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30 Dec 20, 4 tweets, 3 min read
For anyone interested in the Baric interview on synthetic recombinant SARS-like CoVs earlier, see around 38:00 into this video.

There is also some interesting preliminary discussion starting around 36:30 or so, mostly in English.
This provides the video that went missing when a few accounts I had quoted earlier were suspended.

Here are the translations of the transcript of the Baric interview, reference via @TheSeeker268

The database in question at WIV was not public. We know this because the RaTG13 sequence was several years old.

It was likely only one of the >50 novel southern Chinese bat CoVs used for the EcoHealth Alliance grant to make human-optimized recombinants.

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More from @__ice9

ice9 Profile picture
29 Dec 20
@HenkPoley Yes, am familiar with the issue.

I will see if I can locate my earlier findings on this.

So far I have only located some notes from earlier, but not the actual citation yet.

@HenkPoley This paper indicated that a single exposure to 70% ethanol largely preserved filtration efficacy, comparable to dry heat or UV sanitizing. However, further exposure events gradually worsened filtration efficacy.

medrxiv.org/content/10.110…
@HenkPoley Discussion thread here:

Read 6 tweets
ice9 Profile picture
29 Dec 20
To date, anecdotal reports from dual entry inhibition in mild acute COVID-19 remain excellent.

Recovery within 48 hours appears typical, absent significant complications (e.g. secondary infection).

Dual entry inhibition means blocking both:
- TMPRSS2/13/11
- endosomal entry
Dual entry inhibition was tested in the Ansarin et al. RCT, adding bromhexine 8mg t.i.d. to a baseline of HCQ 200mg q.d.

Mortality in hospitalized moderate COVID-19 patients fell to zero.

This remains one of the best results of any COVID-19 RCT to date.

Theoretical justification arises from the fact that endosomal entry is of only secondary importance for SARS-CoV-2 replication in the respiratory tract.

Both TMPRSS (proteases at the cell membrane) and cathepsins (proteases in endosomes) must be blocked.

Read 15 tweets
ice9 Profile picture
3 Dec 20
More evidence that endothelial cells are not directly vulnerable to infection by SARS-CoV-2.

Endothelial dysfunction in COVID-19 is entirely indirect. Image
Discussion thread on pericytes, nearby susceptible cells strongly suspected to mediate some of the damage.

Discussion on infection of pulmonary megakaryocytes, i.e. platelet-forming cells, also strongly suspected of involvement.

Read 6 tweets
ice9 Profile picture
3 Dec 20
People want ironclad proof for everything. It doesn't exist. It never will. Even the best trials only apply to a certain stage of the disease in a certain set of the population at a certain dose with a certain baseline standard of care.
One must weigh evidence and combine signals in a safe way. That is all.
"First, the only certainty is that there is no certainty. Second, every decision, as a consequence, is a matter of weighing probabilities. Third, despite uncertainty we must decide and we must act."
Read 4 tweets
ice9 Profile picture
1 Dec 20
More evidence inflammasome activation predicts severe COVID-19, and acts as a major driver of disease progression.

They release IL-1β, which summons neutrophils and promotes (highly pro-thrombotic) NETosis, plus IL-18, which prompts IFNγ secretion (very inflammatory, apoptotic).
In layman's terms:

Certain virally infected or antigen-swamped white blood cells smash their emergency self-destruct button, explode, and release huge amounts of signaling molecules that summon exploding neutrophils and tell other classes of WBCs to order nearby cells to die.
This strongly contributes to the severe lung clotting and often serious broader lung tissue damage that define the state we call "severe COVID-19."
Read 4 tweets
ice9 Profile picture
1 Dec 20
@Deadly_Statins it's pretty nasty. the systemic inflammatory response is intense and can hit hard and fast. not a cold or flu at all. not like anything I've ever caught before. glad I was able to abort it.
@Deadly_Statins trying very hard not to catch it again. basically just hiding out in my residence as much as possible.
@Deadly_Statins the percentage of people with active infections out in public right now is obscene; it would be apocalyptic if IFR were higher.

unfortunately because there are so many of them, hospitals are turning people away and IFR *is* getting higher, slowly, inexorably.
Read 4 tweets

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