RT @indehisce@twitter.com

Post-mortem exams of COVID patients who’d long recovered—and were no longer testing positive—reveal persistent infection in their lungs. Most died of pneumonia.

“This is consistent with the conclusion that these patients had never cleared the infection.”
onlinelibrary.wiley.com/doi/10

🐦🔗: twitter.com/indehisce/status/1

@White_Bite

Time to drop the ruse: no one ever clears this virus. If they did, you'd see the supporting pathology blasted in every major media outlet in the West, as occurred with that contrived hammer and chisel study.

@noyes @White_Bite
Yup. I'm starting to get tired of all the academics waiting for absolute proof, when the simplest explanation for all of the post infection problems is persistence.

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@mathew1927 @noyes @White_Bite

I suspect we need to define Long COVID more thoroughly. There's good scientific evidence for:

-Persistence of the virus
-Damage done by the virus
-Micro-clots
-Autoimmune/immune dysregulation

I'm pretty sure *all* are happening, and that's why there seem to be distinct Long COVID clusters of symptoms. Not everyone has all of them, but we will probably find that each Long COVID sufferer has at least one.

What I hope happens next is that the trials that are on-going for anti-virals to help clear viral persistence show good results against at least some types of Long COVID, because that will help everyone begin to define what Long COVID really is, and what's caused by what post-acute phase issue.

@BE @mathew1927@zeroes.ca @noyes I've been talking about this with others.
The current definition of LC is very limited IMO.
Viral persistence will elicit inflammation and continuous inflammation results in damage, especially when left unchecked.
Sequelae will happen. This I can say with little uncertainty. So to limit LC to just cognitive dysfunction, clots, etc., is just too early days IMO

@White_Bite
1)I think we have two general flavors of chronic disease:

Subclinical, in which Complement remains largely regulated, and symptoms are non-existent or similar to those of a lingering cold.

Longhaul, in which Complement is dysregulated at one or more 'checkpoints' (C1-INH, Factor H, etc), resulting in engagement of the Alternative Pathway of Complement and subsequent lytic release of the Lectin Pathway pernicious N-protein.

IMO, intact SARS-CoV-2 has a passive Complement
@BE

@White_Bite
2)Complement evasion strategy that allows it to eschew the need for surface NRoCs by displaying a surface that does not interact with the many fluid phase PRRs of the Classical and Lectin Pathways of Comment. At least when the spikes are Down. That changes when the spikes raise Up. It's a super interesting and novel strategy, so it doesn't surprise me that it has gone underappreciated.

SARS-CoV-2 is one chronically underestimated virus. People are too busy telling it what it
@BE

@White_Bite
3)supposed to be to actually listen to what it is telling them about itself.

@BE

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