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Hello, ladies and gentlemen, and welcome back to the Rounding the Earth podcast. Rounding the Earth is a popular newsletter series published on Substack written by applied statistician and educator Matthew Crawford. Topics of discussion range from critical analysis of conventional wisdom to Bitcoin and everything in between. And of course, as basically from the beginning of the show, of course, the COVID-19 pandemic. Our goal is a careful examination of important topics and perspectives shaping the world that too few people talk about. Subscribe to Rounding the Earth on Substack, Rumble, YouTube, and Locals to join a burgeoning research community and to help us unflatten the Earth. My name is Liam Sturgis, I'm a musician, music producer and writer slash editor coming at you live from Vancouver, British Columbia, Canada. And I'll be your host for today, joined as always by the venerable, the intelligent, the handsome Matthew Crawford. Good afternoon, Matthew. Let's go team defense wins ballgames. Haha, rally up, rally up.
Speaking of teams, do we want to jump in introduce our guest right away because everyone's excited? Yeah, he probably doesn't need much of an introduction to this audience, but we might as well, you know, we'll let him do it, right? The man of many names, Jay "do your job" Couey. Oh, that's a that's that's quite an introduction. You guys are nuts. Um, I like yours. Actually, I thought that was really clever. That was that was really fun. Well, welcome back, JJ JJ has joined us from the Starship GigaOhm where he he pilots. He is captain of a vessel that does what? Um, well, right now we talk a lot about, again, the coronavirus and the pandemic, but it's only because that's what I've been reading about for quite some time.
Lately, we've been actually talking a lot about this clone war that's happening. And by that, I mean this argument about the role of RNA infectious clones versus the quasi species swarm and which concept is more important for which part of the narrative that we're currently going through. And talking about those two things has got me a little bit more attention than I had previously. And it's not all great. Some people got really mad because they take it very personal if you walk with them for a time and then decide you might have walked the wrong direction. I'm freely admitting that part of my sort of change of heart about some of these things is, is… The history of that means that at some point I was pushing parts of this story that I no longer believe are necessarily true. And so that that's that's kind of a painful thing to go through as a person, but it's much more bewildering to see what happens to the people around you as that you realize.
You know, it may be good for everyone in the world to take a moment and go, you know what? All of us have been fooled by some things. Right. And but like, it's good to reorient yourself to principles, right? You know, try to figure out what's going on, maintain your morals as you do. Right. Like the big picture, things are still the same as far as that goes. Like the root, the root of what needs to happen, the root of we're going through something huge.
You know, I as I've said many times, I think that we are… that ultimately the core of all of this is that we're going through a major global financial tailspin and that the military banking complex was getting out ahead of it. And a lot of things that that have been part of the matrix for decades got sort of repurposed for the moment. And that, you know, because of that, we're getting we're seeing glitches in The Matrix and every one of us has and will continue to experience certain levels of cognitive dissonance. And to say that out loud to say, I have been fooled, I'm still fooled, you know, but let's at least try to sort things out, right? So people don't get, don't get too angry with each other. But you know, I mean, how many how many things have we been fooled about? You know, I don't know how many of the early treatment medicines actually work because I haven't studied all of the research. Nobody can be expected to do that, right? There are probably things that I'll find that I said that I no longer believe and will probably change my mind about a few more. But, you know, I still think vitamin D works.
I think this is a really important point to make. I really like what you said there, which is that in order for I think everybody agrees that there's some big reorganization that was necessary or bound to happen or already happening and that reorganization requires everybody to be on board. And more importantly, maybe it requires that most people not to understand exactly what organ… reorganization is occurring. And so they've fooled us on so many fronts and now the question really becomes, I think that's, you know, the ultimate issue here and my little microcosm of this thing, in 2019, if you would have asked me to put my chips on the board, I would have put my chips on the board of the University of Pittsburgh School of Medicine knows more about vaccine safety than Robert F. Kennedy Jr.
And I didn't have any real proof why, I just had lived my life and had been socialized in such a way over the course of my adult life to understand that that was a generally good system, with generally good outcomes and because everybody was checking each other, there would be no way… You operate in a world in which often the distance is a tapestry and it's woven by proxy trust. And that's true for every single one of us. Yeah. And that that I think is just something that that over the course of the pandemic, some of us have come very close to that tapestry ,even seen behind it, and others of us are still blissfully unaware that it's there, and that, that huge chasm between us is really the main problem. I don't even know what if there's a solution to it, honestly, the person that I talked to earlier today wasn't convinced that there's necessarily a solution, per se.
Or it's not necessarily, it's not necessary that we know it now, right? Like I think that what's going to happen is, is, you know, stepping forward, let's say that the global powers go bankrupt, you know, before they pull off their plan. And then the rest of the world, all of us, we're going to have to figure that out, right? There's going to be a lot of experimentation with local governments… governance, we're going to be figuring out game theoretic stabilities of our communities. We don't have to know how it's going to work out. You know, we just have to move forward the best that we can, right? I'm going to drop a comment from from Rumble right now.
And you know, what's up with this crazy, what's up with this crazy title? I don't know how to build a super virus by well, so so that goes to the we had another guest we were hoping to have join us today. And it's my understanding that and Matthew, correct me if I'm wrong, he's a science fiction writer. Do you want to explain the premise and, you know, keeping in mind, hopefully he'll join us for a later episode. Yeah, you know, JJ and I talked with him one day and and like, I like the guy. And you know, he he had some insights because working for on a book, he had done a lot of deep diving into all of this stuff. He actually had knowledge of certain publications that helped him make observations before many people did. Right. Almost anyone. And and so I think he has like a lot of valuable insights and contributions to the conversation. And I for whatever reason, I didn't pay attention to the fact that he hadn't responded to the invitation. Or sometimes when you send the invitations, Liam, I don't even know what happens with the conversation after that. Because of the FTX article that blew up so much. And I've had so many interviews lately, you know, I just I didn't pay close enough attention. But he he never responded to join us today. If you're out there watching, you know, if you want to come on again, but maybe we'll steer this conversation in a different direction.
And there's a question that came up from Rubin B infectious clones are still gain of function, right? With the malicious intent behind it. So we still have a transfection campaign to stop. So one thing I want to I want to say is that I view a phrase like gain of function in some sense. It's rhetorical, right? Like it's like, OK, what do you want to define underneath gain of function? You know, what is it and what is it that you're doing there? And I think that there's also a conception of what a virus is and what a clone is that is actually a really difficult conversation. And I've actually thought about it further since the last time we talked and you were on here, JJ. And, you know, maybe now is the time to bring this up, since maybe our conversation isn't quite going in the same direction. But you know what this is actually? the conversation, how do you build a virus?
Let's say that you put an infectious clone out into the atmosphere, you know, and some people, you know, get sick from it and it replicates and some of those replications have mutations and it begins to become a little less pure and a little less pure. On the other hand, it may it may be like those game of life simulations that we saw and I'll bring that up. Actually, I'll let you talk in a minute and go get some game, game of life examples where you have things that happen. Sometimes they continue to happen forever. They just go in a cycle and that would be an evolutionarily stable virus. But they might also peter out and then just disappear because overall, the replication rate may not quite keep up even with like as you go off in like, you know, branches of mutation, you know, some of those will replicate, some of them won't. Will it hit one that replicates well enough to keep the whole thing stable and becoming its own cloud, its own swarm? And I think that that is actually it's a difficult question.
We don't even know if the people who make these things, you know, they may not know the answer to that sometimes when they, you know, if they make one and they put it out, it's hard to know if they know. I don't think they do. I mean, that's Dennis and I touched on it briefly this morning. I think that that's one of the major questions that remains now and one of the things that I'm working on as hard as I can is understanding what we know and don't know about, about how they can or cannot find and track and measure and quantify the presence of virus. So last night on my stream, if I can just, I think this is totally completely on board relevant to this. Last night on my stream, I showed this paper. Where are we here?
I showed this paper, which is this one that's coming up. It's called "Direct RNA nanopore sequencing of full length coronavirus genomes provides novel insight into structural variants and enables modification, modification analysis". So what they do here is they're using nanopore sequencing. They don't have to do any PCR. They can just throw whatever RNA they find in their, in their, in their thingy in through the nanopore and they'll get a sequence. And so presumably if they start with, and in this paper, I'll show you what they start with in this paper, they start with, this is the, this is the actual methods, generation of recombinant viruses in total RNA isolation were performed as previously described. And then it says the briefly full length cDNA copies of the genomes of HCoV-229E. And then it goes list two other ones were engineered into recombinant vaccine of viruses. And then those were those vaccine of viruses recreated that DNA and mass copies, right? And then they use that DNA where does it say, uh, respectively were transcribed in vitro using purified digested genomic DNA of the corresponding recombinant vaccine of virus. So they started from a huge quantity of DNA and they made perfect infectious clones of human Corona virus two to nine E. And now what's here is really special because presumably in a pure culture with a pure infectious clone, you should get an awful lot of, of full reads and guess how many reads they got, they got two full reads. So putting all the RNA they could extract through the nanopore and the nanopore reads everything because it's the newest greatest technology ever. It makes 15% errors, but so what, how many, if you are suggesting that when you start with an RNA infectious clone, you put it in culture and then you extract the RNA that's produced from that and you only get two full reads. What do you get from somebody who's sick? Nevermind. What do you get when somebody is asymptomatic? This paper is just before, sorry, what I was sort of humming to myself. Like I was going, like, that's interesting. Oh, it's really strange because this should have been the optimal situation to get many, many, many, many, many full reads. And instead in this paper, they only saw two. The average, the average length of read was like between 1000 and, and 600 nucleotides. It's still very long, but the, the perp, the point I'm trying to make is that even when you start with what appears to be a perfect pure clone from cDNA and then transcribe it into RNA, when you look for the products of that infectious RNA, they were only able to find two full reads. And that seems to suggest to me that either their RNA capture technology is horrible or what they say happens when a virus copies itself is not what happens. And I think that's the case. And here's what I think happens. And I didn't explain it very well last night, but I'll explain it here. If you look at this figure, you can see the coverage that they get and the coverage is higher, which means that they get more reads on that area. And so it's highest in the sub genomic RNAs that are in the most abundance. So the most abundant sub genomic RNA turns out to be the end protein. The next abundant one turns out to be the M and then the E and then the S protein. So there are many, many copies of these sub genomic RNAs. And when you start to package virus up the vast majority of particles, according to some of our favorites, uh, favorite virologists are non replication competent. I might posit that the reason why is because when there's packaging, there are comparatively few of the RNAs available for the RNA dependent RNA polymerase, but lots of extra RNAs for these, these, these structural proteins. As a result, you get a lot of viral particles that just have structural proteins, but don't have the whole requisite genome, which would jive perfectly with what Robert Malone and other people have suggested about non infectious particles. And it would also jive perfectly with this, with this picture here of all the total number of fragments that they find and how many fragments they find in N, how many fragments they find as E M and almost no full fragments of the most important proteins for replication. And that seems to suggest that we don't fully understand how, how replication occurs then because otherwise there wouldn't be so much imbalance between these sub genomic RNAs when they use what is purportedly the best, uh, sorry, the best, um, technology to find these DNA right now. I mean, this is, is, is direct. They don't have to do anything else, direct RNA nanopore. This is supposed to be the gold standard, even if it has high error rate, that doesn't mean you shouldn't get full reads. It just would be reads with errors, right? So something's not right here, but they just go along with it. It's fine. This seems to suggest, I've found lots of papers like this and it's beautiful because you can go and look for papers in salmon viruses where they make cDNAs of salmon viruses and then do the same experiments. That's extraordinary.
And so these clones, I think are the danger in the sense of if you make this clone and then this clone, look at this paper again, remember what this implies in, I would love it if we could get Kevin McKernan in on here or somebody to talk about this. But I think what this implies is that during viral replication, you are, you are potentially shedding virions that are only having the end protein in a couple spike or only the end protein. The end protein. That's interesting. Other than the S protein, the end protein is one of the ones that was most immunogenic and the one that people most respond to after natural infection. It's beautiful. And one that we had in lots of the PCR tests, if I recall correctly, S was most common, N was second most common and E was third most common. That's correct. I think that's right. And in ORF1A are still the primary ones they do. It's really neat to be just peeling back this because I do think that it's possible that a lot of people are just so compartmentalized in their little field that they don't, they don't know all this stuff, how this stuff kind of adds up to these, to these incongruencies. I mean, it's, it's real hand waving and they don't know a lot about how it works for sure. And when you, when you look for signs, you know, just like I, this, this kind of is the same kind of observation as if there was a new cause of death, do we see it? In this case, if this is a pure RNA infectious clone of a known human coronavirus and you put it in culture and then you get this kind of coverage on the, on the genome, then that means something about how viral replication works. It just has to, and it doesn't, it doesn't work like they say it does, or otherwise there would be at least some significant proportion would be full genomes. So point of clarification. So EMO cell on rumble ask or rather says the mRNA in the quote unquote vaccine is the clone. They can't create a full virus, but briefer sequences and note, they stabilize the mRNA pseudo uridines. Before you address that specific claim, I do want to seek clarification. So this, the notion of the infectious clones and the possibility in, in one theory of what's happened that infectious clones were made in large enough quantities to then distribute in one or more places around the world at one or more points of time, hypothetically. So is it then also the case, are we still talking about infectious clones in as EMO cell says the case where they're being manufactured in the cells of the human recipient of the transfection or are they entirely different things? No, that's entirely different things. So when the MR, the RNA of the vaccine or call it transfection is injected into people, then you are depending on the purity of the RNA, you are making protein somewhat related to that sequence. That's a whole mean, is it a clone, like a 10th of the, the nucleotide sequence, right? Right. And no, the idea of a clone is, is somewhat caught in this, in this picture. So you can imagine that if this is the best a clone can do that out of the whole sample, there are only two really, really good viruses that have the whole genome and there can be infectious if you, if you cough them out. Now if you think about this as the best example of what this virus can do, then you can see why it would travel very intermittently between animals and between people because it's not very good at packaging the whole genome up. I don't know why I can't explain it, but I can tell you that if you had an immune response or an allergic reaction to somebody who was shedding particles of the end protein, you might have a day of infection. You might have a day of symptoms. If you had someone in your house that was shedding these particles while being infected by one of these guys, then yes, you might also have symptoms, but the virus might not even be replicating in you. But you would still shed or you would still test positive for the PCR products of that, those particles. So it's tricky because if the virus replicates like this, then it's making an overabundance of certain sub genomic RNAs and very few of the ones that never leave, right? And so it's really weird. I don't understand this paper. I know it's just one paper, but I do feel like it's a hint as to that the whole model is incongruent. And again, remember what I'm saying that they, what they intended to do here was show that they could use direct RNA nanopore sequencing to get the entire genome of a coronavirus in one shot. The way that they did it is they started with a cDNA purified clone of a known human coronavirus and then they got what? Two shots. That to me is not very impressive. Yeah. Okay. You just like so many things just entered my head in terms of like evidence of what might or might not have happened. Yeah. In the West, in Europe and in the US, we saw way, way more infection than in Asia. Yeah. Also when you look around at where animals tested positive, where in the world did animals test positive? Not many animals ever tested positive in China. There were like a couple of pets or something. But here in the US, we had, like we estimate that millions of deer tested positive, right? We had dogs and cats and other stuff, mink positive in Europe, you had the minks. And like there's something about this where if you were to, if this were released as like an aerosol into the air, then you would expect there to be a correlation between the proportion of animals getting sick and the proportion of humans getting sick. And there is. So, I mean, it's not this huge piece of evidence, but it's a consistency, right? It's a consistency with there being more release in the West. Yeah, the one thing I don't like about it is, is I'm pretty set on not using PCR positivity in animals or in people to interpret what's going on. Okay, that's fine. That's fine. It's a consistency, but a questionable one. But now that you bring up the PCR positivity, you know, now we have to, you know, question, you know, like something like the GISAID database.
And one of, like Kevin McKernan, I didn't, I've had so many things going on, so I didn't get to focus on it, but I did notice a Twitter thread. I don't know if you read it or not, where Kevin was saying, you know, what I don't like about JJ's theory basically is that you have this appearance of mutation moving around the globe. And you know, so, you know, one question might be, you know, do we even trust the genetic databases at all?
No, I think that one of the places that that Twitter thread went with Kevin was that he likes better the idea we put forth a few months ago, which is that some ancestor or related viral swarm has always been there in the background. And therefore the opportunity for overlap with PCR is too great. So it's just an opportunity of when do you start testing and what do you call it? And then what variants do you, if you control the sequencing database and you control the, and but he would say, and this is something that I think has really, has really put me in check for a few days, was that he would say that there's, you can't say that the sequencing is incorrect. You can say it's biased to find SARS, but you can't say it's wholly from whole cloth cut, you know, or whatever, whatever the right thing. You can't say that it's wholly made up. But there are parts of it that you could question. I think the original sequence made by, made by the Wuhan lab done with Illumina sequencing using 30 sets of, of generic coronavirus primers, who knows what that is. But because of the read depth, I think, I do think that Kevin would say that's a legitimate sequence and so then that's where it sort of made me circle back all the way into my head and say, well, then we already had an idea that covers this and that is that the, that the viruses were already there in the background, part of a smaller group of whatever's, but they're there. And when you use something as sensitive as PCR, you can detect them. So I'm traveling back to early beginning of this, this year, the point at which you and I started to talk more was the point at which I, I started publishing the Omicron hypothesis. And one of the things that I want to point out was, and I got pulled off of this to work on the DMED project, which, which in retrospect, seems a little bit interesting to me. Well, you know, and, and that, that, that's been its own interesting ride even since then. But you know, one of the things that I want to point out is that, that, well, you know, GISAID, there was a, there was a guy raising noise about GISAID and, and I can't remember his name. Let's see. What's, what's his name? Oh, here he is. James Taylor. James Taylor was this Johns Hopkins researcher who was kind of shaking, shaking the fence, shaking the trees, saying, Hey, you know, let's go ahead, like, we should be making this open source so that everybody can see and work with this. And then suddenly this, this young man dies. You're joking. I don't know what happens, right? You're joking, right? No. Wow. I didn't know this little story. I think I may have told it to you on the phone very briefly, but I couldn't remember his name. I didn't know the story that well. I still don't know the story that well. It's just, it's an interesting little thread. It sure is. So you know, like I've, I've wondered the degree to which we can know, you know, how, how high fidelity this database is. Now of course that's, that's in addition to the fact that there was something very weird about Omicron, which is that in GISAID, there was the publication of an Omicron sequence in July of 2021. But supposedly it didn't emerge until October, late October, 2021. But this, you know, you know, another researcher Sandeep, Sandeep Chakraborty, which do you follow? Did you follow him, JJ? I did not know. He seems to be a smart guy. You know, I put him on my Twitter and of course, Twitter never shows me his tweets unless I go out and see them. So I'm pretty sure he's one of those, you know, shadow suppressed people. But you know, he found that record and then boom, it got deleted right after he found it. Now I call into question, I do remember this story. I do. I call into question how much we can trust these databases. Can you explain what made that an Omicron, like why, why is it asserted that that was an Omicron strain that was collected? And narratively speaking, it seems it was collected too early. Why do you assert it was an Omicron sample? Well, it's just, you know, looking at where the mutations are. Okay. Okay. Weird. Well, you know what I realized yesterday is, because again, I'm approaching this from trying to put it together without the same level of mathematical or scientific expertise as you guys, but a decent feel on narrative. And it occurred to me that at the time that Matthew was talking about the Omicron strain looking like it probably could have been from a lab directly itself, you then had almost an institutional acceptance of that. Now what I mean is you had Bill Gates on TV saying, Oh, you know, Omicron came out and it sort of acted like a natural vaccine. And which is sort of what a lot of us were saying at the time in a positive sense, like, Hey, look, it looks like it's doing something good. It's either making it so that everybody's going to get COVID and then develop an immune response they may not have had yet if they hadn't caught COVID yet. And then now fast forward, it kind of feels like it's part of the narrative too, hypothetically. I was suspicious immediately when I heard him say that. And I tried to warn people, like there were people going, you know, this is like a white hat operation. Yeah. And I, you know, like the moment I heard white hat operation, I'm like, okay, you know, this is built from the same skeleton. It's just got a few little tiny pieces. Let's be realistic here. And here's why. Here's why. From the same backbone. Because, and it's only with the benefit of hindsight, but, and I've never spoken to Andrew Huff and I have limited interactions with Charles, but it's Charles Rixie. But Andrew Huff right now, isn't that sort of his big assertion that these coronaviruses, Jay, as you've described, the research has been into whether these can be used as essentially what Bill Gates described, right? The ability to transport vaccine, like in the context, not necessarily of a gene therapy, but more like as an aerosolized virus, right? But the thing is you have gain of function is bad, but what we're trying to do with it is good, which is attach things to these viruses for, for benefit. So I, I, I don't know, but it would make it easy to like have releases that are just sort of publicly known about and have people not question them. A pretext for that. Yeah. A pretext. Yeah. There we go. I don't want to lose the topic, so don't let us go off topic, but there are a few papers from recent, um, both recent media coverage of them and also recently written about the idea of whether or not bio enhancement without the knowledge of the population is okay. Yep. Moral bio enhancement and this is where the language gets tricky because I think what some people have pushed back at you over is, is like, you know, what do you define as gain of function? And this is, this is an understandable conversation, right? Like at some level it's rhetorical. When you come up with terminology, you have a set of criteria. Does it, is it part of that or, or is gain of purity? Could we, could we just say, okay, gain of purity is a subset of gain of function, you know, and it's, it's like a subset that's sort of like an edge case in the definition maybe, but it's the important part, right? The important part is the edge case. Like I, and I, I've never answered the question as to what I think about the terminology because I don't even know what the official definitions are or whether the official definitions matter. Right? Right. Like, it may be. So in a way they do think of it this way. If, if teenage behavior was classified as some category which sounded really bad, but wasn't really relevant to what teenagers actually do, then it would be pretty problematic. And I feel like gain of function might be one of those categories where they've created a whole concept and mythology over here, which is not the danger. And it is by specifically describing it as a, a special case of experiments. They have created an illusion where these experiments now really do have danger. You know, maybe that doesn't mean that gain of purity, you know, doesn't fall under it. It just means that they are, you know, casting an illusion to cause us to focus on the rest of it. Oh, well, I was thinking, I was thinking, I was supporting 100% the idea that the semantics of gain of purity are not trivial and that I think actually it might be a step forward in the sense of putting gain of function in a category that we can address it separately from a well-established obvious purity problem. And, and I, I know that the most of the people that are involved in this are not willing to have this discussion simply, it feels like as though, because that distinction would, would undermine something that they, they want to maintain. I don't really get it, but to me, it's a very significant thing to figure out that the biology of coronaviruses is not all it's cracked up to be. And that when you, when you say something like I've said over the last couple of weeks and then people throw a bunch of things at you from all different sides, it's all the same thing. The latest thing that everybody's saying, I wish Jay would read a paper about proofreading in coronaviruses. But then if you look for papers about proofreading in coronavirus, the seminal paper is by Mark Denizen and Ralph Barrett. So basically the, the godfathers of every gain of function experiment in the world as it pertains to coronaviruses are the two guys that have established basically the only proof that nonstructural protein 14, I believe is the one they talk about, but EXO capital N is the name of the protein that it makes. That Gila case is responsible for proofreading and is responsible for what allows the coronavirus to copy this extraordinary genome in RNA. And if it wasn't having proofreading that size of RNA would not be able to sustain itself as a virus. And, and then everybody just cites that paper and now coronaviruses can do proofreading and the real proof in that paper is that they did a point mutation in that, in that, in that protein. And then they showed that there was more mutations in the sequence that they got, but it's not really clear to me if they, you know, mutated something else and didn't get changes or, or mutated a couple other proteins and it's everything was still fine. And it's not really clear to me when I look at other papers, how it is that they can even establish what percentage, for example, of the, of the viruses that are produced during trends or during replication are actually useful. No one's ever really been able to measure that because how difficult it is to measure anything. And so at the same time as that we have, we are assuming that coronaviruses work in these very specific ways, which include again, being able to replicate themselves at high fidelity for three years or more. And we can, we can sequence them and it's, it seems dubious and I'm just not yet fully equipped to be able to tell you where and how. And I hope that with Kevin's help, I can get there because simply there is a difference. There's lots of genetics that we can do and we can do full throttle and all of those genetics tend to start from prokaryotes and they tend to start with bigger organisms that have more consistency in the genetic signals that we're looking for. The best example that I have is that metagenomic sequencing was very famous for being able to take a sample from a patient and look for the different kinds of bacteria that were present just based on shotgun sequencing. But when you look into that deeper, what you will find is that what they did was that they screened ribosomal genes and then they only PCR and sequence the ribosomal genes. And then they looked at the ribosomal genes and made predictions about what bacteria or parasites were present. That's a very different experiment than whole genome sequencing of everything in the sample, which is kind of how they make you feel they're doing it. And they don't mind if that's the conclusion you come to, even though in reality what they're doing is ribosomal. JJ, could you send me that paper? I haven't read many papers lately. I haven't been, you know, it's focused on the science lately, but this is one that I feel like I want to, I want to read. And then I'm going to circle back. I'm going to try to see if I can get Kevin to come on, you know, one of the next few Tuesdays and then invite you back on. And I may ask one other person, but I'll let you know in private who that is, you know, before asking everybody to come. But it's somebody else who's smart that I've been talking with, who knows more about this topic than I do and who I'm trying to learn from. Maybe sending me some information, some reading material, not that I've had time. But since we're on this topic, I, you know, we brought up this analogy last time you and I talked of automata, right? And I pulled up the game of life and it occurred to me that this is a pretty good analogy to help people begin to think about this in their minds because, you know, it took me, it took me actually several months to, you know, it wasn't my focus. So it took me several months to have the conversation with you about the quasi species, you know, swarm. Right. Like when you and I started talking more in January, it was probably, I don't, I don't even know, late February, March sometime, but I was also working on the DMED. But you know, several times I would stop and think about it and go, OK, I can see a little bit more about what this is. Right. And I felt like I was able to converse about it better. But we talked about the game of life and this is an automata, you know, sort of machine here. It's created by this guy named John Conway, who was a very playful, creative mathematician. You know, one of the one of the people who pushed the study about autonomous Ford and if people really want to, you know, look at where modern automata research went, that's what Stephen Wolfram does. That's what his book, A New Kind of Science is all about. And I read that book and, you know, it's an interesting book. There's a lot to learn from it, but it has more uses of I, me, my than probably any three books that have ever been published. So you know, I know that going in, but I'm going to I'm going to reboot this right here and refresh the screen. Let's see what happens. You know, maybe these are like, you know, these are stable sort of virus clouds on their own or something like that. And you know, ultimately, there's replication that can happen, but things sort of peter out over time. And of course, this is not any kind of a perfect analogy right here, but you can you can kind of get a sense that because, you know, what happens to a cell has to do with the cells around it. Right. Do you get, you know, virus in a place, you know, that may depend on how much of that virus, how many viruses, virions have that sequence right now and how many have adjacent sequences that might replicate into it with a single nucleotide polymorphism or something like that. Right. So it kind of makes sense to think of it this way. And you know, an infectious clone might just be any boom, I'll just drop something new in there. Right. And at first, there's a sort of stability to it. But that stability, you know, it's not necessarily permanent, right. It just eventually it's just absorbed by the cloud of whatever's there. And of course, it's much more complicated than this, because each individual pixel here may have its own replication rate that might be zero, or it might be that each very on results in a thousand virions, you know, that are itself or very close, you know, snip away to snips away, you know, whatever mutations away. So anyway, this may I wanted to bring this up because it may help people understand this conversation better and understand why it is that, you know, when we're talking when we talk about a virus versus an infectious clone, it's not that an infectious clone isn't a virus. It's that there is this sort of fundamental distinction between the ones that are out in nature and are stable. You know, they've sort of proved that whatever happens to the cloud, it just keeps on churning. Right. Whereas, you know, one of these infectious clones, you have no idea. It may be that point zero, zero, zero, zero, zero, one percent of things that were sort of seeded as a cloud would would be stable, you know, with with a survival of the flattest with its near neighbors, right, with its pals would be sort of stable in the environment. Whereas an infectious clone is like, you know, taking a shot in the dark. Does your does your dark hit the bullseye, you know, blindfolded. So anyway, I'm throwing this out there. Hopefully, you know, I can see you kind of like this, Jay. I do. I I'm I'm much more interested in it from the perspective of people realizing that that these kinds of distributed processes can at least be cartoonified in a way that that will more accurately parameterize how they should be thinking about this. And I think a lot of people are it's just easy to see like a floor full of matches and then you light one end and the whole room burns. And it's a much more complex system than that. And again, you know, once you get off the main narrative, which is that there's a new cause of death and we have new cures for it and and figure out that that math never happened, then then you can move forward. And I hope that that's part of, you know, what's recently starting to become if we could get the mainstream people to not think about whether this is a lab leak or not, but whether to think that there was a novel cause of death or not and whether they have any good cure for it anymore or not, then you might be in a closer target to waking people up or having them question in a useful way. Because lab leak or or natural virus doesn't make them question what their doctor said about what to do about it. But I think that's where we need to be. I'm going to address good doggy for a second. You know, like one of the things that bothers me about communication in the space is, is people just saying you're wrong. Right. And not really, you know, it's like, okay, what what assumptions is he saying that are unsupported? Right. You know, participate in the conversation, be useful if you're coming to troll, you know, that's not helping anyone. Well, let me stand up. Let me stand up for good doggy, because he did ask a specific question after. And that that is sort of the point I was I was going to want to want to make is ask specifically because I do want to try to understand. And I and that's why I am feeling attracted to Jay's thinking, because I don't get the impression that this is based on a set of assumptions or beliefs. I think that's perhaps a misunderstanding of what Jay's saying, because isn't the whole point to kind of go back and review a set of assumptions from the most basic all the way down to the most complicated and the nitty gritty, as someone else pointed out, we need to get to. So so that so I think it is important what specific assumptions what what is Jay missing if he is, but then also the specific question he had followed up with was if Jay has any predictions for the winter. And I do think this is relevant to what he's trying to understand, even if it doesn't seem totally relevant. So do you have any predictions for the for this winter, which were, I suppose, almost in? I feel really like this is where this is where the sort of the the line where my expertise as an armchair virologist and an armchair immunologist, we don't I don't have that data and I don't have a good sense of how that data has really progressed from year to year, like somebody who's worked in a hospital their whole life. I have the impression that there is the possibility because I've read the same things that a lot of other people read that there are people out there because of their regular inoculation may be in a state of immune suppression. And so maybe they will get more sick this winter. But or the social distancing kept the kids from getting as many bugs and as much immunity as they did for a year and suddenly there's an excess catch up or something like that all at the same time. Yeah, it could be the same time. I mean, that is possible. We may not have flattened the curve. We may have lifted the sheet and thrown it up. Yeah, I tend not to think that the kinds of things that we did really made much of a difference on how kids got sick. And I like to believe that that the the viruses that were there in 2019 didn't change so much between 19 and 21 that when we did go back to normal or almost normal with the kids that they were still fine. I don't know, though, I don't know what to say about this winter, because I think the more important thing is what the TV says about this winter and what they stress and right now they're saying that's going to be a tridemic and they say that that the pediatric wards are filling up and and they keep repeating it. And I don't know why, other than to drive a continual, very, very brittle narrative about how our health care system is in shambles because of the pandemic and we're still fixing it. By the way, I'm going to throw this in here because I wrote an article about it maybe a couple of months ago, is that in the middle of crises, the military sends in people not even like the CIA, but military intelligence sends in people to newsrooms to begin filtering the information that comes out. And that alone turns out to be very interesting in a case like this, you know, maybe maybe they really do know, you know, what this winter is going to be like, because, you know, they already have that information ahead of time. But it's also one of those things that sort of keeps people tuning into the mainstream media because as much as they lie, they're also the sources of some some little pieces of key information. And you may not know which unless you're really, really paying attention to to what's going on. Right. But it may be that they only feed you correct information when it serves their purpose. And maybe that purpose is, you know, a little bit more panic. But I think that everybody I reminded people this and somebody else reminded me of this in 2020. And I've never said it again, but you can go back to the 1970s and see that hospitals operated on a whole different level of capacity back then. And we had excess capacity in all of our hospitals on purpose. And in the modern era, excess capacity has wasted space. And so hospitals and staff and and and space is allocated in such a way that between 60 and 80 percent of it is full all the time. So if they say that the pediatric wards are almost full, what they're really saying is our business model is perfect right now. And I don't see that as, oh, my gosh, where our system is overloaded. If you if you set it up so that you're going to run out of food every day and then extra people show up and people run out of food, you shouldn't be really surprised. Right. And that's how they do it. They set it up so that in the peak of the season, all the beds are full because that's the most economically lucrative model. They don't want to have 20 percent capacity and staff and space all the time. That would be crazy. And you have in the 70s, though. And I'm feeling frustrated now because I'm I'm pulling back. I feel now maybe a bit of what you're feeling in that we're missing the point like we're looking away from what is possibly just direct cause of death, like humans causing humans death in very obvious ways. And we keep getting pulled back into kind of weird, repetitious discussion. And I almost apologize for for bringing us back into there a little bit. But you're totally right. Like we have a hospital system set up that I think everyone kind of understands now works the way that you just described. We have policies now that everyone more or less understands, even if they're not focusing on them, which is the problem. We have policies that are resulting in deaths recklessly or otherwise. And that's why I go back to I think Denny has been right since 2020, where he said this is a genocide. And I kind of want to join you in feeling like I'm in this moment. I'm feeling a bit panicked, actually, about how overtly misdirected we're allowing ourselves to be, perhaps, perhaps. So looking at this question down at the bottom here, how could anyone sequence a swarm accurately? And this is a really good question that I've actually thought about a little bit myself. You know, JJ, you probably could answer it better than I can. But my first answer is you don't get to sequence the whole thing ever, right? Like you know, and you could swab, you could swab the oropharyngeal cavity, you could do lung lavage, you could swab the anus, you're going to get different reads from these places. Is that right? Well, let me let me there is a couple papers that tried to do that. If you use the same primers in all those places, you don't get different reads. I don't know what that means. Oh, really? You get the same reads. Interesting, I wouldn't have assumed that you did, but that's that's good to know. One of the things that Harvard to the big house, for example, said was going to happen that the swarm was going to move from tissue to tissue, and eventually it would revert back to its original form, whatever that was. And I haven't seen any papers when they look for it, they don't see the the kind of single nucleotide changes in different places in the body that they thought they might see. Well, then that that's evidence against the theory that Omicron was like this rapid channeled evolution through like one AIDS patient, which, like, there's part of me that just wants to smack whoever says that every time they do. Yeah, it's it's, it's a unless we can see the original data of these kinds of sequencing experiments, it's hard to really say, but the technology that they use is metagenomic sequencing. So they amplify very small fragments, and then they use a genetic computer algorithm to take those fragments and align them to expected sequences. And so it's not clear to me, except that I guess what they did with the original sequence, what they purported to do was align these fragments up to a consensus coronavirus genome and then allow them to fill in the holes of the SDN, and whatever sequences they found is what they put there. And then the, you know, the percent that it resembled other coronaviruses was calculated now. I can only just show you the paper and you can stay show you the I wonder if I have it. I don't I don't think I have it right away. I can get it though, while we're talking, but they just show you the the the overlap of where the little reads go and it's not it doesn't look wrong to me. It doesn't look like anything disingenuous. It looks like how a meta sequencing should happen if you presume you have a coronavirus. That's what you'd see. So when when Kevin challenged me the other day and said, you know, I think you're going out on a limb here, if you're going to say that all metagenomic sequencing is just kind of fraudulent, because he's pretty sure it's not. It took a little bit of wind out of my sail, to be really honest, because I thought, you know, I had something that I could also give to some other people that, you know, might bring us closer to being a united front. It's a big it's a big leap in in thinking, right, they're going to be wrinkles to smooth out. Yeah. And so, yeah, we'll try to have that conversation again. I just want to answer real quick, you know, isn't immunity done a farce? I think this is Lance responding to the idea that maybe because people social distance, they didn't, you know, get as many bugs and didn't get as much. You may be right, Lance, I, I'll say, I'm pretty open minded on the discussion. I'm just, you know, I was throwing out an idea, but I'm definitely not married to it in any way. Dennis Dennis this morning, brought up this guy named Sheldon Cohen, who were in the times before it was prohibited to infect humans with things. He was doing experiments where he was infecting people with influenza. And the only correlation with disease severity was with the amount of stress that these people were having in their life. So that why did I bring that up? What were you just saying there? It was something very relevant to what Matt was just saying. He asked about, Oh, where is it? Isn't immunity debt a farce? Isn't it? If people have been as a result of being penned home in their homes with their kids or their mother-in-laws or having trouble working remotely, or if the wearing of a mask or not wearing a mask or being around people that are wearing a mask is all stress, then everybody's immune system is going to be necessarily suppressed. And that's at least there are, I think there are quite a few not connected lines of research that have indicated a wide variety of stresses make you susceptible to infection, susceptible to sick behavior, as it were. And so this jives really well with that, that if, if over time we are just stressing everyone out more, then this winter is going to be worse than the last one. And as the stress increases, then the general sickness in the population will go up. And I just want to say, I believe it was his students he was infecting. So it's not necessarily something that we would recommend people do these days. That being said, tremendously valuable insight. Now my question is, has to your knowledge, has that research been replicated in the same formal high quality setting? I know there's plenty of observational, you know, reasons to say it's true, but is there more? Because that was a while ago. Is there any more modern confirmatory research there? If I was to look for it, I would look into something like veterinary lab science stuff where you would look at animal welfare, welfare, and I bet there's some literature that's not used to make this argument, but it's used to make the argument about best hand best practices in animal handling. But if you could find an article that was looking at best practices in animal handling, I bet you could find one that showed that that certain obvious practices that lead to happier animals, let's say make make for less pathogenic problems in a in a in an animal facility. I bet that's very true. I just don't know where we would find it or what we would look under. But that's where I would look first. Makes sense. So we have an interesting question here. Why does Andrew Huff and I hadn't heard this before. Why does Andrew Huff believe that gain of function accelerates evolution by a hundred thousand years? I don't know what this refers to. Do you JJ? Yeah, he was on this interview with Kim dot com the other day and he kept repeating it a few times that gain of function research accelerates the evolution of the virus. I've worked in a part of that interview, I've got it paused right now, but it may be that I was working in that pass by without me understanding what was being said. But I'm going to go ahead and just and just say this out loud. So I and Andrew Huff came in and worked on you know, it's coming. I don't know. I'm just guessing you're you and you ever you warned me you're just going to say something out loud. It's usually something. Well, OK, so when I started working on the de med, which I did about 85% of the work on on that. But Andrew Huff was brought in by Thomas Rintz to work with me because the pile of stuff to do was just so enormous, it turned out to be so enormous that it would just never get done. But basically, Andrew Huff came in and he did what I'm going to call 1% of the work and that his part made no sense. But he was inserted into the chat group where we were discussing the work the whole time. And my wife is in there also, and she's a biochemist and my wife is is is a bioterrorism defense specialist. And she's very good at being a fly on the wall. And she would hardly ever say anything in the chat group. But when when Andrew would say things about, you know, biology, biological warfare, stuff like that, she would very often like turn, look at me and go, that's just not right. Like over and over and over again. And like this isn't something like this isn't something my wife does a lot. Right. I mean, she might she might like if she if she sees somebody who says something and it's not like specific, it's not quite right. You know, she may chime in and go, well, there is this other thing. And you know, like if you if you look at these experiments and they showed this or but I mean, she was just she was just like like there's something very wrong here. And the other thing that my partner Sam noticed in that same set of statements he made was his description of his fellowship and his Ph.D. and his strange educational and then early career path. And Jay, that was your observation as well, if I recall correctly. But what I couldn't explain to Matthew when I was trying to the other night is why it wasn't jiving with how things usually go. Could you just clarify what it is about, you know, about how he went from one field to another and how the fellowship just like it just doesn't get done that quick. Could you could you articulate that for us? So I think what I recall correctly, first of all, this is one particular piece of that interview, but most of what I know about Andrew Huff and some of these other players in this is all Mark Kulak, like that guy has really archived everything that I know and followed up on. It's a it's a how do I say it this way? If you're in the United States and you have a research university, one of the the ways that that factory works is that people go through your university and take apprenticeships, which are called postdocs or PhD positions, and in that apprenticeship, they're not paid as well as they should be paid while you are spending or using millions of dollars of the NIH money to educate them. And so that could go to institutional costs, it could go to equipment, it could go to animals, it can go to, you know, your own salary and their salary. But in the end, you're using NIH money to educate people. But these institutions use 90 percent of the money for themselves and 10 percent for those people that are supposedly the focus of this education. And it's the same with the postdocs. Any postdoc that doesn't bring his or her own money in is pretty much dead weight. And so unless they do really excellent work, you're not going to be in a lab for that long unless you get your own funding. And so that's pretty much the ceiling that everybody works against. If a professor at a university meets a PhD student that has a fellowship, and the fellowship comes from some organization where all the costs of that person are covered, what that usually means is that their salary plus 150 percent of that for institutional cost is provided. And so it's the ideal scenario where instead of me needing to write a grant and justifying why I should have a PhD student, all I need to do is get this PhD student to agree to learn from me. And then the money comes with the PhD student. What Andrew Huff described, as I understood it, was that he did his PhD through a fellowship where he couldn't turn it down because he was getting paid forty thousand dollars a year. And that's good at that time. Probably it's not giant now, but it's for a PhD. It's really good. And that he finished his PhD in two and a half years, which is strange, again, because a PhD project in America would be minimum, a minimum three years. And I guess it's possible that it could have been a three year thing that he's finished a little early. But it sure sounded like to me a scenario where something went too quickly. Something seemed too greased, if you will. But he could have just been lucky. It just strikes me as very odd because I know lots of people whose PhD took six years. Yeah. Really, really, really smart people. Yes. PhDs took, you know, four or five, six years. That's normal. For people. 170 IQs. Yes. One committee member could be the problem that requires two more years of experiments. It's not very usual that a degree granting institution is going to give you a PhD in two and a half years. It doesn't behoove them. Yeah. And I'm going to go ahead and throw this out there, too, since we got on the conversation. I'm just letting it out right now because I've started writing on a lot of these observations I have about people in our space that I found that I personally don't trust. I don't trust Thomas Rintz. I don't trust Andrew Huff. When I found what I found with the DMED, which, you know, potentially indicated a larger story, which is that, no, there wasn't these, like, three hundred and thousand percent increases. But look, the snapshots of the database, the past data changed, right? That was an open door to FOIAs and a potential lawsuit over fraud aimed at the DOD and the contractor that handled that. And Thomas Rintz was like, is my top priority? Five weeks later, nothing's done, right? The whistleblowers all dropped him. But he was focused on Andrew Huff at the time. And like Andrew even showed me, like, I would be able to talk on the phone with Rintz like once a month, even when he told me that, you know, my FOIAs were his top priority, which still never, still never sent. I put him in touch with a FOIA specialist who is a government insider who helped craft the Aaron Seary FOIAs and, you know, didn't do anything with it. But like, you know, I could see from Andrew Huff's phone that he and Andrew Huff were talking like five, six times a day this way, at least at the time. Right. I mean, and it seems like that that that continued to be his priority from there. So you know, what company would have been in charge of the DMED data in the past? It's called Unisant. And this is really interesting because, you know, Unisant is the French word for uniting and it fits into this paradigm that we see over and over again of these organizations that virtue signal with their name, eco health alliance or hack USAID, which, you know, has been long revealed as a CIA cut out. Yeah, that's not even conspiracy theory anymore. But you know, the wellness is the wellness group or wellness trust, right? Like all of these these organizations that that virtue signal their name. But but, you know, saying it in French is even a little bit more suspicious in the sense that the U.S. reached through France to go to Wuhan to build that laboratory, right? That's the best way to describe it. In CERM had the engineers at Lyons, France, who had been running their BSL for laboratory, go over there and do that. And of course, all of the like so many Mac and Fannie Mae, that seems like an incredibly weird dude to have at the head of that. Yeah, this is what I pointed out to Matthew as being the most striking when I was looking into this group. Oh, crap. Yeah, these are these are this is the the deep state. If you're looking for a real world example, I think this is a really good definition is groups like this. You know, you got PayPal down there, too. Chins on there. It is insane. Yeah. And these these are current former, you know, recent positions for these people. And they go in and out. You know, these aren't just passing positions. So this is the group in question. You know, IBM, obviously, a lot of a lot of, you know, United States Air Force, like a lot of them work for the Department of Homeland Security, yeah. General dynamic, tens of millions of dollars a year for a database. You better not have a span that goes months at a time in which your data is highly incomplete for recent years, right? So it's like hundreds of millions of dollars at the very least off this database, hundreds of millions. I'm stunned. I'm excited. That's crazy. I'm going to drop the link to that page in there. It's not complete, but it's worth it's worth a peruse, fully referenced. It is very anti fascist, isn't it? Thanks, Drew, welcome trust, I was saying wellness trust, wasn't I? Yeah, that's all right. Yeah. So but you were saying you were talking about Thomas Renz and how there's this was going somewhere. I can't remember. But and I want to say Andrew Huff, I'd love to talk. I've never talked to him personally. So I'm not trying to talk behind his back myself. I'd love to talk to him directly. It just hasn't had hasn't come up to be clear. If he did want to answer some of my questions, I think I think you you he's doing his rounds right now. I mean, he definitely has a firm opinion and stance on what happened, which which I don't agree with. But he's able to articulate it very well, which makes me think it'd be useful if if no one has done it yet to identify which questions have not been answered, like which questions have not been asked of him and which questions have not been answered just through his breadth of dialogue. And just to be clear, he says a whole lot of truthful things. Yeah. Right. It's exactly like the the coding theory story. The most difficult thing to deal with is when you get close to 50 percent, right? Jay, I want to ask on a personal level and you've talked about this a little bit and we've talked about this now sort of from a different perspective. But how do you handle on the personal level the changes in the relationships that you're that you're seeing? Are they mostly happening in in relationships that have been made in the context of the Scooby Doo adventures, you describe it such that it's not so much the individual relationships, but more the fact that relationships are changing. That's confusing and emotionally, you know, something to manage. Or are you finding it in more ways in your life that are like, is it friends and family to who are reacting to this specific set? The reason I ask is because people watching, I think, are still going through their own version of it, though, with different, you know, different details and different circumstances compared to the unique one you're going through. I just think it's very valuable to hear how people are managing in various contexts. And I I just would not want anyone to think that what I am doing is suffering from this. It's suffering from a from a cognitive perspective, like everyone else is trying to figure out what's going on here.
But when you're trying to figure out what other people are up to, it's a little bit more of a weight on your head. And one strategy is to just not worry what other people are up to and assume or give everyone the benefit of the doubt all the time. And I think I coped with that with the situation for the first two years like that, where I pretty much gave everyone the benefit of the doubt and when there was a time when some of the people that I'm having a disagreement with now, one of them being Kevin McCairn was very, very introspective about Robert Malone at a time when I was just thinking he's a hero and Robert Malone's a great guy. And so we've had a lot of different issues we've we as a group of people trying to cover this online have had different disagreements. But but I'm I am struck by the level of of of certainty that surrounds the fact that people think I'm wrong about this particular thing and why it's so offensive to some people to say that I may have been part of the apparatus for a while that fooled everybody. And why that why that somehow becomes a personal attack, I know that I'm not always wording it the best and I'm always but I also am keenly aware that very few of these ideas that are floating around in my head are uniquely mine and that listening to people and hearing things and reading things these things all spontaneously get reassembled in my head and it's very easy for me to believe that I figured it out, when in reality it was arguing with Kevin McCairn it was discussing with Kevin McKernan and it was talking with Matt and you it was reading the newspaper, and saying what the hell does that mean? And it was listening to the to the PBS NewsHour and going oh my gosh is that wrong? and then collectively processing that and so sometimes it feels like we are lashing out at each other but for me it's really it's all the same processing and if it becomes personal I don't know. I guess we're fighting for something that's so important right now that it's hard for me to see all the time where that personal starts and and where I just need to. If it was my very good friend who needed to divorce his wife I would have to say some very painful things to him, and say like look you're missing something here and if you don't listen to me you're gonna go off into the sunset and live this unhappy life and not understand. And maybe I can help you because I'm your friend and maybe some part of this argument that that occurs over the swarm and the clone is really like that where when people first hear it if it feels like a personal rejection like you're rejecting my ideas or the things that I helped you to understand when I feel instead like I've just had at have have calmed down a little bit and look backwards a few more times and and scratched my head a few more times and then um and I don't think that there's there's as many monsters as there were in the beginning as I thought and and I think there are different monsters than I saw in the beginning and that's all big revelations but but yeah it's it's I'm not really dealing with anything other than the consequences of my big mouth because what the problem is it is very difficult to go in front of a microphone without a script when you're taking all of this stuff very seriously and you've been smsing with people all night and talking to people all week to get to a stage where you can deliver a two-hour objective presentation about what you disagree with with someone else if you think that person is not playing fair right particularly when there's nobody helping you right uh like if if what we did was get um you know and if jj and i got the 10 smartest people that we know who are thinking about the stuff uh in uh an office for a week all of the language would improve we might even invent new terminology to discuss some of it it would be um you know presentation would be clearer this is actually unfortunately one of the asymmetric advantages that um you know people on the aggressive side of an information warfare game you know have if you're on the side that is more opaque you know let's say that this is all the results of um you know military banking complex and deep deep you know military um you know uh bio weaponry and psychological warfare uh that side is going to be able to talk with greater eloquence and be able to uh talk with without uh as much uh i don't know sort of conflictious debate in the room it's one of the reasons why is i'm writing my chaos wars articles there are a few people that i that i i will say my opinion is i i feel certain that this person is some sort of chaos agent in one way or another um but there aren't many people that i'll label that right like you know i i think this carolina bonita person is certainly something you know something not it's my opinion i can't prove it but i think somebody you know sent her on a mission to cause chaos um i i think that uh i think that of a few people but most people i just have question marks for and you know it's important like it and in fact i'm gonna i'm gonna mention this just because and i plan to write this in an article too like i haven't stopped to do a deep dive on robert malone but everybody like pokes me like will you take a side will you take a side will you take a side everybody's poking me about him too and and and you know part of it like here's part of the thing is you don't necessarily need to right um even if somebody is controlled opposition well you may hear a lot of things that are right that that if you if you use discernment you can still gain value from them you know always hold everyone at a distance that you don't know well use your instincts i had a great conversation with a woman from california who was a mayor before before the pandemic and talking with her about certain people on the phone she just had she had great instincts and she was like you know people better start to learn to use their instincts again or they're you know they're toast um and i agree with that but uh you know use your discernment you don't necessarily have to judge people as all good or all bad either there is you know without going deep on the subject there's a very real thought in my mind that you know certain people whether it's robert malone or andrew huff or anybody else may have been put in certain situations they did not understand when they got there they you know they may have or they may in the future change course uh or you know like we all have lots of information revealed to us over time and everybody has different interests you know there may be you know that there's very little black and white you know there's a whole lot in the gray zone there's a lot in the gray zone people have vested interests people have hidden interests use discernment as much as possible learn as much as you can the the truth though the matter of of the whole thing you know it if this is some sort of global revolution let's say of the financial system which i i believe from beginning to end even though my view on what it is has changed a little bit right like we have more texture for that conversation um there are only a few things that are really important to talk about one is um that you know there's certainly this aspect of the pandemic that it was just causing panic causing chaos it's totally suspicious the way people would suddenly change their mind in one you know unipolar you know polar direction um that we pay attention to these things that we can absolutely say for certain most everything else is secondary or tertiary don't let the noise of those things overwhelm your view of the big picture the simple things first yeah i agree i think that's always what i i go two steps forward and one steps back and and and uh i i'm not afraid to say that i have i am still considering the fidelity of the sequencing even though even though um i really had to check myself after talking to kevin um i'm still i still think that there is something there is an edge to be understood in all aspects of this science and it is to their advantage if we don't know where the edge is it's to their advantage if we think that the the edge is where they say it is and that kind of general principle has what really got me free of the trap that i think i was in which is that well i figured it out it's a lab leak um and i do think that that was a trap i do i do think that's the reason why now the mainstream media even the view and the ladies on the view are talking about it probably being a lab leak because this was kind of a we've been we've been scripted to be here it doesn't seem like even that complicated of a psychological operation to call it a scooby doing where they make you think you figured it out and then both sides accept it um i don't know i i you know one one thing about the zoonosis story is it's so paper thin right zero animals ever tested positive um you know there was there was so much obvious you know if you did any research at all there were obvious holes if you did a lot of research there were a billion holes and then you have the social media engines coming in and just raining fire on anyone who's trying to open those doors and and you know shed some light in uh all that fire all the fire the suppression fire um that makes it feel like it was more of a struggle when it wasn't really right then then when everybody goes oh it was a lab leak after all it feels like that's overcoming the drama when the problem solving was actually real real thin and that that's an indication that what they've allowed us to drop into is itself at the very least not the the full story but probably not the right story yeah now there's one suggestion that's been made by miss weasel on rumble um where did it go sorry hold on it was basically that the she wonders if part of the reason people are so attached to the the scooby-doo narrative of it was a gain of function lab leak is that that right now is possibly the core of some lawsuits and that right now a lot of progress has been made lining up to hold people accountable for that now i i think that's a oversimplification because it's also just not necessarily true there's a lot of different lawsuits in the works a lot several by rfk junior and children's health defense robert barnes both with children's health defense and brooke jackson and those are just a couple there's so many but do you think there is an element of attachment and feeling as though if we let this go we've lost a good chunk of our first couple of years of work trying to unveil not just on the narrative side but on the legal side too now i think there's that's the problem is that there are two battles here so you can you can win the battle about coronavirus biology and still convict these people of saying everything they said and doing everything they did um and so if these people want to claim that they can make gain of function viruses and they did it and we can convict them on that i don't know that that in some ways seems like a very simple solution to the problem and we should do it but my argument is that then there's case law that says the gain of function viruses can kill millions of people instead of public health measures implemented incorrectly can kill millions of people and i think that that's why some people are very upset is that if they really believe that there is some amorphous number of people that have been killed by this etiological agent, it could be a few, it could be a lot, but we don't know and so we better assume a lot so that we can convict these people. I think that's a… that's that that plays into their long-term plan, and then their long-term game because then we haven't actually rejected their story. um In the… in a very similar way that i find it very, very much now part of the same fight, that that if we're going to win the FDA is going to probably disappear, if we're going to win the CDC is going to be either removed or revamped, or reorganized or something. Like all kinds of parts of our system are are in need of revamping or full burning to the right down to the studs, and and so this isn't an argument about what happened in february of 2020 so much as what allowed whatever purported to happen in 2020 to be an open door to completely ruin our system or or revamp it that's yeah that to me is is is so much about what this is about and when you start focusing on the birds um and and saying that it's really this bird it's this bird over here it's this bird over here you're ignoring this you know huge pile of of other things going on i don't know and and to be clear because the department of homeland security is our third fourth guest for the day uh we don't mean literally burned to the ground to be explicitly clear um like no i don't want anything to be burned to the ground i like the buildings i just i think bureaucracy as it exists right now is something that needs to be revamped yeah and so figuratively that would be yeah silly little disclaimer for the dhs well you know what um i i think i'd like to move toward um wrapping things up we've been going for about an hour and a half uh but one thing that you know um everybody let let jj know uh you know um how good he looks in the captain's chair if you haven't if you haven't gone to see the starship you should go check out his feed uh over at uh uh oh gosh what you like you go by i only go to okay twitch i only go to twitch to to watch you so i half the time i can't remember that it's called twitch um but yeah everybody can go over there and check out uh go and biological on twitch and uh i i mean his his stream has been fire uh a lot of the last couple of months um and uh and thank you drew remember uh stick to the fundamentals defense wins ball games yes any closing thoughts um i'm not dividing i don't want to divide i don't want to fight about it but i do think that we have to stick to parsimony and a lot of times um right now i think that there are people that are set in narratives that have been reinforced by television and social media and there are very few of us as you said earlier that aren't fooled by something still and it would do everyone a good thing right now to recheck what we're sure about and and make sure that we remind ourselves that it isn't very much that we're sure about and even though i'm very good at coming off as though i'm sure about it um it really only works with my wife and it shouldn't work with you um you should be doing your own research and uh yeah and check in my work uh i welcome it i hope it i hope it continues right and this is science you know uh it should be formed on a foundation of doubt you know it's always keep looking around there's always a new vector you can shine light in and learn a little bit more so if maybe the only other thing i would say is that we have to stop discounting everyone is having these bad motives um but at the same sense i do believe we are at the stage in our progress as a movement to where we are now facing resistance from from growing as a movement from the inside not the outside yeah and you know i i said this in an article in just in the last few days um i i think that it's wrong-handed for us to think that we all have to be one unit right um we should be decentralized you know when you can't when you can't squash any one thing all at once um when you can't make the same mistake together right uh it on wall street we sometimes call this the common investor effect you know if everybody's invested in the same thing and you all make a mistake at once even if you're really really good at not making mistakes it doesn't matter right it's one of the reasons why people shouldn't have too much power but you don't all have to be on the same page in the medical freedom movement you just have to value liberty and you know what up your game you know your epistemology your way of researching uh your instincts uh your way of your way of life like everything right that that's really and truly uh you know the best reason why we're here that you know what we're going to do to move forward those the core values you know defense wins ball games stick to the fundamentals i love it i'm going to make a slide that says defense wins ball games and put it in my startup i think it's great i'm gonna find a bobby knight picture to use with it i'm really excited well good stuff guys the last little reminder i want to uh put out there is that we are now on locals and we have seen a glorious um increase in attention there um in terms of both free members who are coming in to be part of the community and paid supporters um so thank you all very much and here's the great thing we want you to come join us roundingtheearth.locals.com and as you can see here we've got a free promo code um look your support is appreciated absolutely but the number one priority is bringing people into this decentralized bigger thinking critical thinking picture so the link to that uh discount and it's a great place for us to like drop like you know we we drop numerous interviews of different people sometimes we drop jj's stream or um you know i i dropped one from mark kulak actually i thought mark was going to be talking but it was just the it was it looks like it's just the twitter interview um.com uh but you know it's a great place to just be able to drop like lots of news that relates to everything that we're doing too so yeah and it's a good it's a good funnel point i think we're figuring out all the utilities for it and one that i find is that we can in fact put uh for example in this one post pinned to the top uh all of the relevant links for today's show so you can go there get a notification that we're about to go live and you see rumble youtube odyssey and then of course a link to giga ohm biological so anyway thank you all for um joining up on there and jay thank you again so much for coming on to our lovely little uh unflattened the earth think tankathon um anytime you have a seat at the table in your clubhouse i love to come by fantastic okay matthew any final thoughts before we play that iconic outro music defense wins ball games you
*Kevin*, *kevin:_*
https://mccairndojo.com/
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Principal Investigator at the Korea Brain Research Institute Systems Neuroscience and Movement Disorders Laboratory (Retired)
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*Matt*, *Matthew*, *Matthew Crawford*, *matthew-crawford:_*, *stream-crawford-2022-11-08:_*
https://roundingtheearth.substack.com/
Rounding the Earth Newsletter
Pandemic, Bitcoin, education, finance, science, health, economics, statistics, and other topics that need attention.
Mathew Crawford
Educator, Entrepreneur, Statistician, Finance Specialist
*PCR*
https://en.wikipedia.org/wiki/Polymerase_chain_reaction
The polymerase chain reaction (PCR) is a method widely used to rapidly make millions to billions of copies (complete or partial) of a specific DNA sample, allowing scientists to take a very small sample of DNA and amplify it (or a part of it) to a large enough amount to study in detail. PCR was invented in 1983 by the American biochemist Kary Mullis at Cetus Corporation; Mullis and biochemist Michael Smith, who had developed other essential ways of manipulating DNA, were jointly awarded the Nobel Prize in Chemistry in 1993.
PCR is fundamental to many of the procedures used in genetic testing and research, including analysis of ancient samples of DNA and identification of infectious agents. Using PCR, copies of very small amounts of DNA sequences are exponentially amplified in a series of cycles of temperature changes. PCR is now a common and often indispensable technique used in medical laboratory research for a broad variety of applications including biomedical research and criminal forensics.
One major limitation of PCR is that prior information about the target sequence is necessary in order to generate the primers that will allow its selective amplification. This means that, typically, PCR users must know the precise sequence(s) upstream of the target region on each of the two single-stranded templates in order to ensure that the DNA polymerase properly binds to the primer-template hybrids and subsequently generates the entire target region during DNA synthesis.
Like all enzymes, DNA polymerases are also prone to error, which in turn causes mutations in the PCR fragments that are generated.
Another limitation of PCR is that even the smallest amount of contaminating DNA can be amplified, resulting in misleading or ambiguous results. To minimize the chance of contamination, investigators should reserve separate rooms for reagent preparation, the PCR, and analysis of product. Reagents should be dispensed into single-use aliquots. Pipettors with disposable plungers and extra-long pipette tips should be routinely used. It is moreover recommended to ensure that the lab set-up follows a unidirectional workflow. No materials or reagents used in the PCR and analysis rooms should ever be taken into the PCR preparation room without thorough decontamination.
Environmental samples that contain humic acids may inhibit PCR amplification and lead to inaccurate results.
*kary-mullis:_*, *PCR*
https://www.youtube.com/watch?v=Xc0Kysti6Kc
Kary Mullis about using PCR to diagnose AIDS, in 1993
00:25 If you can say, if they could find this [HIV] virus in you at all, and with PCR if you do it well, you can find almost anything in anybody, it starts making you believe in the sort of Buddhist notion that everything is contained in everything else, right?
00:42 I mean, because if you can amplify one single molecule up to something that you can really measure, which PCR can do, then there's just very few molecules that you don't have at least one single one of them in your body, okay?
00:56 So that could be thought of as a misuse of it, just to claim that it's meaningful.
1:00 But, the real misuse of it is… you don't need to test for HIV, you don't need to test for the other 10,000 retroviruses that are unnamed, also in the subject, because someone that's got HIV generally is going to have almost anything that you can test for, because they have just… HIV is a fairly rare virus. There is only 1 million out of 250-300 million people in America that have that virus. So you have to get around, either you mother has to have it and pass it to you, or you have to really be paying a lot of attention to people that do have it, and paying attention to them and get a pretty good chance of getting it that way. It's hard to get it, but if you have it, there is a good chance you've also got a lot of other ones, because you've been in the market for… you've been… it's been possible for you to get a lot of… so to test for that one just doesn't have any special meaning is what I think is the problem, not that PCR has been misused.
*gain-of-function:_*
https://en.wikipedia.org/wiki/Gain-of-function_research
Gain-of-function research (GoF research or GoFR) is medical research that genetically alters an organism in a way that may enhance the biological functions of gene products. This may include an altered pathogenesis, transmissibility, or host range, i.e. the types of hosts that a microorganism can infect. This research is intended to reveal targets to better predict emerging infectious diseases and to develop vaccines and therapeutics. For example, influenza B can infect only humans and harbor seals. Introducing a mutation that would allow influenza B to infect rabbits in a controlled laboratory situation would be considered a gain-of-function experiment, as the virus did not previously have that function. That type of experiment could then help reveal which parts of the virus's genome correspond to the species that it can infect, enabling the creation of antiviral medicines which block this function.
In virology, gain-of-function research is usually employed with the intention of better understanding current and future pandemics. In vaccine development, gain-of-function research is conducted in the hope of gaining a head start on a virus and being able to develop a vaccine or therapeutic before it emerges. The term "gain of function" is sometimes applied more narrowly to refer to "research which could enable a pandemic-potential pathogen to replicate more quickly or cause more harm in humans or other closely-related mammals."
Some forms of gain-of-function research (specifically work which involves certain select agent pathogens) carry inherent biosafety and biosecurity risks, and are thus also referred to as dual use research of concern (DURC). To mitigate these risks while allowing the benefits of such research, various governments have mandated that DURC experiments be regulated under additional oversight by institutions (so-called institutional "DURC" committees) and government agencies (such as the NIH's recombinant DNA advisory committee). A mirrored approach can be seen in the European Union's Dual Use Coordination Group (DUCG).
Importantly, the US and EU regulations both mandate that an unaffiliated member of the public (or several) be "active participants" in the oversight process. Significant debate has taken place in the scientific community on how to assess the risks and benefit of gain-of-function research, how to publish such research responsibly, and how to engage the public in an open and honest review. In January 2020, the National Science Advisory Board for Biosecurity convened an expert panel to revisit the rules for gain-of-function research and provide more clarity in how such experiments are approved, and when they should be disclosed to the public.
*rna:_*
https://en.wikipedia.org/wiki/RNA
Ribonucleic acid (RNA) is a polymeric molecule essential in various biological roles in coding, decoding, regulation and expression of genes. RNA and deoxyribonucleic acid (DNA) are nucleic acids. Along with lipids, proteins, and carbohydrates, nucleic acids constitute one of the four major macromolecules essential for all known forms of life. Like DNA, RNA is assembled as a chain of nucleotides, but unlike DNA, RNA is found in nature as a single strand folded onto itself, rather than a paired double strand. Cellular organisms use messenger RNA (mRNA) to convey genetic information (using the nitrogenous bases of guanine, uracil, adenine, and cytosine, denoted by the letters G, U, A, and C) that directs synthesis of specific proteins. Many viruses encode their genetic information using an RNA genome.
Some RNA molecules play an active role within cells by catalyzing biological reactions, controlling gene expression, or sensing and communicating responses to cellular signals. One of these active processes is protein synthesis, a universal function in which RNA molecules direct the synthesis of proteins on ribosomes. This process uses transfer RNA (tRNA) molecules to deliver amino acids to the ribosome, where ribosomal RNA (rRNA) then links amino acids together to form coded proteins.
*rna:_*, *mrna:_*, *ribosome:_*
https://en.wikipedia.org/wiki/Messenger_RNA
Messenger RNA
In molecular biology, messenger ribonucleic acid (mRNA) is a single-stranded molecule of RNA that corresponds to the genetic sequence of a gene, and is read by a ribosome in the process of synthesizing a protein.
mRNA is created during the process of transcription, where an enzyme (RNA polymerase) converts the gene into primary transcript mRNA (also known as pre-mRNA). This pre-mRNA usually still contains introns, regions that will not go on to code for the final amino acid sequence. These are removed in the process of RNA splicing, leaving only exons, regions that will encode the protein. This exon sequence constitutes mature mRNA. Mature mRNA is then read by the ribosome, and, utilising amino acids carried by transfer RNA (tRNA), the ribosome creates the protein. This process is known as translation. All of these processes form part of the central dogma of molecular biology, which describes the flow of genetic information in a biological system.
As in DNA, genetic information in mRNA is contained in the sequence of nucleotides, which are arranged into codons consisting of three ribonucleotides each. Each codon codes for a specific amino acid, except the stop codons, which terminate protein synthesis. The translation of codons into amino acids requires two other types of RNA: transfer RNA, which recognizes the codon and provides the corresponding amino acid, and ribosomal RNA (rRNA), the central component of the ribosome's protein-manufacturing machinery.
The concept of mRNA was developed by Sydney Brenner and Francis Crick in 1960 during a conversation with François Jacob. In 1961, mRNA was identified and described independently by one team consisting of Brenner, Jacob, and Matthew Meselson, and another team led by James Watson. While analyzing the data in preparation for publication, Jacob and Jacques Monod coined the name "messenger RNA".
*complementary-dna:_*
https://en.wikipedia.org/wiki/Complementary_DNA
Complementary DNA
In genetics, complementary DNA (cDNA) is DNA synthesized from a single-stranded RNA (e.g., messenger RNA (mRNA) or microRNA (miRNA)) template in a reaction catalyzed by the enzyme reverse transcriptase. cDNA is often used to clone eukaryotic genes in prokaryotes. When scientists want to express a specific protein in a cell that does not normally express that protein (i.e., heterologous expression), they will transfer the cDNA that codes for the protein to the recipient cell. In molecular biology, cDNA is also generated to analyze transcriptomic profiles in bulk tissue, single cells, or single nuclei in assays such as microarrays and RNA-seq.
cDNA is also produced naturally by retroviruses (such as HIV-1, HIV-2, simian immunodeficiency virus, etc.) and then integrated into the host's genome, where it creates a provirus.
The term cDNA is also used, typically in a bioinformatics context, to refer to an mRNA transcript's sequence, expressed as DNA bases (deoxy-GCAT) rather than RNA bases (GCAU).
*robert-malone:_*
https://en.wikipedia.org/wiki/Robert_W._Malone
Robert Wallace Malone (born 1959) is an American physician and biochemist. His early work focused on mRNA technology, pharmaceuticals, and drug repurposing research. During the COVID-19 pandemic, Malone has promoted misinformation about the safety and efficacy of COVID-19 vaccines.
In the late 1980s, while a graduate student researcher at the Salk Institute for Biological Studies in San Diego, California, Malone conducted studies on messenger ribonucleic acid (mRNA) technology, discovering in what Nature has described as a landmark experiment that it was possible to transfer mRNA protected by a liposome into cultured cells to signal the information needed for the production of proteins. With Philip Felgner, he performed experiments on the transfection of RNA into human, rat, mouse, Xenopus, and Drosophila cells, work which was published in 1989. In 1990, he contributed to a paper with Jon A. Wolff, Dennis A. Carson, and others, which first suggested the possibility of synthesizing mRNA in a laboratory to trigger the production of a desired protein. These studies are recognized as among the earliest steps towards mRNA vaccine development.
https://www.rwmalonemd.com/
As the original "inventor" of mRNA and DNA vaccines… I am concerned about how the technology is being developed and implemented.
Robert W Malone PhD
https://sites.google.com/housatonicits.com/home0003/research/robert-wallace-malone-b1959
2017-biography-omicsonline-org : "Robert W. Malone - CEO, Clinical Trails, Atheric Pharmaceutical, USA"
Robert W. Malone, M.D., M.Sci. CEO, CSO, co-founder and board of manager member of Atheric Pharmaceutical, LLC. Dr. Malone has extensive research and development experience in the areas of clinical trials, vaccines, gene therapy, bio-defense, and immunology. He has over twenty years of management and leadership experience in the academia, pharmaceutical and biotechnology industries. His FDA, HHS, and DoD agency knowledge is extensive. Dr. Malone is an internationally recognized scientist and is known as one of the original inventors of "DNA Vaccination." Dr. Malone holds numerous fundamental domestic and foreign patents in the fields of gene delivery, delivery formulations, and vaccines. He has over fifty peer-reviewed publications, has been an invited speaker at over thirty-five conferences, has chaired numerous conferences and he has sat on numerous study sections. Dr. Malone is in the Harvard Medical School Global Clinical Scholars Program in 2015-2016. In August 2014, colleagues at the Department of Defense/Defense Threat Reduction Agency asked Dr. Malone to step in and help NewLink manage the Ebola project and develop the contracts necessary to move the "orphan" PHAC/rVSV ZEBOV vaccine forward quickly. Dr. Malone got the project on track, recruited our client Focus Clinical Trials to team with USAMRIID/WRAIR to develop the immunoassays, put WHO leadership in touch with Pentagon leadership to expedite the initial WRAIR clinical trials, recruited the government of Norway to help fund the clinical research, used social media (LinkedIn) to recruit Merck Vaccines to join the project, recruited a management team, and lead the development of the BARDA and DTRA contracts - yielding over 200M$ in resources. Those were frightening times, but now we have a remarkably effective vaccine, developed in record time. Dr. Malone was CEO and co-founder of RW Malone MD, LLC, a very successful consulting and development firm focused on clinical trials and USG medical countermeasure proposal capture and management. As a capture and proposal manager, Dr. Malone has an extraordinary funding record. In the past five years, he has been involved in ten billion dollars of successful government contracts and awards.
*conways-game-of-life:_*
https://en.wikipedia.org/wiki/Conway%27s_Game_of_Life
The Game of Life, also known simply as Life, is a cellular automaton devised by the British mathematician John Horton Conway in 1970. It is a zero-player game, meaning that its evolution is determined by its initial state, requiring no further input. One interacts with the Game of Life by creating an initial configuration and observing how it evolves. It is Turing complete and can simulate a universal constructor or any other Turing machine.
The universe of the Game of Life is an infinite, two-dimensional orthogonal grid of square cells, each of which is in one of two possible states, live or dead (or populated and unpopulated, respectively). Every cell interacts with its eight neighbours, which are the cells that are horizontally, vertically, or diagonally adjacent. At each step in time, the following transitions occur:
Any live cell with fewer than two live neighbours dies, as if by underpopulation.
Any live cell with two or three live neighbours lives on to the next generation.
Any live cell with more than three live neighbours dies, as if by overpopulation.
Any dead cell with exactly three live neighbours becomes a live cell, as if by reproduction.
These rules, which compare the behavior of the automaton to real life, can be condensed into the following:
Any live cell with two or three live neighbours survives.
Any dead cell with three live neighbours becomes a live cell.
All other live cells die in the next generation. Similarly, all other dead cells stay dead.
The initial pattern constitutes the seed of the system. The first generation is created by applying the above rules simultaneously to every cell in the seed, live or dead; births and deaths occur simultaneously, and the discrete moment at which this happens is sometimes called a tick.[nb 1] Each generation is a pure function of the preceding one. The rules continue to be applied repeatedly to create further generations.
*PCR*, *christian-drosten:_*
https://en.wikipedia.org/wiki/Christian_Drosten
Christian Heinrich Maria Drosten (German: [ˈkʁɪs.ti̯an ˈdʁɔs.tn̩] (listen), born 1972) is a German virologist whose research focus is on novel viruses (emergent viruses). During the COVID-19 pandemic, Drosten came to national prominence as an expert on the implications and actions required to combat the illness in Germany.
On 23 January 2020, Drosten, along with other virologists in Europe and Hong Kong, published a workflow of a real-time PCR (RT-PCR) diagnostic test, which was accepted by the World Health Organization (WHO) and which sent test kits to affected regions.
On 19 February 2020, Drosten, along with 26 other scientists, published the Lancet letter in support of scientists and medical professionals in China fighting the outbreak and condemning theories suggesting that the virus does not have a natural origin, which it referred to as "conspiracy theories."
On 17 March 2020, Drosten was appointed to the European Commission's advisory panel on COVID-19, co-chaired by EC President Ursula von der Leyen and ECHSF Stella Kyriakides. On 23 March 2020, The Guardian described Drosten as "the [German] country's real face of the coronavirus crisis", and also noted that the Süddeutsche Zeitung had described Drosten as "the nation's corona-explainer-in-chief". He was a counterpart to Lothar Wieler, head of the State's Robert Koch Institute in Berlin, in consulting to German federal and state authorities.
*complementary-dna:_*, *plasmid-vector:_*
https://en.wikipedia.org/wiki/Plasmid#Vectors
Plasmid, Vectors
Artificially constructed plasmids may be used as vectors in genetic engineering. These plasmids serve as important tools in genetics and biotechnology labs, where they are commonly used to clone and amplify (make many copies of) or express particular genes. A wide variety of plasmids are commercially available for such uses. The gene to be replicated is normally inserted into a plasmid that typically contains a number of features for their use. These include a gene that confers resistance to particular antibiotics (ampicillin is most frequently used for bacterial strains), an origin of replication to allow the bacterial cells to replicate the plasmid DNA, and a suitable site for cloning (referred to as a multiple cloning site).
Plasmids are the most-commonly used bacterial cloning vectors. These cloning vectors contain a site that allows DNA fragments to be inserted, for example a multiple cloning site or polylinker which has several commonly used restriction sites to which DNA fragments may be ligated. After the gene of interest is inserted, the plasmids are introduced into bacteria by a process called transformation. These plasmids contain a selectable marker, usually an antibiotic resistance gene, which confers on the bacteria an ability to survive and proliferate in a selective growth medium containing the particular antibiotics. The cells after transformation are exposed to the selective media, and only cells containing the plasmid may survive. In this way, the antibiotics act as a filter to select only the bacteria containing the plasmid DNA. The vector may also contain other marker genes or reporter genes to facilitate selection of plasmids with cloned inserts. Bacteria containing the plasmid can then be grown in large amounts, harvested, and the plasmid of interest may then be isolated using various methods of plasmid preparation.
A plasmid cloning vector is typically used to clone DNA fragments of up to 15 kbp. To clone longer lengths of DNA, lambda phage with lysogeny genes deleted, cosmids, bacterial artificial chromosomes, or yeast artificial chromosomes are used.
*nanopore-sequencing-paper-jc:_*
https://www.mccairndojo.com/library/2022-12-06T0400Z-Sinterklaas-Clone-Wars-Special-Gigaohm-Biological-High-Resistance-Low-Noise-Information-Brief/#t=5558.2
Sinterklaas Clone Wars Special: Gigaohm Biological High Resistance Low Noise Information Brief
*nanopore-sequencing:_*, *nanopore-sequencing-paper:_*
Direct RNA nanopore sequencing of full-length coronavirus genomes provides novel insights into structural variants and enables modification analysis
Sequence analyses of RNA virus genomes remain challenging owing to the exceptional genetic plasticity of these viruses. Because of high mutation and recombination rates, genome replication by viral RNA-dependent RNA polymerases leads to populations of closely related viruses, so-called "quasispecies." Standard (short-read) sequencing technologies are ill-suited to reconstruct large numbers of full-length haplotypes of (1) RNA virus genomes and (2) subgenome-length (sg) RNAs composed of noncontiguous genome regions. Here, we used a full-length, direct RNA sequencing (DRS) approach based on nanopores to characterize viral RNAs produced in cells infected with a human coronavirus. By using DRS, we were able to map the longest (∼26-kb) contiguous read to the viral reference genome. By combining Illumina and Oxford Nanopore sequencing, we reconstructed a highly accurate consensus sequence of the human coronavirus (HCoV)-229E genome (27.3 kb). Furthermore, by using long reads that did not require an assembly step, we were able to identify, in infected cells, diverse and novel HCoV-229E sg RNAs that remain to be characterized. Also, the DRS approach, which circumvents reverse transcription and amplification of RNA, allowed us to detect methylation sites in viral RNAs. Our work paves the way for haplotype-based analyses of viral quasispecies by showing the feasibility of intra-sample haplotype separation. Even though several technical challenges remain to be addressed to exploit the potential of the nanopore technology fully, our work illustrates that DRS may significantly advance genomic studies of complex virus populations, including predictions on long-range interactions in individual full-length viral RNA haplotypes.
Adrian Viehweger, Sebastian Krautwurst, Kevin Lamkiewicz, Ramakanth Madhugiri, John Ziebuhr, Martin Hölzer, and Manja Marz
https://genome.cshlp.org/content/29/9/1545.full.pdf
https://www.mccairndojo.com/library/2022-12-06T1900Z-Denis-Rancourt-LIVE-Gigaohm-Biological-High-Resistance-Low-Noise-Information-Brief/
Denis Rancourt LIVE: Gigaohm Biological High Resistance Low Noise Information Brief
GigaOhmBiological
https://patents.google.com/patent/EP0871780B1/en
A basic technology in the field of molecular biology is the conversion of poly(A)+RNA (mRNA) to double-stranded (ds) complementary DNA (cDNA), which then can be inserted into a cloning vector for generating a cDNA library or expression in an appropriate host cell.
Several procedures for generating cDNA libraries which have been used during the last 15 years are comprehensively reviewed in Wu, ed. Methods in Enzymology (1987), voL 152. For the most part, cDNA library construction technologies use poly(A)+RNA as a starting material. The intact poly(A)+RNA is characterized by a polyadenylated "tail" at its 3' end and a characteristic "CAP structure or cap site" at the 5' end. A critical requirement for cDNA library construction is to completely copy poly(A)+RNA to full-length cDNA and retain the complete sequence information on the structure of the protein encoded by mRNA.
One generalized and commonly used method by which the poly(A)+RNA is copied into cDNA employs reverse transcriptase, which starts at the 3' end of the mRNA from an oligo d(T) primer and proceeds towards the 5' end to generate a cDNA:mRNA hybrid (Gubler et al., 1983). The RNA strand is then removed from the hybrid by action of RNase H and a second DNA strand is then synthesized using DNA polymerase I. The resulting heterogeneous mixture of ds cDNA molecules can then be cloned into suitable recombinant DNA vector molecules using a variety of techniques. Unfortunately, for the majority of mRNAs, this method does not allow for the synthesis of "full-length" cDNA because reverse transcriptase can not efficiently copy them into full-length cDNAs. The efficiency of copying is inversely proportional to the length of tnRNA; thus, the problem of "full-length" cDNA synthesis is more acute for longer mRNAs. Moreover, the current technology can generate deletions at the 5' and 3' ends of the cDNA.
In an alternative approach, poly(A) tails of mRNA molecules are first annealed to oligo (dT) linking with linearized vector DNA (vector primer)(Okayama et al., 1982; Pruitt, International Patent, Appl. No. 89110816.9 ). Then, the first strand of cDNA synthesized by reverse transcriptase is tailed at the 3' end by oligo dt which facilitates subsequent cloning by circularization into vector primer. This method also generates greater numbers of cDNA clones that contain truncated cDNAs due to non-full-length cDNA synthesis.