you define bio warfare? It was really just an outbreak that they seized opportunity, the response opportunity on. Oh, man, that's a hard question. But I don't know, man. It's something that really rapidly needs addressing. You know, it's up there with, you know, I see two primary fronts that we have to push on. One is the legal with respect to informed consent. And, you know, that's wow. I got a flyer on that one, too, Kevin. OK, awesome. There are certain parameters that are required of medical professionals to to give informed consent, and I guarantee they're not doing it. But what I was going to say about the gain of function, if you deny the ability to gain a function to be bio warfare, you're letting everybody off the hook. And if we can follow along with, you know, what Brin's law has done with Adrian Puff coming out and attempting to call them out on this gain of function. Now, the moratorium was reversed in 2017. So let's not forget that. But they can attempt to I don't I don't remember all the legal terms, but extend the court case based on whatever the preliminary evidence is and get get attention around it and push back on negligence of biocontainment. You know, they have certain responsibilities to contain everything properly. And so that's one legal avenue that you're you're ignoring when you say, well, gain of function research doesn't do anything. Yeah, it certainly does. It's it's a you're boxing yourself into a very, very limited corner by trying to argue that that aspect because it applies to all pathogens that they could be potentially modifying. And, you know, if what Nick is saying that they, they had this history going back and are you still are you still with us, Nick? Well, I just did you explain sort of how the defense changed into the special virus cancer program and I didn't I didn't discuss the origin so much as the integration at the end. That's the more important part is that everything that they spent that money on all that intelligence didn't just you know, they didn't put it in a library in a special collection, it became an active, quiet department, you know, within the National Institutes of Health. But originally, yes, the, we see at in 1962, for example, there's a project called investigations of viral carcinogenesis in primates. And one of the noted scientific officers is Robert Gallo. And that's 1962. And according to the history books, the special virus leukemia program, which was its original name, wasn't formed until the 1960s, wasn't formed until 1964. That 1962 project was paid out to Lytton Bionetics, which was one of the large bio weapon ears for the Fed at the time. So that's that's part of that, that at the beginning, it was a lot of small bits and pieces, individual projects that needed a home. And they sort of gathered together under a banner of a war on cancer. And while you miss it, miss out the bit where they take change. Henry Kissinger, bring in Henry Kissinger. Oh, boy. That's the best bit. This is going to have to I'm gonna have to run. It was nice to meet you. Yeah. I hope you guys can continue the stimulating conversation. Maybe we can be back in touch in the future. Yeah, sure. Yeah, it's a real pleasure. Thank you for your time and working through this, like I say, having black-minded bench active virologist is you're a precious thing. We need to get you armed guards. Yeah, no, I'm just trying to keep my job. All right. Until next time. Yeah. Thank you, Mary. Thank you, Mary. Take care. Thanks, Mary. Well, Nick, go on, tell us, tell us about Henry Kissinger.
Well, I've got to say, he's been talking some sense about Ukraine, but tell us about him. Don't underestimate his ability to be clever and aware of his street value and cred and to shift and pivot so that he can, you know, keep the hoards, the masses of pitchforks and torches away. Well, it's, you know, it's, it seems to be woven into the body research that I worked on and the others and also rearing its ugly head today as a senior, you know, a principal advisor to Klaus Schwab and the, and the WEF. And there's, there's been excellent, excellent analysis from David and Mark and others on, you know, Kissinger's fine granular details. The part that seems to be really dangerous is when he becomes the national security advisor.
And that's this, I've heard Mark describe sort of the legal and operational autonomy and their sort of unique position in the executive branch in relation to the seat of the president and their, you know, he, he went into some fascinating details about it that I, I'm, you know, would love to learn more about, but yeah, it was, it was his real rise to power because he sort of cycled out in, in smaller roles during the earlier sixties and then came back in as, you know, a very, very powerful role and had a fascination with microbiology and surreptitious agents and agents that could be applied or distributed or deployed in a variety of ways. I say poisoning wells. Just poisoning wells. I mean, yes, yes, yes, yes, yes, yes. And then, you know, it's very important for everyone to think this is BS or I don't believe that. And that's just, you know, hocus pocus or it's, it's a scapegoating. It's very important for you to have that gut reaction. And we would encourage you to go back and do your own, just dig a little bit. And you'll find in conversations in the 1970s, there were hearings. It was all the big news about what did the CIA do? What would, what was Henry Kissinger doing with them? What was Dr. Sydney Gottlieb, the poisoner in chief doing? What in the hell were our federal intelligence and defense groups up to, particularly after Nixon's stood up on camera in November of 1969 and said, we're no longer going to do anything offensive, which, you know, we all understand was was showbutting.
I would just say bullshit. But yeah, it's bring up the paperwork. Let's have a look at it.
What would you like to see? Well, you know, the emergence of the special virus can spread your little presentation. I haven't seen it in a while. Okay.
Let's have a look at that.
Have you are you seeing? Okay, so you probably are. Let me stop that just a second. Let me go back. The screen share is on.
Okay. Okay. Well, yeah, let's look at let's go back and just do the classic. Let's look at a paper. And this is this is the Gallo project from sixty two. We were just touching on.
And it's a it's a two prong multi year project that begins here. And I tracked the project code and watch that split into a couple of other children, you know, their branch tips with other people involved later later down the line. But it had two major thrusts. One identify pathogens in the primates that were that were oncogenic to maintain and manage a network of primates for any kind of use in this space across the U.S. so that they could eliminate the problems that they were having with importation. They were having a lot of challenges getting through the scientific barriers and the testing requirements of importing the animals from overseas. So the most intelligent thing was to bring in females and begin breeding and sustain those programs.
So that move. That's what I was saying, Chad. Yeah. Yeah. Now, coming back to one of the things I say in the 200 level course about some of the materials and something that I found interesting is that they discuss the use of anti-lymphocytic serum right here in 1962. So anti-lymphocytic serum is generally produced from the blood of, you know, if you're using two components of a source animal for an experiment or a product, you would use isologous or matching materials. And if you were using chimpanzee kidneys for a vaccine or a transplant experiment, then you might suppress the immune system deliberately biologically through employing this tool called anti-lymphocytic serum. It's exactly what it sounds like. You don't have to, you know, listen to the name. That's what it is. That's what Mary brought it up at the beginning of her talk. Antibody mediated shutdown of CD8 positive immune cells as a way of modulating your model system to encourage, well, things like this, leukemia and other joys brought to us by this program. 1200 models. Yeah. And it would be great to have her take a look at maybe two or three key artifacts, not drag her through, because there's thousands of pages and there's many redundant concurrent activities. And in that, we saw Dr. Johanna was talking about the, you know, different, her awareness of the different teams and projects and experiments that were occurring in parallel on primate pathogens in Germany. And we see that in the literature, particularly towards, I mean, you can see all through the course of who the assigned scientists are, who got these contracts, you'll see a variety of nationalities, clearly. But at the very end, in the 1977 final progress report, there's a who's who. There's a massive list of the current folks that are kind of in the international scientific exchange program.
And, you know, I'm stunned. That's the part that kind of confounds me as to how or why would they leak and expose these capabilities so broadly? If not, with a clear intent of keeping a certain echelon, a certain level, a certain cadre of institutions or known parties involved in the progression of the technology. That's pure speculation on my part, but I've never been able to sort that out.
Reading that paragraph there, during the past year, macaques were inoculated at birth, were in utero, mason-physer, Epstein-Barr, herpes virus, Marek's disease. Epstein-Barr virus was given with immunostimulation and immunosuppression. ALS, and Australian antigen, otherwise known as, say it with me, hepatitis B, was given to newborn African green monkeys. I don't know how, you know, it's done, right? The deed is done. You know, how do it? You know, I was asking Mary, how do we, how do we put this back in the box in such a way that it just, you know, has, you know, it's just, you know, it's just, you know, it's just, you know, in such a way that it just, you know, has minimal impact on the population at large. And, you know, the problem is, is, you know, those virology departments are treasured by the defence industry. And, yeah, pharma, academia are the glove, and DOD intelligence is the hand. And it's been very convenient for that arrangement to continue since 1945, since before then, you know, really, probably, you know, more on the lead up to World War II. It's been a continued and strengthened alignment. It's a brick, you know, it's a brick house. And I think that, you know, I will speculate or just opine about your question to her if I might. And that's, I believe that we do want to continue having universities. I think we do want to continue having a broad spectrum of life sciences if we're, you know, talking specifically about the risk area here. How do we interpret, you know, who has the competence to interpret and score and mediate risk with potential research? You know, that's right there. It's like, who is qualified to say this could lead to disaster? This is another, you know, crack in Pandora's box. Don't do it. We can't do that. Who's got the reject stamp? And who's qualified to use it? That's, that's a, I'm sure there are people who would come forward and say, give me that stamp. Yes. Yes. Yeah. And you wonder who, where the puppet puppeteers are behind some of those people. But, you know, you don't have to look far. Just look up. Yeah. I think, I think I didn't, I'm not offering a solution yet. I'm just sort of saying, I think that we do, we, I, I don't believe in dynamiting out the old universe. I think that transformation and change management are possible. And I think that making people eat their words, like bringing forward the, uh, the Stanley Plotkin deposition, bring forward key snippets. No one is going to listen to nine hours. I listened to nine hours and I needed, I needed therapy afterwards. It was horrible, but there's, there's all sorts of key items in there that could become very important legal instruments considering, you know, in light of your, your discussions and who you've, you know, Doc Keck and all the things we've been talking about recently, those are the bits and pieces that are needed to make incredibly strong foundational arguments. And if you can illustrate the ill science, the, uh, you know, the deformed or deficient or lacking standards for safety and efficacy that are supposed to be there, that are there in the law, they're there in the recipe book, then when they're not there in practice and you demonstrate that, um, then unfortunately we're left to deal with what he brought up about what just recently happened with his decision. Uh, and that is the sort of overarching, well, it's national defense, what sort of overarching, well, it's national defense. Well, you know, that sort of big brother Trump card. And that's another hurdle that I think there are probably minds out there who have, you know, his, him, him, him included, but it's, it becomes this very compound. It's like a knot. It's a series of knots that have to be, you know, untied, um, carefully. And if you go forward and your case gets rejected in certain circumstances and in certain areas, I believe that contributes to how it makes it more difficult for people in the future to have success, uh, arguing the same, you know, making the same arguments. Yeah. You know, much as I would like to blow up those instances in a Minecraft way, census, um, you know, it's, it's, it's reform that has to be aimed at, um, the, the, the problem we have now, I would again suggest is existential because, um, um, the bureaucracies are so penetrated by, um, I don't know, wef, wef toadies just to try and hang a label on them. But, um, the, you know, the discussion we had the other day, which, which was, you know, maybe, maybe all their goals have been achieved, you know, some, you know, something that Mark talks about with the, um, the harvesting of sort of genetic material and diversity, et cetera.
Um, and they, maybe they've got it already. They've got what they need. Um, and so they're, they're free to, um, I don't know, where's, where's the, uh, club of Rome document bring, bring that up, uh, which I'm sorry, which the club of Rome. Oh, I don't, I don't, I don't think I have that one today. Um, uh, no, no, no, I, I have, I have thousands and thousands of pages. I don't have everything and everybody keeps dumping. I mean, there's so much stuff I wouldn't go get Kevin. There's new things, you know, I want to go and spend time, you know, using just search and digging through, by the way, this is another step. This is Merck. Remember our paperclip friends that gathered, they, they preferred to work in their, their company of others. They wanted to be with their friends. Uh, eventually I would assume all of their families came over initially, you know, they were allowed to communicate and mail Christmas presents back to their families in Europe. Uh, but the biologic scientists here, I wonder how many were somewhere nearby to Maurice because Maurice was an American nobody. He just, he was adult in my opinion. He just sort of stumbled in, um, as far as what he got, what he, I think he got to play with other people's toys. I think he got to be sort of the front man, but there's a mythology around Maurice. Um, Mark has really explored him and, you know, I'm, I'm, I'm constantly making mention of the other researchers because they do such a fantastic job of, uh, you know, they, they dissect these people, but, uh, the science here is, um, I think this came to mind, this paper came to mind when, uh, Jonathan was talking about mass distribution of infectious clones. And I didn't just throw the baby out with the bathwater. I'm like, you know what? I can't prove anything yet. I'm going to listen to his argument. Uh, the, you know, I've got bits and pieces. I have not done an AB comparison, but what brought me, it came, brought me back to this era where they're talking about producing huge amounts of, uh, lab, you know, just massive, you know, massive volumes of it. And later in the seventies, you see evidence of the, uh, current stores that they had produced already. And, you know, that stuff doesn't have a shelf life of 20 years, not going to sit around on it. So I wonder how much got operationalized. I wonder what got moved into commercial stores. Uh, I mean, commercial distribution and, you know, in doctor's offices, I, I, that's, that's in and of itself, something that's fascinating to me, but he was talking about distribution. Uh, this is obviously, we're talking about vaccine products. You and I have talked about some of the darker, you know, unfortunately verifiable technologies of aerosol, aerosolization, um, uh, drying and crystallization of viruses. You know, there's, there's lots of military documentation about that capability. And so it's like, I don't worry about when I watched Charles working so hard on the amazing maps and the data points around, uh, the, the Wuhan lab and all of that first cases, the wet market analysis, all of that. I was like, you know, you're, I wanted, I wanted to say, don't, don't, don't, I didn't want him to off the case, but I wanted to say, don't, don't get so sapped by that because clearly it looks like a multicentric origin. And, um, you know, we could look at the genetics with, and we did early on, we saw in that paper that got squelched, you're not supposed to look at certain parts of the genetics. And that's where everybody had shown a bright light on that topic. But this is one of those points where I just want to say that, you know, Charles, Charles work in sort of plotting those cases, um, where, where, where its power lies is, um, being able to push back against the, those that have tried to argue zoonosis and try to make it, you know, the, you know, the vanilla explanation just to replicate the masses. And, and, you know, their strategy is again, it's long-term because they want to load the literature in such a way that, you know, the students coming through are going to buy into their narrative.
And we, we, we need someone, you know, with Charles skillset, you know, that's, that's his training, right? Um, Oh, absolutely, absolutely. And, and I don't in any way criticize, and I'm, you know, I didn't do that work, you know, so, so respect to Charles, nothing, no criticism of it. I, when I saw how much detail he was going into on it, I, I felt like, um, you know, I was like, ah, let's go after the NIH, let's go after, you know, Barrick and eco-health and all of that, keep going, you know, let's follow the route. Yeah, he is. And we, we have a hell of a lot more than just the mappings. So yeah. And the, you know, it's in my mind, we have to hold these people accountable. And, and we, we've got a small window in which to do it. And so we have to take as larger bite out as we can at this point, and then hope that enough dominoes topple, um, as a consequence.
But what's the age on this document? I'm just, I'm, I'm reading through it and 1970. Yeah, you know, yeah, you know, already the, um, the techniques are, uh, startling. Yeah. Yeah. Impressive. And, um, you know, we didn't, we didn't pop out here out of nowhere, right? That's the, that's the sort of take home from this, that they're, um, they've been doing this a long, long time. And you know, the, I'm, I'm, you know, I wonder when the sort of realization came to the controllers that, oh, we should pursue this avenue towards the sort of medicalization and control. I wonder, I wonder, you know, what's that back in the seventies? Um, no, no, no, no. This is about, this is about Rockefeller medicine and the creation of cancer and the cancer industry. And there are fantastic historians who have told this, um, you know, these different aspects there, there's great material that, um, can talk to us in, in documentary and, and written form, but this is, you know, this is a well, well studied, uh, problem that just simmers because most people, it's just really invisible to most people. It's just not in their sphere of concern or priority. And, and, and they shouldn't have to worry about something insidious, but it has been, and it's what a lot of, you know, you think about hippie medicine, I'm sure everyone has had fun making fun of the granolas and the tree huggers will bless their hearts. Cause they were the first warriors to help us come back to, you know, at least in the American space, um, uh, phenotypic medicine, plant medicine, uh, you know, the, the archetypes of which most pharmacology analogs are built on and, and, and go back into that space. And they keep sounding the alarms when we have challenges to access to integrated medicine, different sorts of treatments and therapies, et cetera. Um, but yeah, this is, this is a long story as far as that piece of it. And we can go back and look at, uh, uh, you know, look at the history books and look at those documentaries to get a real clear understanding of how they planned the takeover of the academics and the regular regulatory, you know, right. You hear regulatory capture. That's what they mean. It started a hundred years ago. So, yeah, yeah. And where does the reform start? Well, in my mind with, uh, a lot of, uh, a lot of people being made, uh, unemployed fired. Well, that's the, that's the whole part. That's the, when you say change management, I, I, I, that's that, that's a, it's a, it's a word. It's a Pat phrase. Uh, it means career changes and I have compassion for, so I've thought about that. I'm like, Hmm, could I, could I think of some, uh, some 12 step program for virologists? You know, is there some way we can take all of that amazing competence and channel it someplace else? Talking to Mary, I mean, that was a, quite an astonishing conversation. And, uh, an astonishing conversation. And thank you for Mary, for being there. If you're still with us, uh, or you hear this again, that was really an important, um, you know, to hear your opinions and your insights was, was really, really good. But, um, the fact of the matter is, is it will hobble a lot of careers if we say no more to certain channels of medicine. And how do you put, like you say, how do you put, put it back in the box when there are people who will just say, you know, some private pharma or bio weapon here will say, Hey, we've got funding, come over here, work with us, you know, don't, don't bother putting it up on LinkedIn. And, you know, we, we know what you're capable of doing. How do you put out the fire? So that's you, if you can't appeal to the ethics of the people that right now are paying their mortgage and their credit card and their Amazon prime and their, whatever is their, their lifestyle with money that is derived from activities that ultimately threaten life across the planet. If you can't convince them in this state to speak up, you know, if you can't take that away from them, if you can't threaten that, um, and, and again, they'll, they will be seen as the frontline soldiers who is writing their objectives, who is funding their grants, who is reading this massive vinculum of insight about the biological vulnerability of the species that we're learning about through this work.
You know, that's, it's, I, I think there's, I think there's multiple levels that can be addressed. And I think that nonviolent confrontation in a decentralized, non-advertised way.
Think about the Maquis from deep space nine, right? They had their own little individual cells and they didn't know the cell above or the cell below. And we give away, we, we put a lot of our cards in the table in spaces like this. So I think it's going to take some very good people willing to engage in some specialized research and presentation and assembly of data, and then a, you know, an intelligent approach legally and through mass communication. I think Pandora's Pandora's box cuts both ways. We can show the history, the risks, the intentions and the results of these activities across multiple diseases, across multiple continents for multiple, you know, for years. Uh, and if we can translate that into five languages and make something palatable to most people, you could start a counter fire. You could, you could start, you could get the whole world aware of it and pushing and helping push that stone. So, you know, those are some thoughts. Well, yeah, my, my concern is that it's, we're just too late. The, they've, they've bided their time, sprung the trap and you know, they're, whilst we're trying to sort of clear our head as to what's, what's gone on there, you know, their next 10 year, 10 year stage is being loaded into the chamber and getting ready to fight damn rangers. Is, is this the Saturday night meeting of the people's front of Judea? Yeah. Yeah. Why not? What have the Romans ever done for us?
First, you know, the, well, how do you, how do you get round the, cause they'll turn around and say, Oh, look at all the developments we have done. You know, the diagnostics, the what have you. And this is in my mind, the, I could see the diagnostics and the sequencing being a thing, just can't they just get into like categorization rather than manipulation? And, you know, I don't, I don't have an issue with monitoring, right? It's the, it's the industry that sprung up around the idea of, you know, medical countermeasures, DOD driving all this such that they, well, I always, I always come back to Andrew Webber and his, you know, he was a true believer in that we'd, we'd conquered the, the existential threat of bio warfare through MRNA platforms. And everybody that has a patent and a product and a stake in a market, you know, a horse in the race, as they say, is going to be enthusiastic about that horse. You know, we have to take, take out the, de-incentivize these, these behaviors. And, you know, remember in the 1950s and 60s, four out of five doctors preferred Paul Moll. I recommend Geekvape. I'm glad you found your vape.
You went through your vape renaissance. That was so fun. I was flipping you shit. I did yesterday. I was in panic mode. I sort of fell asleep and I fell asleep with the vape resting on, what do you say, the outer ample gut. And it sort of, it sort of just slipped down the side. I sort of wake up and find it, go to use it. And it didn't work. No display coming on, no nothing.
Did you plug it in? Did you unplug it and plug it back in? Yeah. I was doing everything. I was like, what's going on? What's going on? And, you know, I knew the batteries were full and I was like, oh God, it's dead. Why didn't I order two? And now apparently there's a, I don't know how it switched off, probably because I was leaning on it in my sleep or something, but you have to switch it on. Like you've got to rapidly click the button five times.
Yes. There's a safety sequence. So you don't accidentally turn it on and burn your luggage or your pocket or whatever. Yeah. You got to go beep, beep, beep, beep, beep. So I didn't know. And that to me just, that tickles me because you are sitting there when we were talking a year ago, when we first were getting acquainted about working on a particle accelerator and you're asking me about the engineering inside of a particle accelerator. I'm like, I'm sorry, but I, you know, that's outside my lane, but you can't turn your vape on. That kills me. I love it. Now this is something I should have, I should have, would have, could have, but I really appreciate it. Thank you very much for bringing me in. And as soon as I saw who it was and saw the kinds of, you know, competence she was bringing and her real direct and clear opinions, I'm like, oh, she's unchained. She's not, you know, I mean, I heard her say, I don't want to lose my job. So she can't be a rebel, but she was speaking her mind and I was very appreciative of that, but this would have been, this is her bailiwick. This, this, so that I had that one, uh, you know, simian virus isolated in 73 or 72 by Gallo. I had that little, that snippet up. This is what became of those cells. That patient is HL 23 and her cell line became an entire fascinating thing, much like the Henrietta Lacks Hella cell line and a couple of others that took on a life of their own, you know, no pun, but this is, this is them literally taking four different baseline. Are you supposed to change the screen? Are you not seeing, are you not something new? Oh, sorry. I thought you were seeing everything. You're like, dude, I'll just share screen. There we go. This is what I'm talking about. And maybe it froze. No, I think I was on another actual one. I just shared a window. That was my bed, my bed. But, um, this is, this is as exactly as it looked for four baseline cell cultures then cross contaminated specifically with target viruses for the purpose of examining the chimeras and they, and this paper, you and I could go through this if you want. At some point, I may could pull up the paper tonight, but I don't, you know, this is not, this is not the HIV show, but this, this would have been for her. She could, she could talk us, you know, forwards and backwards through this, including, um, uh, I would have been interested to hear her, uh, suggestions or experience on risks, on what cross contamination risks might be, uh, non-target pathogens. Cause you know that for every single one of these bases, there's gotta be a little short list or a long list of non-target pathogens that came along for the ride and are part of the magic of the recombinant technology, you know, spin the dice, spin the dice, roll the dice and see what you get. And so he, they describe later in the paper, um, the progeny, the results. Um, and of course they focus on those that were, uh, you know, most mutagenic, uh, highest variability things of that nature, which would, you know, which would speak to multi-species swarm, uh, mutagenesis of something that was seeded into the population and then branched out immediately from a central clade that lines up to what Dr. Gerald Myers was doing. He was the DNA, HIV DNA specialist at Los Alamos. And he was the one that I was talking about previously who said there was a big bang with HIV one in the middle of the seventies and it, it branched out from that point.
And considering that Africa had ongoing vaccine campaigns and then the hepatitis campaigns in the U S, um, that, you know, that's one of the pieces that aligns. Yeah. Um, you know, we have the, the potentially, well, now I'd say the signals are there already, but, um, you know, the unleashing of this next generation technology on such a massive scale. Um, who knows what we're going to see in three years, five years, um, because of what they've done. And, um, yeah, okay. Maybe they won't wipe out three billion, but, you know, it could be significant amounts who, who, who do take a, uh, a hit. And and even if it was, uh, something sort of more concealed, like loss of fertility, that type of thing. And, um, you can, well, how much, how much can we trust them to be honest about, uh, data that they're, they're bringing up? Like I had this, uh, clip that I was, I was, I wanted to investigate it a little more, but apparently, uh, Euro Momo has suddenly lost, um, hundreds of thousands of deaths. And, you know, this is something that I've, I've raised repeatedly is that if the fallout from all that they've done is so bad, then they'll, they'll go and retroactively start changing the data and who's, who's keeping an eye on them at a, you know, high resolution enough level and has the, you know, reputational chops to sort of bring, bring that data forward. And there's an argument that that's sort of happening now, um, in the US backups or backups or backups, Kevin. Yeah. Yeah. Um, there are people who have been building you, they call them universes and data lakes and, you know, data warehouses and cubes and pivots, you know, there are folks who live, um, on, on that. And so there's got to be a good, that's one of the problems with replication with the internet is that you, you can't put there, there are lots of situations where putting the genie back in the bottle, um, applies. This is a good one. You can't take back something that's been duplicated. Somebody's got a back of it and they show, I mean, that is, that's what I love seeing are the examples of disappearing ink. That's another piece of it. And there are some people who are really turned on by that. They enjoy the mystery, you know, they, that's, that's their thing as far as helping, um, you know, solve the mystery. If we're all the Scooby Doo gang, um, then, you know, they, they love looking and finding those discrepancies and doing the comparative analysis. Uh, and it's pretty simple because you don't have to look at the whole universe. You look for certain, um, you know, certain databases where there are sequences. You don't have to find 20 examples of data manipulation and, uh, erasure, you know, digital, digital shredding. You have to find two or three key examples that are about the germane data like sequencing, uh, early, you know, early registration of bat sequences years and years ago papers that tie in and have matching sequences in the text in line in their peer reviewed papers. They call that out. That's what they can't take back. The digital footprint is indelible. So now it's a horribly, you know, it's like being an auditor or being an actuarial for an insurance firm. It's, it's, it's a horribly, horribly droll and awful and boring work. Um, but we all have to be chartered accountants, you know, you know, we have to, we have to find those examples and they are a basis for our arguments and those arguments need to be absolutely clear and externally verifiable. And we don't have to worry about solving for all of it, um, where we use it, when we use it, what is the format? Because, you know, I, I have compassion for what you've been through with the case in Europe and the loss of, uh, your, your associate, your colleague, uh, and all of that. I, I, you don't whine and bellyache about it, but I want you to know, we, you know, we're, it's gotta hurt. And we watched what happened for Doc Keck and that, that hurts that smarts. Um, but we have to, uh, as Jonathan's backdrop says, learn to rest, not to quit. So, you know, I know I'm, I'm, I'm insufferable that way. I'd probably piss you off with that attitude, but it's, you know, how do you, what else do you carry on? But I'm just, you know, within the last week we have had, um, you know, from Israel, basically them turning around and saying, oops, we can't find the contractual agreements we signed with Pfizer.
Which stand out in the public eye. It's about, it's about a critical mass in public opinion. That's what we're fighting. We're not worried about winning the case and arguing, fearing cleavage sites and sequences in court. We're worried about winning hearts and minds about, you know, we turn, we're using their own tools against them. We're worried. We're trying to convince everybody that this is all worth stopping and saying, whoa, Nellie, and taking a look at these new draconian policies, first and foremost, power that has been grabbed. That's the big danger and then continuing back into the science and making sure that there's good, a good balance. Like, you know, I don't know how you feel about Twitter. It seems like a weird mixed bag right now. And I didn't expect it to be a magical cure for everything, but what are your, what are your thoughts on that as a space where we can continue this conversation unimpeded?
I think it's great what's happened in the last couple of weeks. And the, you know, maybe it's naive to think, you know, when Trump, you know, he made a statement this week, right, that he's, he's going to restore, you know, properly apply first amendment principles and, you know, I'm, well, I hope, I hope that this is a turning point in that direction. I'm still, I'm still of the opinion that we need to be holding people to account such that it's, it's so shocking to those that went along with all of this, that the, yeah, there's, you know, it'd be a hundred years before they think about doing or trying to do something like this again. The, you know, that's, it's not much to be resting your hope on. Yes, but there have been unanticipated synergistic effects. I think we're also at risk of a whole ton of countermeasures and counterintelligence. Another, another learning chore for everybody to have to come up to speed on the fact that that really exists and how to, you can't recognize it. There's no magical glasses you can just put on to recognize bullshit, but you've got to unfortunately turn the squelch up on your scrutiny and not just get sucked into everything. And, and you begin seeing the patterns of where critical thinking is actually coming from and where collective narratives are gathering. So I, you know, there's, there's, I think there's hope there. I think people, I think there's a whole, I'm seeing a whole lot of quiet from folks who seem to be full of vaccine hyperbole and we're doing all of the most, you know, the real brutal, you know, let them, let them die, you know, the horrible, horrible, disparaging people that were questioning the safety of the products. I haven't seen them bearing their teeth. I, you know, I still see what appeared to be a simple, you know, basically I think of it as an ad sale when any major quote unquote news or journalistic outlet comes forward with some of the rot that's coming out right now and making excuses about why people are dying and making, you know, just, just doing the astroturf job over, you know, that's hello gaslighting at a global level. I think, I think you guys said that the other day of, of what we're all seeing that the data, you know, you, you, we can't ignore our eyes. So anyway. Wow. Yeah. May it long continue. It's just, are those organizations going to, well, that intelligence defense going to relinquish their grip on, and I don't, I don't think they are. And, you know, maybe, maybe the shackles being taken off right now. Maybe, maybe that's just a more data gap. Now maybe, maybe that's just a more data gathering for the next, the next clamp down. I don't know. I wish I, I wish I had more, more data, you know, more, more insight, but it's interesting that we have a situation where they admitted that they were literally scouring Twitter. It didn't matter the size of the account.
Right. This just came out in the last couple of days. If they, if they thought something was inappropriate, and, you know, in this instance, it just means against their narrative pushing. They, they took it out. And I guess a big angry finger needs to be pointed at the FBI and their involvement in this. Again, you know, how do you, how do you reform that institute? And, you know, how does that happen globally as well? Right. Because, you know, we don't want to, we don't want to be an situation where we completely shoot in the foot, the United States, such that it, it becomes chaotic and ungovernable more than it already is. And I was going to say, weren't you just here on vacation? What are you talking about?
I thought you had some fresh insights. Well, hang on. Someone's asking me, why is Japan there on that eighth or ninth wave of COVID? Because, like, as Marie was saying, that these are endemic viruses. The problem, the problem we have right now is that, as she explained, a trait that gets injected in, that confers advantage, will, will stay in the, in the swarm. And, you know, the, and look, biology isn't like the smooth graphs that they show you of like exponential growth, like a bacteria colony, et cetera. The, the mathematical models are extremely limited, and you can expect this to drag out for some time. And so, yeah, of course, you're going to see wave after wave. And the problem we have is that they've picked it as a, a control mechanism to leverage against the population. And I, well, you're doing people's front, right? Sitting here. We go in, we go in, we kidnap Violet's wife. And it's, it's, it's, it's never going away. That's the, it's, it's like anything. And I've, you know, and I've tried to say this a lot from the beginning, that we have to come to equilibrium with it, right? We have to come to equilibrium with it, right? We have to come to equilibrium with it, right? That we have to come to equilibrium with it, right? Much, much like anything and, well, large library of pathogens that we, we do deal with. And, you know, the, the danger is, is just just them convincing the population that we need to be on, or subject to a constant sort of track and trace. And, you know, I see someone, splitters, yeah, talking about the Well Cup, but, you know, apparently MERS is floating around now. And we could, you know, maybe, maybe part of their planning and gaming out is you get, or you, or you unleash the more, more benign version and get people running off in different directions. And then when the pushback comes, which it is, which is what we're doing, then something much, much more dangerous emerges on the, or in the environment. Again, I don't know. What I do know is that I think we're dealing with psychopaths and they, they will do anything and everything to maintain their privilege positions. And, you know, but they've never seen it from our perspective. They've never had a collective or compassionate worldview. It would seem, and I'm not equivocating for them. And I'm certainly not excusing them. Hello. You know, we're talking about life and death. Yeah. I don't want one of those rich Roman imperialist tidbits. Oh, bag of ocelot noses. Okay. My favorite that I still get people with, and they don't, most people don't know what it's from, but they always laugh about it as I, oh, two points, two flats and a packet of gravel. Right. You know, when they're going to the stoning, every, everybody should know that every single line. But yeah. So back, you know, back to it, back to the black pill. So I, I thank you very much for giving me some time with you tonight and for, you know, being able to tie it together with a real life virologist. That was fascinating. And I'm going to be, I'm still working on the 300 level program, which is going to be, I don't want it to be a history lesson about eugenics. So there's going to be a little bit about eugenics there. You know, it's going to be, try to not cover the same material as the one and 200 levels, but go back and show a bit more of the framing of what appears to be the best, you know, the best explanation, best evidence for how and why all of this stuff happened.
And then also come back in right here, like we're doing on the screen and get back to some of the key moments. Now, this is 1977 and he's bragging, this is Gallo, you know, as the lead scientist in the lab. I don't know if he had any assistance. They are not named here. Certainly this is, this is interesting to me because I never found Tony Fauci's name in any of the SVC papers. I certainly didn't find Dr. Judy Mikovits. She was just beginning her career as HIV hit the scene. So she was, I believe, I don't recall her timeline, but she was not in the agency at this time. But this is him demonstrating that he can characterize leukemia causing or leukemia related viruses from a variety of primate sources. And in particular, he likes or is specializing in the category of the primate type C RNA tumor virus. Now that's a mouthful for a specific little categorization in the RNA virus family. And that's what SIV is. And it really is genetically primarily what HIV 1 and 2 are as well. So to me, since this predates the emergence of the disease in the West, and he ties into this strange patent fight behind the curtain all during the 80s that was terminated by President Reagan, he jumped in and negotiated a 50-50 split with the Pasteur Institute. You know, there's many, many other pieces to the evidence. But this is for me something that resonates specifically about Gallo. It's like, yeah, he did go looking for these things, and he was successful as an investigator. And he wasn't doing this, you know, on, you know, he didn't have a buy me a coffee account. He wasn't doing it in his, he wasn't Bill Gates doing it, you know, out in the garage. He was doing it to the best of other people that we have to stay semi-detached from and take a look at the institutions. Who were the institutions? Lytton Bionetics was just one of the dogs of war. They took the money, and they spent it, and they said thank you, and they delivered. Who paid Lytton? Who told them that those were scientific priorities? And who was in charge of the ethics and the oversight? And all of that is available in some place, you know. You said again and again, it has to start in the U.S., the U.S. has to do it. Well, this kind of, I hope, factors in and dovetails in with work that Mark has done, certainly work that Doc Keck has done, and others in gathering a body of data that we have to make a map to. It's too much for anybody to just get their arms around. We have to say this is where the good stuff is. This is where, you know, basically index it for the world and then replicate the hell out of it. And then no one is at risk because there are thousands and thousands of copies of the database around the world. And people can begin really pushing on media and other investigators and academics to say we've got to look at this now. This is a now or never type of situation. And I think that there's enough folks that are turning the tide. I'm watching allopaths start suddenly turning the corner about vaccines and looking at the science, looking at the outcomes in their patients, doing real, you know, being healers. And that's very encouraging. And so I think there's multiple levels. We know the nurses know what the hell's going on. They're the most intelligent. You know, they are really, you know, they are the healers in the world. And they already know they're five steps ahead of us. So we have to pull these people together. We have to get more cohesive in the spaces where we can where it can be interactive. And I think you should bring your best Sunday behavior and become a Twitter spaces person on a regular basis and just make a regular scheduled pit stop for 60 minutes. Make it a very brief interaction and you will begin accumulating and it will ripple and other people will pick up the material material. It's not you. It's not signing up for, you know, getting behind anybody like RFK or anyone. It's about the truth and it's about the mission of what we have to accomplish. But I think you'd have I think you'd have good success in that space. And, you know, like I saw you in the up at the podium when you were doing the presentation and you were a bit nervous. I know you knew you're jet lagged and all of that, but you did a great job. And I think that if you present yourself in a little more coherent, meaning, you know, agenda every time there's something we're going to be covering. And today it's X, Y and Z, whether it's a paper or a topic or a change in legislation or legal case or whatever. You know, I don't know what kind of scope you want to expand to, but I think that your voice would be effective in the Twitter spaces. And, you know, you should consider it. I am the. Well, you know, maybe maybe my work here is done. No, not at all. Not at all. Not at all. No, there's going to be army of raccoons at my door burning my house down. No, no, this is this is your no, this is your space. This is your platform. But as a small side salad, you could take the best. You could just take probably the most important two or three items that have occurred in the last cycle or you're in the middle of and say, let's talk about this. You're restricted because you have to do it in the radio format. People can tweet stuff you can do. You know, there's there's now you can you can have a thread and chat links and all of that, but it's not the same as presenting and reading through and doing all of that. So doing science without visual aids is very, very difficult, especially when buying to parlay with the the public. It doesn't doesn't have the maybe the background. And, you know, that's something that I constantly sort of wrestle with. And I'm I'm getting old and there's the stuff's moved on so quickly. Anyway, you know, I don't know how much relevance I can I can sort of bring to the larger discussion. Well, there's there's a lot of overlap. So if we talk about the Venn diagram of topics and conversations, there's a lot of concentric stuff in the spaces. There are people that are I attend a couple where there are frontline care providers. So these aren't these aren't research careers. These are these are providers and practitioners. And they cross, you know, a number of specialties. And one, you will come into contact with some resources and insights and new data that might be beneficial period for you, for anybody that you know, you can bring back to the raccoon cave if you like to. I think that the opportunity to sort of magnetically attract interested minds and like minds is going to be I think we've we've turned the corner and you you have that platform as another space where you can get more folks involved, more fresh folks in the raccoon cave if that's where they arrive. But but again, a 60 minute framework with your mind and the amount of knowledge that you've got across the board about these things, the way that you can approach some written content, just queuing up two or three items and making, you know, really considering, you know, watch the clock and considering you'll maybe surrender 15, 20 minutes of it as Q&A. You won't give out any microphones until you're done with your share, you know, sort of the download and then say now let's talk and people will fill in the rest of the time. You don't have to create a 60 minute framework every time you do it. And if you just do it once a week, that's manageable. I mean, look at you, you're on every day twice, twice a day sometimes. So I can't feed the little raccoon cubs.
Yes. Yes. And I repeat, I was not indicating that he should leave the raccoon cave. I don't want to start rumors anyway. Well, let me know when when you want to talk again. Thank you so much for having me spend some time with Mary and with yourself. And I hope she can come back. And yeah, yeah, I'd love her to get into, you know, the weeds of this sort of conversation. And sure, you know, the work, you know, I'm convinced that, you know, the history of it is so important to, well, people need to understand that this isn't just something that just spontaneously emerged in the last couple of years, right? There was a long winding path through the institutions to get us here. Yes. And we have to be meticulously and triple checked prepared so as to not be swept aside. We have to make a compelling argument that bites and leaves even if it's a small percentage, a percentage of people who are experienced or come into contact with it, sort of with that itch to go in and verify it. And they'll open the data and they'll see it for themselves. So, you know, you keep it very simple. You reduce it, you reduce it down. You're Italian, you know, in the genetics, you just reduce the sauce down to the beautiful tomato, just very fine sauce, yeah, and a little bit on the top of the pasta. Don't drown your pasta. So, we bring just critical pieces that align to the specific topics so that we maintain a manageable amount of information. That's easy enough to tweet. You can do three tweets and say today we're going to be talking about these three tweets that I put up in the nest or down in the in the thread. But the point of it being is that you are inside of it. You are probably not the best person to look at yourself and your reach and your impact and the value of what you've done over time. You know, I'm not saying you're unaware of yourself, but you do what you do. And what that means to others is none of your business. We get to interpret what, you know, the value of it. And it's been very valuable. And the way that you have managed and negotiated the changing and emerging information and data from the research and from, you know, patient outcomes has been spectacular. And so I think you should continue. I'm just giving you a rah rah. Yeah. Thanks for the ego boost. Yeah, I say no, no, no, no, no intentions of stopping right now, folks. I think, well, I think they've still got some surprises lined up for us. If any of the past couple of years go by. So all right, I'll let you go.
Okay. Thanks very much. Have a good weekend. Yeah, you too. Take care. Cheers. Cheers. All right. Yeah, I hope that was a value to people. And I will.
I don't know, I might take a day off. I've been streaming hard last couple of days. And, and yeah, it's nearly Christmas. Okay, time flies. All right. So with that, I'm going to wish everyone a dear take care. God bless. I will see you in the next one. You don't know how angry I am. You do. I was just leaving for work. You do not understand. After reading that all on, I will be arrested for not taking a fucking vaccine. I will fucking kill you.
This is fucking dead serious. I am fucking dead serious. These people don't know who the fuck they're insane. No fucking vaccine or MRA will ever fill through my fucking blood. Never. I will fucking die. Fucking fighting for my fucking tears and my fucking blood. Fuck these motherfuckers. Fuck this shit.