Baric Transcribed Interview (Redacted) — page 98
of 155 pages
← p.97 p.99 → · this page in the original PDF · package
DC.Scheduling@LexitasLegal.com
different tasks? So they're doing something to gain
function and they're doing something to spread --
DR. BARIC: No. So you're confounding experiments.
The first aim, again, is to sort of walk through this
process of what makes a threat virus, how do you identify
it, and how do you then try to counter that threat
approach.
MS. SALAZAR: With, so --
DR. BARIC: 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.
MS. SALAZAR: But this is all under one proposal.
You're saying that these were separate technical aims.
DR. BARIC: That's correct.
This is our OCR of the page, with running headers and footers removed. The
Committee's PDF
is authoritative; quote from it. Machine-readable, including the uncleaned
text: /api/page/baric_ti/98
Records on this page
| Record | Date | Type | Pages |
|---|---|---|---|
| baric_ti:utt:00856 | 2026-04-10 | transcript segment | 97–98 |
| baric_ti:utt:00857 | 2026-04-10 | transcript segment | 98 |
| baric_ti:utt:00858 | 2026-04-10 | transcript segment | 98 |
| baric_ti:utt:00859 | 2026-04-10 | transcript segment | 98 |
| baric_ti:utt:00860 | 2026-04-10 | transcript segment | 98 |
| baric_ti:utt:00861 | 2026-04-10 | transcript segment | 98–99 |