A single line often inverts meaning once you see what it
answers, so neighbouring messages are always shown.
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Secondly, if you're doing work that's related to the development of vaccines or serology, it's also except from the gain-of-function policy. DC.Scheduling@LexitasLegal.com
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Or national security. That was also an exemption.
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I don't know what you mean by that.
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Yeah. I'm just saying it was. I wasn't --
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2026-04-10 09:00
Ralph S. Baric
So anyway, all the work with pseudotypes was not subject to gain, right. These are single-hit vectors that can't cause disease. As soon as we made full molecular clones, or chimeras, they were done in a WIV backbone, which meant that they're putting a zoonotic spike into a zoonotic strain, to eventually identify vaccine formulations that would be used in the cave, that's not subject to gain-of-function.
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It's not.
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That's not, according to my records. And in the grant in the very beginning it says that's not subject to gain-of-function. Now, if I remember correctly there is one sentence in there somewhere that says that we will consider potentially moving spike gene, or furin cleavage site into SARS coronavirus. That is definitely gain-of-function and would have to be reviewed before anything else was done. But that occurred boom, boom, boom, boom. You know, we're talking about eight steps down the line, where you gain a significant amount of data about the role of each spike, its ability to use different DC.Scheduling@LexitasLegal.com receptors, and the role of the furin cleavage site in the ability of that virus to replicate and cause disease, before you do anything about moving it into another strain. So there was a huge amount of data that would be available to say this could be safe or we shouldn't do this.
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So is it only gain-of-function in that scenario if you know it's --
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Well, again, you're dealing with -- okay. So prior to 2015 paper, we had little if any evidence to indicate that any bat sarbecovirus was capable of replicating efficiently on the human receptor, especially in the context of a primary cell derived from the lung, the airways of a human. And so there was no data to support the idea that these were important threat viruses. After that paper, it said that there are threat viruses, followed by the WIV1 paper, that said there are threat viruses in nature, in bats, that can have the potential to cause serious human disease. We don't know for sure. A good example of this is there are strains that use the DPP4, no, let's say the ACE2 receptor of SARS coronavirus, and you put them in K18 mice that overexpress that ACE2 molecule, you can find genome equivalents but no live virus. In other words, the virus gets in, it makes a bunch of those progeny RNA molecules, but it doesn't make any progeny viruses so it can't spread. DC.Scheduling@LexitasLegal.com So the idea that just the virus receptor interaction and entry is the whole key to driving a virus to become a pandemic is just nonsense, and it's always been nonsense. In the case of coronaviruses, there are 49 genes in each of our bodies that regulate disease severity, and the person who gets really sick has a very common loci on chromosome three, with five genes on it, that we inherited from Neanderthals, according to the reports, based on people that do the sequence comparisons. And if you have that loci you're going to get really sick with sarbecoviruses.