Will Dove 0:00 Well over two years ago, as it became obvious to many of us that the injections manufactured in the billions by big pharma were not vaccines, but rather a bioweapon, I confess that I believed at the time that it wasn't a very good bioweapon. Even now, with the work of doctors Denis Rancourt and Joseph Hickey, showing that to date, approximately 17 million people worldwide have died from the vaccines, they still do not appear on the surface to be very effective at achieving the goal of the globalists to kill, maim and sterilize a large percentage of the human population. As obscene as it is for any decent person to contemplate killing 17 million people, that is still well less than 1% of the global population. In fact, it's only 1/5 of 1%. From the perspective of the globalists who may want to kill as much as 90% of us, this bioweapon of theirs seems ineffective. Unless of course, we have not yet seen the full effect. New evidence keeps coming to light as a virologist, Dr. Geert Vanden Bossche said, the vaccines have a million different ways to kill you. Early this year, we learned that the shots contain not just RNA, but a substantial amount of DNA. Then we found out about the inclusion of SV40 simian virus protein strands. Recently, Dr. Phillip McMillan released data on the fact that the more often the person is reinfected with COVID, the greater the risk of a severe effect on their long term health. But the latest revelation is the one that concerns me the most. Very recently, we learned about something called ribosomal frameshifting, the ability of the shots to corrupt key proteins in the bodies of the injected. Everything, but everything that happens in our bodies is controlled or regulated by proteins. Dr. Jessica Rose holds a PhD in computational biology, a rare degree. In the past, I have interviewed Dr. Rose on the vaccine adverse events reporting system. But Dr. Rose also holds post doctoral degrees in molecular biology and biochemistry, and a master's degree in immunology. She understands the harms caused by the shots, not just on a deep biological level, but also in terms of real numbers from her statistical analysis of the VAERS system. She joins me today to give us all a thorough explanation of just exactly what ribosomal frameshifting is, and how it can potentially affect the vaccinated. It's never my intent to engage in fear mongering. I prefer to focus on message of hope. But it's also my responsibility to bring you the truth. Dr. Rose, as with all ethical scientists, will freely admit there's a lot we don't understand yet about how the COVID shots affect the body. It is my genuine hope that the information revealed in this interview is not as grim as I fear. Because if it is, the COVID shots could be a ticking time bomb. One that sooner or later will go off inside the bodies of everyone who has been injected. Will Dove 3:51 Jessica, welcome back to the show. Dr. Jessica Rose 3:53 Thanks for having me back. It's great to be here. Will Dove 3:57 Now when I invited you to do another interview, not long ago, I wanted originally to talk about more information, we found out about how they're monkeying with bears because in our last interview, you provided proof positive that they have removed huge amounts of data, almost certainly to hide certain safety signals. But recently, I read some articles on your substack on ribosomal frameshifting. Now, Dr. Trozzi and I covered this very briefly in a previous interview. But the more I read about it, and you're very good at explaining it, where a guy like me with a very basic knowledge of biochemistry was able to, looking up a few terms, understand it. And it's very concerning. It really is. And this is very new data. So I think we need to get deeper into it. So we have to start a course by explaining what is ribosomal frameshifting. So, I'll get started. For those of you folks who maybe didn't take biology in high school, a ribosome, it's just a structure that makes proteins. So, the ribosomal frameshifting, now I'm going to let you explain that, Jessica. Dr. Jessica Rose 5:01 Okay, so just for some background, on December 6, not so long ago of this year, a paper was published in nature, like the real nature, called N1-methylpseudouridylation of mRNA causes +1 ribosomal frameshifting. So this piques a lot of interest in the small community of people who are kind of waiting for this paper to be published, quite frankly, it didn't surprise a small handful of us because, in fact, a couple of us, including Kevin McKernan and Peter McCullough, wrote a paper predicting things like this, that paper's on the preprint server and you can you can read about it there. But basically, what this means is that proteins that we're calling off target proteins are being produced a, a percentage of the time up to 10% of the time, or about 10% of the proteins that are being produced are these off target proteins. And what that means, whenever you hear on target, that refers to the the intended spike protein, spike proteins, or the fragments, however much template you have to work with. So these are off target proteins are, they're like, proteins that we we don't even know what they are. And they could actually be aberrant, which means that they could be inflicting harms that we we didn't predict. So there's a couple of reasons why this was easily predictable, if you know a little bit about what they did to produce the modified mRNA itself, and the reason why it's modified mRNA and not mRNA. So first of all, what they did, in order to produce the optimal amount of protein in a species, using code from another species, you do something called codon optimization. So this is a little bit of high level biology, but I'll explain it as best I can. We all know about DNA and RNA, and they there are DNA bases. And there are RNA bases. And these bases are read by a ribosome, which, like you said, is this protein machine making thing in triplets. So this triplet is called the codon. And each, each entity, species... Will Dove 8:05 Can I just jumped in there, Jessica, because, you know, obviously, I'm trying to act as a bridge between your immense knowledge, my basic knowledge, and then the knowledge of our viewers, which may not be much at all. So what Jessica is talking about, these codons, if you took any biology in high school, you know that there's something called nucleotides that's the guanine, cytosine, thymine, okay? It forms the DNA. Now in RNA, the thymine gets replaced with uracil. Now there's something in those are called nucleotides, three nucleotides form a codon. And that's all you need to know about that. But I'm also going to sort of jump ahead because I know where Jessica is going with this. Like I said, in RNA, the thymine that exists in DNA is replaced with uracil. Now that's a nucleotide. There's something called a nucleoside, which helps to form those nucleotides. And in RNA, that's uridine, except in the modified RNA, as you were speaking about, they replaced that with pseudo uridine, which you mentioned earlier. So I think that catches people up to the codons part. Please continue. Dr. Jessica Rose 9:10 Yeah, that's right. And I'll bring some more detail into that too, because that's the second part of what they did. That probably causes frameshifting. So each animal species entity uses their, they have preferences for their own codons. This is called codon bias. So the codon bias in a virus is not the same, for example, as in a bacterial species, like E. coli, is not the same as a homo sapiens. You get the idea. So they're not going to use the same sets of codons in the same proportions. The reason for this like the whole surrounding idea is that in addition to the The way that the codons are read and translated into an amino acid is by base pairing with an anticodon, which is the reverse of the codon. So this this is coming along, with this anticodon as a transfer RNA. So this is a different kind of RNA that's really essential to translation. And this transfer RNA is carrying this amino acid. So the transfer of this amino acid to to this binding event via this ribosomal pairing is what translation actually is. That's the translation to the amino acid. So each entity has their own transfer RNA set. They have the clouds of transfer RNAs, let's say and some of these are rarer than others. So in humans, we have arginines, for example, just one of the amino acids, that's rare, it's considered a rare amino acid. So there are fewer transfer RNAs carrying the arginines that base pair with this codon. So basically, that's it's probably a little more detail than you need to understand. But they codon optimize this mRNA for optimal protein production in humans. And basically, what that did is that it increased the CG content. So because of the codons that humans use, where there's a lot of G's and C's, there was an increase in this content and the byproduct of that Will Dove 11:53 By, by CG content, what you mean is the cytosine guanine nucleotides, right? Dr. Jessica Rose 11:58 Exactly. Will Dove 11:59 Yes. Dr. Jessica Rose 11:59 Yeah, that's right. So the byproduct of that, and this is new to me. But I understand the implication is that you're going to get more potential for actual mRNA misfolding, or kinkiness. So there's also this whole subject matter, which is its own realm, you know, every time you, you take the top off one can, there's a whole world in there. So there's a whole world of mRNA structural biology as well. And I'm like, you know, I thought, I'm a protein level person. So I, this is new to me. But of course, it makes sense. So there's structure to these, these mRNAs as well. And they can form kinks when there's increased GC content. So if you imagine a little ribosome, they the- the diagrams in textbooks are probably really wacko, but whatever they make them look like burgers, because the top button is like the the larger episomal unit, and the bottom button is like the small ribosome. And there's binding to the small ribosomal unit and then you know, they, it rides the, the mRNA to look for a start codon. Will Dove 11:59 Yes Dr. Jessica Rose 12:13 A start codon is just one, a sequence of three bases that is very specific. It encodes a methionine. And that's how the ribosome knows where to start translating from, so, then this large ribosomal unit, like, creates a complex and then you get translation ensuing. So, so if you have an mRNA, that has, I'm just going to use the word kinks, that has a bunch of kinks in it. And you imagine, just imagine pulling a string through a burger, okay. And so your string has a bunch of knots on the on the arse end of the burger, okay? Your, your string coming out of the burger is going to be your nascent protein, okay? It's going to be a string of amino acids that just comes out of the burger. Will Dove 14:15 That's quite alright. I think it's actually quite a good allusion. Dr. Jessica Rose 14:17 Right. It's the way that I imagine it but it's probably no, no, this, anyway, follow me down the burger path. So your nascent protein, which is just a string of amino acids comes up comes out the head end of the burger, and say your percent of the burger has kinks. You can imagine. Well, the first thing you have to know is that as your nascent protein leaves the ribosome, folding will happen. So, folding of the protein can happen without these little chaperones or with them, whereby this this guy's going to fold into a certain conformation based on on its amino acid sequence, so, and based on, you know, the, the energies involved. So it's not a complete protein. So it's it's not, it's just going to kind of do the like the initial folding. But, and this is a key thing, if you have kinks in the back end, you might actually run into a slowing down of translation. Because it's I don't know if this is true, this I mean, it's been, this is what I suggested in literature. But again, this is not my field. So I'm just trying to imagine how this would happen. And Kevin McKernan actually confirms that this does happen. What's going to happen is that instead of the steady stream of string being pulled through, and the amino acids being added on like tuk tuk tuk tuk tuk like a little machine, it's going to go nuh ngyeh ngyeh ngyeh ngyeh. And it's going to pause. There's a number of reasons why the ribosomes will pause, but this is one of them, if there are kinks in this mRNA. So when you have ribosomal pausing, this is when frameshifting can occur. So if it's if it's kinda like, ngyeh ngyeh ngyeh, like it's kind of stuck on this one place, that it might actually skip a spot and end up in a different frame. So that's exactly what the codon, so that's exactly what the codon, or the ribosomal frameshift is, when you move outside of the codon that's supposed to be being read into a new frame. And then you can imagine if you're not triplet, triplet, triplet, triplet, triplet, if you go triplet, triplet triplets get duplet with something else, that little guy there, that new trio is going to encode possibly a new amino acid that's not really supposed to be there as part of the encoded protein. Will Dove 14:43 Right Dr. Jessica Rose 15:07 So that's one possibility. That's one reason why. Go ahead. Dr. Jessica Rose 16:47 Before you continue, I'm going to attempt to give a very simple translation of what you've just told us. So... Dr. Jessica Rose 17:12 This isn't wine, by the way. I'm not a wino. It's water. Will Dove 17:15 No, I assumed it was water. In fact, that's, that's what's in my coffee cup as well. So, we've already explained folks what the codons are, it's just a trio of nucleotides, and the ribosome is moving down that RNA chain, and it's using, probably getting a little too sciency, something called anticodons to copy those and make a duplicate. And what Jessica saying is, okay, something to remember is that proteins are supposed to fold up, but they're supposed to fold up in a particular way. And so, if you're running into problems where it's folded up, and it's kinked, as you were saying, and it causes it to pause, what may happen is that that ribosome is going to skip that codon. So you move to the next one. So that codon never got transcribed properly, or at all, possibly. And so what you end up with is not a duplicate of that protein, but a, well, I don't know, frankenprotein is what I've been calling them, because you don't know what you're gonna get. Dr. Jessica Rose 18:16 So it's more of a replacement of the amino acid that potentially encodes a new protein. So at the at the mouth end of the burger, you're getting a nascent protein, but you're being, you're feeding in an mRNA. So there's two different things here. This transfer RNA that comes along is feeding the amino acids as part of the translation process. So you got a lot going on here, and it's going tac tac tac tac tac tac, look, it's a really fast process. Will Dove 18:45 Yeah Dr. Jessica Rose 18:45 I wish I knew exactly how fast but Will Dove 18:49 I believe we're talking about fractions of seconds. It's Dr. Jessica Rose 18:53 Yeah, it's, it's fast, and and it's doing this all the time. And it's like, it's it's a really good system. So yeah, it's, it's about, the reason why I bring up the mouth and and the the protein. It's called cotranslation. So you, cotranslational folding. So as you're actually ticking on the amino acids and producing, producing, producing chain, chain, chain chain, it's it's leaving the ribosome, and folding at the same time. There's a little animation that I posted on Twitter. God, love the people who are making animations. They're brilliant. And I don't like Twitter, but I'm gonna send everyone to my Twitter to go watch it because you'll see in in one minute visualization exactly what I'm talking about. And then, you'll realise... Will Dove 19:44 If you will send me the link to it, we will actually insert it right here in the interview. Dr. Jessica Rose 19:49 It's @JesslovesMJK. So just type in @JesslovesMJK, and I'm a highly shaddow- shadowbanned, so you'll have to probably put a bit more effort into it but it's a little bit down on my wall or whatever it's called on Twitter. But it's an animation of how translation occurs. And it's, it's really cool. It's really cool. It's very cool. Will Dove 20:11 And I looked up some animations myself when I was researching for this interview. So it really does help a great deal to visualize it. I mean, we have to understand the animations don't look anything like what it actually looks like, but it Dr. Jessica Rose 20:23 Well, it might! Will Dove 20:23 ...allows our brain to understand. Dr. Jessica Rose 20:23 Which is really cool. Yeah, yeah! Now, it has the burger and Will Dove 20:25 Yeah. yeah. Dr. Jessica Rose 20:26 the nascent protein and the mRNA. And little, you know, the feeding of the of the, the, the, the nucleus, the bases, and, okay, so yeah, go there. And look at that, it'll really help if you're kind of confused about my burger. Will Dove 20:47 We'll find it, and we'll insert, right here, so we can assume at this point that people see it. Video clip 20:52 What you're about to see is DNA's the most extraordinary secret: how a simple code is turned into flesh and blood. It begins with a bundle of factors assembling at the start of a gene. A gene is simply a length of DNA instructions stretching away to the left. The assembled factors trigger the first phase of the process, reading off the information that will be needed to make the protein. Everything is ready to roll. 3, 2, 1, go. The blue molecule racing along the DNA is reading the gene. It's unzipping the double helix and copying one of the two strands. The yellow chain snaking out of the top is a copy of the genetic message. And it's made of a close chemical cousin of DNA called RNA. The building blocks to make the RNA enter through an intake hole. They are matched to the DNA letter by letter to copy the A's, C's T's and G's of the gene. The only difference is that in the RNA copy, the letter T is replaced with a closely related building block known as U. You are watching this process called transcription in real time, it's happening right now in almost every cell in your body. Dr. Jessica Rose 22:43 But before I lose the momentum of the the analogy, there's another really important concept to understand when talking about frameshifting, and that's that is this replacement of the uridines with not just pseudouridines, but N1-methylpseudouridines and I've done a lot of research on this. And there's a huge difference between a huge difference between pseudouridines and N1-methylpseudouridines in terms of base pairing. I'll get into that after but so there are 801 positions where uridines occupy spaces in the code for the Pfizer product, this BNT162b2 thing, it's 4285 bases, I think, and 801 of those positions is occupied by uridines. So they didn't swap out a percentage of uridines. They swapped out all of the uridines for N1-methylpseudouridines. And the reason why they did this, or at least what they're telling us is the reason why they did this is because it imbues this I love that word imbues this modified mRNA now with the property that it can evade detection by the immune system, specifically by toll-like receptors of the innate immune response. So basically, what that means is that these mRNAs, because mRNAs are fragile. This was always a problem with developing this technology. It's like how do we make these things stick around longer so that they can, you know, get to the ribosomes and get translated? So this was the key need to swap out the uridines. The I don't know if they did any testing for swapping out proportions, like maybe swap out 10% of them and you'll imbue the same property of stealthiness but they they went all the way and they swapped them all out what the problem would do it and there's a lot of problems and I'm going to get to something else. If I remember. The problem with doing that right off the bat, if you think about in the in vivo setting, which is the human being the cells of the human being, that get transfected by the LNPs is that we have no idea what the effect is going to be of barraging a cell with so many pseudou... N1-methylpseudouridines, we don't know, because our cells aren't used to seeing that proportion or that many. So we can only anticipate if we have half of a brain cell, that the outcome might not be good because it's out of balance. It's, first of all, it's unnatural. it from the point of view that we're introducing these things by force, we're using these Trojan horse lipid nanoparticles, we're also introducing them in horrifically high numbers, like also the amount of modified mRNAs that are encased in these lipid nanoparticles that are being dumped into the cell. It's, it's an insane amount. And so there's no real way to know studies were done. That should really concern people, no studies were done. The study is kind of being done now. But we're not actually collecting the data in the right way. We're not doing studies to determine, like exactly what I just suggested, like, what would be the differential effects of substituting out 10% 50% 80% 100% of the pseudoUs in certain, you know, settings, for example, even from, you know, innate immune detection. So this is a big problem. And it could also be causing genomic instability, and I'll get to that after. So the thing about this sequence is that there are triplets, there are codons that actually have triple Us, or they did have triple Us. And when they substituted these guys out for N1-methylpseudouridines, all of a sudden, they have triple N1-methylpseudoUs. And sometimes you have four in a row, like if you have two triplets together. This, this might be a U here, sorry, I can't bend, there we go. These might be N1-methylpseudoUs in these two. So what that does is it increases the chances, this is called a slippery sequence. So when you have like three Us in a row, three Us, three As, whatever. So it increases the likelihood that the ribosome can slip past this and frameshift. So this is another mechanism of action by which, that this is actually what that nature paper showed explicitly, that the substitution of the N1-methylpseudouridine causes this frameshifting, that's the conclusion of the paper. They modified the uridines in different ways. And they did beautiful experiments. Don't ask me to explain them now. Because it's like, way out of my brain. But they really did fantastic experiments, the paper is brilliant, to show definitively that it is these N1-methylpseudouridines that caused this particular problem. So again, this is coming out a little bit too late. It's a few years after billions of people have been injected with this stuff. And like we said at the beginning, the problem with frameshifting is that you're going to end up getting proteins produced that are off target. And we again, we don't know exactly what these proteins that are being produced are, and we don't know the biological hazards, but we can anticipate that there might be some because what the hell are the proteins being produced? And and I mean, at the very least to their releasing an immune response, because that's what a foreign protein would do. And at the very worst, they're causing protein misfolding or they are misfolded proteins. This is a big problem because that can wreak... Will Dove 29:52 I think we need to touch on that because as we talked about earlier in the interview, the proteins are supposed to fold up, but they're supposed to fold in a particular way. So when you produce errors into the proteins, they don't fold properly, as you said, misfolding, and we know that misfolding of proteins causes problems, such as... Dr. Jessica Rose 30:14 So, um, most people are familiar with Creutzfeldt-Jakob disease. This is a prion, um, a prion disease, which is very serious and... Will Dove 30:25 Colloquially called Mad Cow Disease, for those of you... Dr. Jessica Rose 30:28 That's right Will Dove 30:28 Right. Yes. Dr. Jessica Rose 30:29 Yeah, that's right. So it happens when a particular protein which is necessary for, you know, in our brains, that's produced by our brains, is not folded properly, if I'm remembering correctly, God, I hope I'm remembering very fast. I've written like 2000 substacks in like, a year, so it's kind of messing me up. So this particular protein misfolded, called scrapie, is is very bad. It can cause pathology, which we know as Creutzfeldt-Jakob disease. So that's one thing. There's also Alzheimer's, which we think, data suggests that this is a byproduct of amyloid, amyloid proteins. So I again, I've written a bunch of articles on this. So if you need more details, please go read them. Now, amyloids are basically they're like the, without getting too detailed, beta sheets, how, well, I won't go into that. So they're, they're a protein of a certain kind, that are very durable. Most proteins have, like, enzymes that can break them down, if they're, if they're not supposed to be there, like a lot of these aberrant proteins that might be being produced by ourselves from frameshifting are probably just being chewed up and you know, removed, they're, they're sent to the garbage. So don't everyone freak out about that. I mean, our bodies are remarkable things. And if it detects something being you know, manufactured that isn't supposed to be there, there are mechanisms in place to, to balance this equation. But in the in the case of amyloids, these guys are tricky because they they don't break down. This is the problem with them. They tend to stack on top of each other. And they can also make normal clots as part of the clotting pathway with fibrin and platelets much more durable, which actually might be why we're seeing all this micro clotting and macro clotting issue with the shots. It's possible. So the reason I'm talking about amyloids is because of the on-target production problem. So what have we just discussed there is is the off-target production problem and remind me to get back to the auto immunity and molecular mimicry issue. Will Dove 33:13 Yes Dr. Jessica Rose 33:15 So, the, I'm jumping around a little bit, but I hope people can follow. So the proteins that are supposed to be produced as a byproduct of this modified mRNA template is the spike protein supposed to be pretty complete, right? The reason why we're doing this is so that the body can mount an immune response to this foreign protein to various epitopes on this, this thing ta-da-da, that that was the design. The problem is, and this has been this has been discovered and written up in a couple of peer reviewed journals. I've also written a number of articles on this. So anything I'm talking about, you can go read about in my substack. There are amyloidogenic peptides in the sequence of the spike. This is this has been shown. Now what I mean by amyloidogenic peptide is that there are short strings of amino acids within this protein, the spike protein that is produced by our cells that have that are imbued with the properties of amyloids, which means that when those are translated, if they're let's just say they're, they're snipped in the right place, and they have they get the potential to to stack onto each other and form an amyloid plaque. This could be very bad pathologically. We're seeing a lot of things that look like what I just described, associated with the shots. I absolutely think this is what's going on, I think amyloidogenic diagenesis is is running rank because of the production of amyloids from this spike protein. I could be wrong. But it makes a lot of sense based on what the literature has shown so far. Will Dove 35:17 And we should also point out that the amyloids aren't just going to necessarily cause the large clots that everybody's heard about, they can also cause very small problems, microscopic. Dr. Jessica Rose 35:29 Exactly. And this brings us back to what I was saying before we got on camera. All of this is going to, like, even before we get to protein production, what's what's most important to visualize in terms of potential harms is where these lipid nanoparticles traffic to, and which cells and how many actually get transfected because in a lot of cases, you're probably going to, you're not going to get a lot of transfection. Mark Girardeau has a theory called the bolus theory whereby you need, by the injection that we're all getting, you get a concentrated dose, which in, say, a narrower vessel is going to increase the chances that you're going to get transfection in a narrow vessel if you have a lot of LNPs, lipid nanoparticles. So you can visualize it a number of ways. The body's, like, claim to fame is to distribute, disseminate, to wash out, to not have concentrations of anything, especially fats in the bloodstream at once, because it's not good, right? You want free flowing, you want, you know, linearity, you want blood cells that aren't, like, clumped together, you want lipid nanoparticles if you get injected with trillions of them to not be in a big glob, because that could probably cause a lot of problems. So the body itself, as I'm visualizing, this is all my own thinking, there's nothing to back this up, is going to try its best to disseminate those lipid nanoparticles into like a single stream. If it can, it's going to try and prevent the concentration as much as it can, by whatever mechanisms it has. Maybe it's going to coat those guys with ApoE and send it to the liver. For example, you can look that up, ApoE, Apolipoprotein E. Maybe it's already embedded with Apolipoprotein E. Anyway, nevermind. So getting back to what I was saying, if you have, let's just say you have some lipid nanoparticles that make it to your brain. Okay? If you have manufacture of these things in your brain, and there's an amyloid problem, it's going to be way worse for you than if you, say, have a few cells in the lining of your blood vessel transfected and producing these guys, it's still probably going to cause a problem locally in that blood vessel. But it's not going to be as bad as if it's in your brain. At least that's how I'm envisioning this. Will Dove 38:33 Yes Dr. Jessica Rose 38:33 So I think the reason why some people are, one of the reasons why some people are experiencing specific kinds of serious adverse events is is location, location, location, and also, what they were injected with. This is the other thing, it's like, there's so many bloody parameters here. We have no idea what's actually in the vials, according to like what we know. At best, the percent mRNA integrity is about 60%. So we don't even know what that thing is going to be, like, set to encode in the frickin' first place. It's tragic, all these things. So one of the immunological chaos is that we can envision very easily happening is an auto immune reaction. So, James Lyons-Weiler, has published a paper on this called pathogenic priming go look that up, go read that paper. And there's a number of other people who've authored papers on the subject of molecular mimicry. So, what molecular mimicry is, is that is when you have a cross reaction between two, let's just say, two sequences of amino acids that are the same But they come from different places. So if you have a human entity that has, you know, a TLR QQ or something like these are the the sequence of amino acids in whatever protein this is that are bindable as an epitope, we call that an epitope. And you also have the same thing in the spike protein, let's say, that's also bindable as an epitope by an antibody, let's say. So antibodies come and they're specific, and they they bind with high specificity to these epitopes, which are just these sequences of amino, these short sequences and amino acids that it recognizes. So you're probably getting at, you're probably seeing where I'm going with this, if you have an immune reaction that's already poised against this specific sequence. And this also exists in human beings in some, you know, cell or whatever, or some protein, then the the reaction can cross over to the human stuff. And that's where, when we get an autoimmune reaction happening, so you can actually start having a reaction against your own body, let's just say body or cells or proteins. This is well established, we, I mean, the auto immunity levels in the clean West. They're off the charts. We don't see them in India, for example, we don't see autoimmune conditions happening there. It's rampant here. There's all sorts of theories for that. But Will Dove 41:03 Well... Dr. Jessica Rose 41:33 I mean one of them Will Dove 41:35 ...it's just pretty much in direct proportion to the number of shots that have been taken, is it not? Dr. Jessica Rose 41:38 Exactly this is actually one of the best explanations for it. It's also the clean hypothesis whereby the, like, most Westerners, as opposed to people who live in India, and you know, I'm not making any, like, I'm afraid woke people are going to, like, launch an attack on me for saying this, but there are more worm infestations in the East than there are in the West, that that's a fact I'm not saying anything against anyone. I mean, I think a small worm burden is a good thing personally. There's a branch of the immune system that actually is responsible and dedicated to keeping worm populations at bay in the human body. There are probably mutualistic relationships between many worm species and human beings. Probably not all of them like ascaris worms, but we have dedicated mechanisms to help. Like the the the class of antibody called IgE is dedicated to binding to worms. So anyway, I won't get too far into that. But there's also, it's interesting to think about in terms of auto immunity, because there's a connection. It's been a long time since I thought about this. So I'm just going to mention it for everyone to go off and research and not dwell on it. There's a connection between certain autoimmune conditions and the mechanisms that it happens and this same branch of the immune system that's in charge of removing worms, so I had an hypothesis and I don't think this is mine. I think it's just, you know, it's it's one that is in the science community, that it's kind of like this branch of our immune system and it's dedicated to getting rid of worms is just kind of like, Hmmm I'm bored what are we going to do in the West? And so maybe they're, you know, they're just excited about having something to do. We are in still all these these these new ideas know these these new toxins coming into the body. Anyway, never mind. Look that up. It's an interesting subject matter, look, look up inflammatory bowel disease and and treating it with with tapeworms. It's, it's a really fascinating. Will Dove 44:10 Okay, now, I want to get back to the broader spectrum of the autoimmune disorders in a minute. But first want to back up a few minutes to what you were talking about earlier, with the potential possibility that we're getting large concentrations of LNP in the brain, combined with the amyloids, high concentrations. And if I understand that correctly, and please correct me if I'm way off base here. What you're gonna get from that, quite likely, is plaques, brain plaques building up, you're gonna get really, I would think symptoms very similar to what you were talking about earlier with the Mad Cow Disease, prion diseases. Dr. Jessica Rose 44:47 Alzheimer's Will Dove 44:49 Yeah, and that's, if that's correct, the thing that scares me about it is the long onset. I mean, I realized we're not talking about actually having a prion disease. We're talking about something similar to it, but prion diseases are A. always fatal... Dr. Jessica Rose 45:04 Yes Will Dove 45:05 ...and B. very long onset. You're looking at five to 40 years incubation period before the symptoms hit. But once the symptoms hit, you're generally dead in a year. Dr. Jessica Rose 45:05 Yep. Will Dove 45:05 So if this is producing something in the brain that's very similar to that, that could be catastrophic. We could be looking at all of these injected people who have these ticking time bombs in their brains that are eventually going to manifest and the part of the, I think the really bad risk scares me about that is knowing that pretty much the number one side effect of the shots is brain fog, which tells us that it's having an effect up here. Dr. Jessica Rose 45:44 Yeah, yeah, I don't quite understand brain fog yet. But that's a real thing. It's also associated with, with how latent viral infection's coming back, but anyway, that's also connected to the shots. But you're right. And you know, the thing that bothers me about it is because of all the censorship, and because of all the condemnation of the simple idea that these shots could be causing any adverse events, let alone neurological adverse events, which we know that they are, this has been a signal from there since January 2021, I published this. There's no way to reverse engineer this to actually prove it. You know what I mean? It's like, they're gonna say, oh, it's probably this, this new food additive that was added to these products that's causing these alarming rates of neuro degeneration in young people. They're going to come up with some crap, you know what I mean, and everyone's going to, I imagine everyone's going to probably buy it because it couldn't be the shots. Because of all the programming, the propaganda, it's like, there's nothing wrong with the shots, it's not possible your government wouldn't lie to you. So it's, it's it bothers me a lot, that there's a huge cover up going on here. And there's a huge community of people who will will persist in making sure that the masses will never trace back their injury to those shots. You know, what I mean? Will Dove 47:33 I understand exactly what you mean, Jessica, but I think your own research is the answer to that, because you're pulling data out of VAERS that they're trying very hard to hide. But you are, of course, you know, you've got a PhD in computational biology. You're very, very good at analyzing data, extracting data, and some of the couple of charts that you published recently in your substack show, when you compare the COVID vaccines to the flu vaccines, an 800% increase in autoimmune diseases, and almost 900% increase in multiple sclerosis, or which is a form of autoimmune disease where the body's attacking the myelin sheath. Dr. Jessica Rose 48:11 Yep Will Dove 48:11 Your own data from their, their database... Dr. Jessica Rose 48:15 Yep Will Dove 48:15 ...proves that lie. It is the shots that's causing this damage, and it's causing extreme damage. Dr. Jessica Rose 48:21 Yeah, and that's exactly right, what you just said, it is causative. They're, like, if it's not, right now, I challenge the people who own this data, the CDC, the HHS, FDA, whatever, whoever is going to be or is in charge of the safety, the assessment of the safety signal, I challenge you to explain to me how when you normalize per million doses, you see this discrepancy? If you go back three years prior to the COVID shots, and look at all that we're looking at the flu, adverse events in the context of autoimmunity, or specifically multiple sclerosis, just pull out the multiple sclerosis. That's the measure code. And in contrast with the three years since the advent of the COVID shots, explain that to me. And then tell me how that this pharmacovigilance database is designed precisely for this. It's to generate signals for assessment of potential dangers associated with products. Tell me how, if by your own assessments using Bradford Hill Bayesian analysis or PRRs that this does not satisfy a causal situation. Will Dove 49:48 Yeah, exactly. Dr. Jessica Rose 49:49 I'm willing to be wrong, but show me how. Will Dove 49:52 Yeah, well, it doesn't seem very likely. Jessica, I'm going to attempt with my own, once again, very meager knowledge to give kind of a summary of what we've talked about and the impact of it, because, of course, this ribosomal frameshifting, it's a very recent discovery. We've known for a long time about the toxicity of the spike proteins, and they cause damage to chronic inflammation, like chronic inflammation is going to cause cellular damage, which is going to cause organ damage, which is going to cause disease. But this is a completely different mechanism. Now, what we're talking about now is basically genetic damage, it's it's mistranscribing proteins. And as you said, probably a lot of them just end up getting discarded, because they're, they're just not functional, so the body breaks them down and gets rid of them. But we get some that are close enough that the body keeps them, but they misfold, and, as we've explained that misfolding, we know causes problems, this has been known for a long time. And over time, if this process is going to keep going, so you're, it's, it seems to me that it's going to be cumulative, that you're going to get more and more faulty proteins that are folding incorrectly, they're going to be causing problems. And because this is very new, I mean, we don't know how far this could go. But it seems to me if it remains unchecked, eventually, this is going to cause a very serious problem in a large number of people. Dr. Jessica Rose 51:20 Well, the thing about it is, it's it's like anything. If you introduce something that's not kind of part of the, the the system that was designed by nature, even if it's a natural thing, if you if you bombard a cell with with something, even natural, like water, is not going to be good. That's the thing. It's like, this is all about, it's a combination of things, I mean, these these are absolutely not natural, by by any stretch of the imagination, if you ask me. And the introduction methodology, the transfection is not natural. It's these lipid nanoparticles are, they're similar to to chylomicrons, which which are little fat bubbles as a byproduct of fat metabolism. But they're exogenously injected into our muscle tissue and probably make it pretty fast to the circulation. So I really want to remind everyone of that, like, all the downstream effects from mistranslated proteins from properly translated proteins, whatever these proteins that are, you know, encoded for by the modified mRNA, the swap outs of the N1-methyl, like, all of these things, individually, lend to potential problems physiologically, because they're not supposed to be there. Anybody who keeps thinking that this is this was an innocuous vaccine, or very, very, very misled. These are, they're called the vaccines because they were designed in order to induce a specific immune response, but they're nothing of the sort by any by any way that you look at it. Vaccines require decades to go from concept to arm. The vaccines are are typically attenuated. Guys, viruses or just proteins, it's not something that can self replicate. It's not something that is, like, that has software that's installed, that's produced by your hardware for an unknown amount of time. This is completely different, as a con- as a concept. And I just want to, I know that we're finishing off but I just need to finish off on this note. Another recent discovery is this residual DNA that's been found in the vials. This is a big problem, this is another problem. If the possibility of integration of any of these DNA bits, fragments is there, which it is because there are a lot apparently in some of the viruses there are a lot of small pieces of DNA, the foreign DNA that is the byproduct of the manufacturing the modified mRNA that got spilled over brought over. Not good. You can have a ton of problems from an onco- oncogenesis point of view, which is cancer. Will Dove 51:22 Yes. Dr. Jessica Rose 51:27 You could have genomic instability Um, you could have double stranded DNA repair mechanisms becoming defective, which we've seen, all of these things I'm talking about are in the literature. So that's why I'm saying them specifically. And it begs the question on this particular subject matter of the DNA contamination, does this change the definition of these products to gene therapy, because the definition of a gene therapy is like modification of a gene intentionally. And what that means necessarily is that you have to get DNA to the nucleus, into the, you know, that that nuclear center via the nuclear pores and integrated into the genome in a specific way. You know, you can swap out a defective gene for an effective gene, for example, the concept is brilliant, but that's not what these things were meant to be. So I'm not saying they were designed as gene therapies, they certainly aren't, as they were proposed to have been designed because what we were told is that these are modified mRNAs encased in lipid nanoparticles, there was no mention of DNA. Now, there's not supposed to be any DNA in here. They're brushing off these new findings aside by saying it doesn't matter doesn't affect the safety profile of the product. Sent them like, how does it not affect the full safety profile of the products? You can't say that because you have admitted that a certain DNA fragment called SV40 promoter is is there in sequence, but you're saying it has no effect. It's it anyway, I can go on for another hour, and I shouldn't. So I implore everyone to just read the few articles I've read, the preprints that Kevin McKernan, David Speicher, Maria Gutschi, and David Wiseman and I have put up recently on, it's on OSF Preprints, on this DNA fragment thing. We've also written a response to this Nature paper about that, N1-methylpseudoUs causing frameshifting. And I've also published something that got into the Brownstone Journal, which is awesome, talking about the effects of on and off target protein production. So I think that's it for everyone's brains for now. And mine. Will Dove 57:40 Yes, and thank you, Jessica, for the work that you do do to to make it easier for those of us who, you know, obviously don't have several degrees as you do to understand this stuff. Right, folks... Dr. Jessica Rose 57:52 I just read a lot. Will Dove 57:54 But I think that we've explained it to at least enough to understand the gist of it. You will find a link underneath the interview to Jessica's substack. Do go read the articles. You know, I, Okay, I have a little bit more knowledge than most people because I was a paramedic when I was younger. I found that I was able to get through Jessica's articles. I did have to look a few things up. But once I understood some terms, really, I got it. I understood it was. So Jessica, thank you for the work you're doing. Yes, you've been amazingly prolific. I think I mentioned to you that I don't have time to read nearly as many substacks as I would like to. I probably read yours more often anyone else's just because of the quality of the content and the things that you find and reveal. So once again, thank you for your hard work and for your time today. Dr. Jessica Rose 58:41 Ah, thanks a lot. I appreciate that. It's it's been a great use of my time in the last three or four years Will Dove 58:50 Yes, indeed, and and of your extensive expertise. You don't talk about yourself, but you are one of the most qualified scientists I know. And I've spoken to a lot of them. So, once again, thank you for all the work you've put into this. Dr. Jessica Rose 59:04 And the secret is I just want to be a longboarder. So...