Couey vs Wilson debate (30 Oct)
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This article will be regularly updated over the next few days and therefore you will need to refresh your browser to get the latest version because I intend to add new material and links over the next few days. I have ripped the audio and transcribed it using word online but it is rather messy and unstructured and is 94 pages long! This is therefore a work in progress. The first timestamps are just rough indicators (my own) before I used the automatic transcribe. I am hoping that I will get some input from the “Racoon” Discord. You should be able to download the transcript here: gig2.docx
This is the debate between Dr Jonathan Jay Couey the neurobiologist and the molecular biologist Dr Daniel Wilson from Debunk the Funk.
Debate (1:21 min)
Pre- Show talk (starts at 00:06:38) In the Pre-show talk Jonathan was critical of Dr Kevin McCairn and remarked that pointing out the contamination in the vaccines and the blood work was a distraction. I beg to differ and think Jonathan is wrong. We are at the point of the mass vaccination of children and not everyone has the time or the mental capacity to engage in an academic discussion about immunology. Science has thrown sand in their eyes. Most people need a simple message to focus on and contaminated vaccine is a good starting point. We know there is contamination as people died in Japan and batches were withdrawn. We simply no longer have the luxury of the cut and thrust of academic debate and most people are simply bamboozled or find it overly complex. Setting the academic niceties aside the message must be simple and clear. When in the trenches you are forced to fight dirty, and it is time to go for the jugular. They have a huge propaganda machine and the medical establishment and pharma behind them. The demonstration of how the vaccine reacted with blood was powerful and simple to understand and with the help of Dr Fleming Kevin was able to reach a huge audience. We need to support each other otherwise we will go down the DRASTIC route. We all need to focus on our strengths and focus all our efforts on the enemy. Hold the line. Play to your strengths. You are all doing a great job keep the pressure up.
10:00 Ribosomes Dr Wilson’s doctorate?
19:00 Dr Wilson introduction
21:00 Natural antibodies and IgG and IgM
Dr Wilson: ( 00:21:55) What I think Geert got wrong was this idea that natural antibodies can neutralize and clear Sars-CoV-2 infection all on their own. We have antibodies in our body that could theoretically recognize any epitope to any pathogen….we have antibodies that can recognize any epitope from any pathogen that is due (22:42) to hypersomatic gene shuffling…… but those antibodies are not from class-switch mature antibodies so they are typically really low in abundance, and they are not going to be really good at binding…so you can detect them in cell assays…so they exist…they are a thing…but they are not good at binding…..the B cells making the antibodies that might bind Sars-CoV-2 need to undergo class switching and further hypersomatic mutation to create better antibodies IgM is typically not going to do much against a virus.
JC: 24:00 …when T cells are responding early to infection, they are not responding to spike protein epitopes, they are responding to the earliest expressed epitopes in viral infection….and when they then activate apoptosis in those infected cells there are viral particles and fragments of these digested cells and the viral particles that get digested by the macrophages that are there, that are then processed, and those need to be cleaned up. That is what the antibodies do in a natural “well done” infection…the antibodies are cleaning up the viral debris, they are not the primary way the body is stopping the virus from infecting cells. How would any antibody that is in your blood stop a virus infecting the epithelial cells of your lungs? It won’t. That is what T cells do and when they fight the infection they create debris which the body has to clean up, and that debris is often times very much the same from infection to infection and that is the reason why those IgM antibodies work at low concentrations and low affinity. And the only reason why you need to enrich antibodies for specific antibodies is for when the viral load reaches a level where it is systemic and that does not happen with every infection because T cells take care of that…and I think most of the TV biology ignores the fact that asymptomatic infection in a healthy person is T cells responding to the first genes expressed in viral infection and that is not the spike protein.
Dr Wilson. 26:00 The spike Protein is the first thing the body sees. JC: That is not true- the first thing the body sees is are the proteins presented on the HLA receptors when the cells are infected, and those proteins are viral proteins and that is how it works. Dr Wilson interjection: Including spike. J.C. (26:27) No, it is the first proteins that are expressed the spike comes afterwards, you first have to express the proteins that hijack the cellular machinery of the epithelium, and those proteins must also be expressed on the outside and they are the first T cell epitopes available. There is no other way to debate that, those are the first and most prolific T cell epitopes, they are identified in at least 10 different papers as the most immunogenic epitopes in the genome and that is because T cells respond to the earliest proteins.[i]
27:00 Dr Wilson….Geert is saying antibodies alone can clear an infection JC response…you are parsing things out (semantics) because Geert is a vaccinolgist with 20 years’ experience (of course he knows about T cells) but….vaccinologists have to look at antibodies because it is the only read out that they have got. Dr Wilson interjection: No, you can measure T cells
JC response: You can, but not all of them…because the memory T cells resides in the lungs and anyone who works on the immune system of a mouse knows that because you have to sacrifice the mouse to get the memory T cells you can’t measure them in a human, you have to get them when they are migrating. Dr Wilson interjection. No, you can get them from germinal centers JC…but they are not the memory cells, they are not the ones residing in the lungs, you can’t…it is not possible and there are no papers except for in mice. Dr Wilson refers to a longitudinal memory [ii] and they measured T and B cell responses. JC. Right, they are stimulated memory B cell responses…they are not the same thing….as the ones residing in the lungs…there are memory cells that migrate back and memory cells that stay from colonial expansion and from antigen affinity enrichment and there are also memory cells that reside at the site of infection. Wilson: And in germinal centers which you can assay. JC: Right, but you can’t assay the ones that matter the most…the ones which they only understand from mouse experiments and monkey experiments because they can remove the lungs. They can sample from the lungs…you are arguing against nothing though…because you are still not admitting that T cells do the job. What other cells are getting rid of the infected cells? Wilson: Macrophages. JC response: NO Macrophages cannot get rid of infected cells the way that CD8 positive cells can because they cannot target…(macrophages) they clean up. The primary response to any infection is CD8 and CD4 positive cells. It is not antibodies DUDE (30:18)
00:30:19 Wilson Antibodies are a frontline defense. JC They are not…..
Wilson If the titer is high enough, they are. If the titer is high Enough, yes, they are.
J.C. That’s that’s exactly why the titer does not stay very high in a healthy person because they are cleaning up. Wilson 00:30:28 They neutralize them, neutralize. If antibody titers are high, the virus will not be able to infect or spread very well. 00:30:38 JC Oh, is that is that, is that what you see in the data now that that that antibody titers correlate with people who can get? That’s ridiculous.
You know, that’s not true. Wilson 00:30:47 Well, we know that neutralizing antibody titers correlate with outcome and with infection and everything so. JC But but you you know that you know that I’ve done like six months worth of streaming to show that that’s not true. There are paper after paper………… 00:31:28 JC But they’re not as important as you think they are. Would you like to hear a virologist? 00:31:32 Wilson Admit that like? ……. JC 00:31:38 That they don’t know what antibodies mean. Would you like? They don’t, they don’t. JC 00:31:43 They don’t know what antibodies mean. They do not know whether antibodies are a correlate of protection or not, and that’s because that’s because….
— Moses Eleftheria (@EleftheriaMoses) October 28, 2021
Wilson 00:31:52 So so, so there’s a difference there. OK, a correlate of protection has not been determined for SARS-CoV-2 so. That means that if you have really high antibodies from, say, a natural immune infection and also really high but lower titers of antibodies from a vaccine. From that difference. Is it we don’t know the significance of it. We don’t know the immune correlate of protection, but we do know that higher antibody titers do correlate with better outcomes for patients…..
David LV Bauer ADMITS to viewers how the Pfizer jab WEAKENS your natural immune system.pic.twitter.com/wjS80ivCNu
— Lisa (@lisaf15021) October 3, 2021
Dr Wilson adds the following papers under the video (on his Debunk the Funk website). I have taken the time to add citations from those very papers:
Wilson Heading: Most neutralizing antibodies elicited from SCV2 infections target spike:
Convergent antibody responses to SARS-CoV-2 in convalescent individuals“Affinity measurements and mapping of naturally occurring and in vitro-selected spike mutants in 3D provided insight into the potential for SARS-CoV-2 to escape from antibodies elicited during infection or delivered therapeutically”.
SARS-CoV-2 neutralizing antibody structures inform therapeutic strategies“Antibody sequencing revealed the expansion of clones of RBD-specific memory B cells that expressed closely related antibodies in different individuals…..Although there is currently no vaccine, it is likely that antibodies will be essential for protection. However, little is known about the human antibody response to SARS-CoV-2……In conclusion, most convalescent plasma samples obtained from individuals who recover from COVID-19 do not contain high levels of neutralizing activity”.
Wilson Heading: Presence of neutralizing antibodies is predictive of patient outcome:
Neutralizing Antibodies Correlate with Protection from SARS-CoV-2 in Humans during a Fishery Vessel Outbreak with a High Attack Rate“In addition, our study shows only that neutralizing antibodies are a correlate of protection: we cannot be sure that protection comes from neutralizing antibodies per se rather than some other immune response with which they correlate, such as T cells”.
Wilson heading: Multiple antibodies recognize several sites on the spike protein post-vaccination:
Convergent antibody responses to the SARS-CoV-2 spike protein in convalescent and vaccinated individuals“While these clones initially offer protection, this property could be lost as widespread selective pressure on the virus is exerted on a region with genetic and structural plasticity”.
JC 00:33:19 And it’s never, it’s never seen a coronavirus before? Wilson 00:33:23 Not Sars-CoV-2 JC Oh, I see. And so what’s so different about SARS Co V2 from the rest of the coronavirus is is it all the proteins or just a few? ………. JC 00:33:35 How different it’s 61% different in what’s that? 61 percent? Is it all spread out evenly, or is it found in certain proteins that are highly conserved across all coronaviruses? Or don’t you know that answer? Wilson 00:33:47 I know that it’s a 60% a 60% a 60% difference in the genome is huge. JC Yeah, it’s huge unless it’s not, unless it’s not all spread equally. My friend and it’s not, it’s not, it’s spread, it does because the immune system remembers the genes that don’t change. ……[iii]
Wilson 00:34:10 No. but it Doesn’t, it’s it’s clearly not able to recognize unclear source code B2 value though, when millions of people have died. JC 00:34:14 So how come 50% of the people who get infected don’t even get sick, don’t even know they’re infected. How do you explain that? That doesn’t happen with flu?……….
"Based on the available literature, we found that there is scant, if any, evidence that asymptomatic or presymptomatic individuals play an important role in influenza transmission. As such, recent articles concerning pandemic planning, some using transmission modeling, may have overestimated the effect of presymptomatic or asymptomatic influenza transmission. More definitive transmission studies are sorely needed".
Estimates of the asymptomatic fraction are affected by the study design, and the definitions of infection and symptomatic illness. Considerable differences between the asymptomatic fraction of infections confirmed by virologic versus serologic testing may indicate fundamental differences in the interpretation of these two indicators.
00:34:22 JC: Do you get high viral loads of flu and not show symptoms? You do not. Sorry, but you don’t. That’s complete baloney. Wilson: Yeah, in some cases we do you do. It’s it’s it’s. Very common to have an asymptomatic carrier of something that happens. It does happen. JC AGREES: Yes, it does happen, but it’s much more likely to happen now that we have these silly transfections going around. Wilson: TRANSFECTIONS? JC: Yeah, transfections, you know the…..Wilson: The yeah, no transfection is it’s a choice. 00:34:59 Wilson: It’s a choice to call the M RNA vaccine in a transfection but… JC: It’s not, it’s what it is. JC: It’s not a vaccine, it’s a transfection. Vaccines, have an adjuvant and a pathogen in them…… 00:35:12 Wilson [They] Have an adjuvant…It’s the mRNA….the adjuvant is the mRNA. They designed it specifically not to be immunogenic. Did you not read about how they did it? JC: I don’t know. 00:35:20 Wilson: Oh, I read about how they did it and it does act as an adjuvant because they’re able to purify it with HPLC that increases recruitment of dendritic cells to the site. They also pseudo-urodilate = (Pseudouridine) it, which also increases dendritic recruitment to the site that acts as an adjuvant.
00:35:36 JC: Oh my gosh, you are actually totally wrong. You know that, right? It’s actually the opposite.00:35:42 Wilson: You’re just saying I’m wrong, that’s. 00:35:43 JC: No, but I …. Wilson: That’s what happens. JC: I’ve interviewed, I’ve interviewed both Robert Malone and Luigi Warren. Luigi Warren is one of the guys who invented this. He’s the guy who came up with the pseudo you’re the idea of using this alternative. Wow man, you are shocking me right now. 00:36:02 Wilson: I mean, that’s literally how it works. pseudo-urodilation and HPLC purification increases dendritic cell recruitment. 00:36:09 JC Of what? where at? Do you mean at the site of injection? Wilson: yes JC: Because the mRNA acts as an adjuvant. I would love for you to give me a reference for that. I would love for you to give me a reference for that because it’s my understanding that the reason why they needed to use this alternative basis so that it would not be immunogenic because RNA is one of the most immunogenic things in the body. 00:36:46 Y Wilson: Yeah , yeah they went through a lot of trial and error to get this right. JC: To get it not to be immunogenic and now you’re telling me it’s the adjuvant and it’s completely wrong. Wilson: Oh, it’s that that’s definitely how it works. 00:36:58 JC: I’ve heard other people tell me it’s the lipid nanoparticle that is the adjuvant. You guys are crazy. Wilson: No, no. JC: There is no adjuvant. That’s the whole point of this. If the mRNA was the adjuvant, you would have such a problem. 00:37:09 Wilson: It is an adjuvant…OK, let me just get this reference for you. 00:37:19 JC: Is it from Moderna or Pfizer? Are you giving me a scientific reference from Pre con? 00:37:23 Wilson: No, this is a review of mRNA vaccines before COVID existed. JC: Cool, cool, cool. Send it to me please. Do they talk at all about the fact that they had to reduce the immunogenicity of the mRNA? Or how do they? Wilson: Oh, yeah, they had to try to figure out how to make it stable enough that the immune system wouldn’t totally just chew it up right away then. 00:37:48 JC: But the immune system doesn’t chew up mRNA dude. You’re a molecular biologist. You know that that’s not the immune systems job. There are just RNase that do that. Wilson: It’s passive immunity. JC: OK yeah OK. Well, I mean just don’t say that’s like the immune system, that’s that’s silly. Wilson: It’s, it’s a defense against foreign invaders that is part of the immune system. 00:38:14 JC: I’m so confused as to how this could be the adjuvant and also not immunogenic. I don’t get it. Wilson: It’s a balancing act. JC: It’s it’s not. Wilson: The immunostimulatory properties of mRNA conversely, can be increased by the inclusion of adjuvant…… blah blah blah blah blah.
Wilson was quoting this:
“The immunostimulatory properties of mRNA can conversely be increased by the inclusion of an adjuvant to increase the potency of some mRNA vaccine formats. These include traditional adjuvants as well as novel approaches that take advantage of the intrinsic immunogenicity of mRNA or its ability to encode immune-modulatory proteins”. mRNA vaccines — a new era in vaccinology
Three decades of messenger RNA vaccine development "Finally, we discuss the mRNA self-adjuvant effect as a critical, but dichotomous parameter that determines the safety, efficacy and strength of the evoked immune response. Notwithstanding, the potency of this self-adjuvant effect of mRNA must be weighed against the risk of any adverse reaction inherent to it, including inflammation reactions and auto-immune event".
00:38:31 JC: inclusion of an adjuvant…you just said the words you dope. Are you reading Oh my God, you just read the words and you’re telling me I’m wrong? Wilson: I’m leaving, I’m finding it hard. JC: Find another paper dude. Holy **** I mean. Wilson: Chill out, chill out. JC: Dude, you’re starting to bother me because nothing you’re talking about is right. It’s the opposite. ……. 00:39:20 J.C. You cannot, but you can’t have it be not an adjuvant and an adjuvant or not immunogenic and immunogenic…..It’s like you just read the article today. 00:39:35 Wilson: It’s a balancing. 00:39:35 JC: You just read the text that said mRNA can be added with an adjuvant and then you stopped reading it because you knew you were putting your foot in your mouth.…00:39:50 JC: You should know it already because I’m talking about general principles of immunology and that is that mRNA is immunogenic and you’re telling me that this is the adjuvant. That can’t be true because otherwise the vaccine would not work like it’s supposed to, which is expressing a ton of spike protein so that the body will build antibodies to the spike protein. It’s one or the other. Dude, it’s crazy. It’s like you work for Moderna and you’re tripping over yourself to give us a stock portfolio presentation. 00:40:24 Wilson: Uh-huh sure. Yeah, so that’s that’s exactly what they do. HPLC and pseudouridilation recruit strength dendritic cells. JC: What there…you’re just said the same thing you said before. You’re not explaining to the biology of it. 00:40:46 Wilson: Yeah, it’s it’s in… it’s in this paper. JC: What is the biology behind it though? You explain that to me. How does that work that the mRNA gets in disguised in the lipid nanoparticle? So, then it doesn’t attract the immune system and it expresses spike protein and then it attracts the immune system.
How? What’s happening. Can you explain that? Because when a virus does it, a virus hijacks your cells and your cell’s machinery and the cells then signal out saying that I’m hijacked both by presenting the proteins that they have to express, and by sending out signals what?
What happens here, does it send out similar signals? 00:41:26 Wilson: It’s there by your body reacting to the foreign RNA. JC: I thought it was to the spike protein? 00:41:32 Wilson: No, that’s the recruitment of dendritic cells. JC: What is the recruitment of dendritic cells? The mRNA? 00:41:38 Wilson: They’re reacting to the mRNA, yes. JC: But the mRNA is in the cells. I thought the M RNA was in the cells, so then how is the? 00:41:47 Wilson: It’s foreign mRNA, not all of it is going to be encapsulated in lipid nanoparticles. Some of it’s going to be free floating some of its…. 00:41:53 JC: Oh wow, oh, this is all kinds of crazy **** that I didn’t know about the vaccine, yeah. 00:41:59 Wilson: Well, that’s what happens in a tube.
The mRNA question has been treated in a separate blog article which can be found here:
[iii] Even though it could be argued that 60% similarity still means that 40% of the virus is “unknown” one cannot argue for a “novel” virus. It depends how that 60% is distributed. It depends on the importance of that 60% (structural, functionality etc of the proteins). One cannot argue that the immune system has never encountered it before. Would you be able to identify a car if only 60% was photographed? Probably. Especially if you photographed the badge. And why would you repurpose other coronavirus drugs unless you knew they could be effective? Genetic comparison among various coronavirus strains for the identification of potential vaccine targets of SARS-CoV2 “The whole-genome sequence alignment of CoV revealed 54% identity among varying CoV strains, whereas, the genome sequence alignment of the nsp-coding region alone of CoV shows 58% similarity and that of the structural protein-coding region shows 43% similarity, suggesting that nsps (non-structural proteins) form the conserved region of the genome with high percent identity, contrarily, structural proteins in need of adaptation to new hosts are more diverse” (Chen et al., 2020). In the conclusion they state: “So, drug/vaccine repurposing is the current hot research area and researchers are aiming for the use of potential target antigen sequences of previously known coronavirus strains to come up with a suitable vaccine for novel SARS-CoV2 strain”.