A single line often inverts meaning once you see what it
answers, so neighbouring messages are always shown.
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So there were two approaches that were discussed, that were presented in that grant. One was the use of small molecule, double-stranded RNA to induce, let's call it innate immunity. These involve proteins that are induced in every one of our cells that regulate the replication and pathogen assists of viruses, and bacteria for that matter. So most people in the scientific community feel that what determines whether you live or die following a virus infection is the efficiency of inducing these innate immune molecules that regulate virus replication efficiency. And there's about 1,000 different genes that host cells make that target key steps in virus replication to knock it down. And it all starts with interferon signaling. Okay, that's the basis for it.
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But this is all under one proposal. You're saying that these were separate technical aims.
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That's correct. DC.Scheduling@LexitasLegal.com
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So when you have a separate technical aim you just have two completely separate experiments that are never going to meet, that have zero connectivity? That, to me, I don't know, but that doesn't make logical sense to me that you would have -- why wouldn't you have separate --
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2026-04-10 09:00
Ralph S. Baric
I think you're making an incorrect intuitive leap. I was trying to describe the two approaches that were being used to control viruses in a cave setting. The other approach was that having identified strains of viruses that had spike genes that could infect human cells and potentially cause human disease, those spike genes would be isolated and placed in virus vaccine vectors that would then be delivered to the bats in the cave, is the second approach. The first approach is immediate innate immune knockdown so that the virus burden in the cave goes down and it's less likely that a soldier will be infected. The second approach is to immunize the bats in that cave so that a virus burden would be very, very low, and it would be long-term protection so the cave could be used for a much longer period of time. So they are linked but they're different approaches to abrogate virus replication.
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Okay. Would this have been subject to the gain-of-function pause in 2017? DC.Scheduling@LexitasLegal.com
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So the short answer is no, up to a point, okay.
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What's the point?
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I'm going to get to that. So if you go back to the NSABB P3CO regulations, the regulations state that viruses, like flu, SARS, and MERS coronavirus, are highly pathogenic viruses, and highly transmissible viruses are covered by this program. And if you do anything on these particular viruses that are highly pathogenic or highly transmissible, and you do any manipulation to increase that, then that's considered gain-of-function and regulated by those documents, based on my read of them. There are exemptions to that gain-of-function regulation framework. The first is that if you work with zoonotic viruses, like WIV1, which has never been show to infect a human being, that has never shown to be transmissible in humans, it is not subject to the gain-of18 function regulatory framework. It has to be reviewed, but the review process would require that it be -- the review process would, based on the regulations, say it's not subject to those gain --