Transcript segment

Baric Transcribed Interview (Redacted), pp.102-103 · baric_ti:utt:00877

Date: 2026-04-10 09:00 (day precision)
Type: transcript segment · interview
recipient: Christina Salazar, Harry Kazenoff, David T. Lambeth III, William Henderson, Clark Ervin, Jake Greenberg
speaker: Ralph S. Baric
Topics: Furin cleavage site and molecular features Intelligence community assessments Wuhan Institute of Virology collaboration

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.

Extracted statements

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Statement	Grade	Attribution	Stance
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.	quoted / not their view	paraphrase_third_party third-party reporting verb	asserts
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.	quoted / not their view	quoted_external message body appears to be pasted content	instructs

Statement

Grade

Attribution

Stance

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.

quoted / not their view

paraphrase_third_party third-party reporting verb

asserts

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.

quoted / not their view

quoted_external message body appears to be pasted content

instructs

In context

A single line often inverts meaning once you see what it answers, so neighbouring messages are always shown.

2026-04-10 09:00 Ralph S. Baric open

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.
2026-04-10 09:00 Christina Salazar open

It's not.
2026-04-10 09:00 Ralph S. Baric open

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.
2026-04-10 09:00 Christina Salazar open

So is it only gain-of-function in that scenario if you know it's --
2026-04-10 09:00 Ralph S. Baric

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.
2026-04-10 09:00 Christina Salazar open

But so --
2026-04-10 09:00 Ralph S. Baric open

And it's nothing to do with entry. You can have scenarios where the virus grows to the exact same titer, and one person dies and the next person doesn't even know they're sick.
2026-04-10 09:00 Christina Salazar open

But so the actual moving, the cleavage site --
2026-04-10 09:00 Ralph S. Baric open

Yes.

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