Baric Transcribed Interview (Redacted) — page 132
of 155 pages
← p.131 p.133 → · this page in the original PDF · package
DC.Scheduling@LexitasLegal.com
asymptomatic. It's an enteric disease. It's when you lose
the furin cleavage site that it becomes a fulminant, deadly
disease that is 100 percent fatal in cats. So loss-of-
function of that furin cleavage site kills you dead, the
cat.
In mouse hepatitis virus, a couple of researchers had
removed the furin cleavage site and said what happens to
the pathogenesis? There was no change.
Another group, taking pseudoviruses, had introduced
furin sites into the SARS-coronavirus 2003 strain, and the
only thing they found was slightly increased infectivity.
Nothing big. Nothing that said "eureka."
So now let's compare SARS from 2003 and SARS-2, and
let's ask the question, what experiments were done to prove
that the furin cleavage site drove severe disease in SAR-2
pathogenesis. What they did was a loss-of-function
experiment. They deleted those four residues that were
introduced by whatever means, and they asked what happened
to the virus. It was less pathogenic, and it was less
transmissible. Eureka. Furin cleavage site causes that
phenotype. Except when you look at the other figures in
the paper, where it shows that it also knocked down the
ability of other proteases to cleave at that S1/S2
boundary.
So it wasn't a furin cleavage site-specific knockout.
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/132
Records on this page
| Record | Date | Type | Pages |
|---|---|---|---|
| baric_ti:utt:01125 | 2026-04-10 | transcript segment | 131–133 |