ice9 Profile picture
4 Jan, 5 tweets, 2 min read
More autoimmune exacerbation in COVID-19:

Fatal cases have higher levels of autoantibodies to Annexin A2, vs. non-fatal severe cases and non-severe cases.

Inhibiting Annexin A2 promotes thrombosis and pulmonary edema.

Similar to Abs against β2GPI in antiphospholipid syndrome.
Interestingly, antibodies to SARS-CoV-2 S2 are also somewhat cross-reactive to Annexin A2.

Not relevant to vaccines using stabilized Spike.

Relevance unclear for natural infection.

May matter during the exaggerated antibody response in severe COVID-19.

Anti-S2 antibodies do not appear to be neutralizing either. Overall, this is arguably a form of ADE.

stm.sciencemag.org/content/12/550…

Note again this can only arise during a COVID-19 case, 'natural infection'.

All leading vaccines use stabilized Spike, so the vaccines cannot do this.
For a medical audience, the main conclusion from this is more evidence in favor of APS as a contributing factor in severe COVID-19 thrombosis and pulmonary edema.

For a non-medical audience, the main conclusion is to try to get a COVID-19 vaccine ASAP.
In the meantime, keep in mind there is extensive clinical evidence that early antiviral treatment (including prophylaxis) reduces risk of progression to moderate or severe COVID-19.

Most effective options:


High risk: also consider dipyridamole-aspirin.

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More from @__ice9

4 Jan
@coolnidal @farid__jalali First off:

Because Zaid et al. already directly demonstrated that plasma serotonin is indeed greatly elevated in hospitalized moderate to severe COVID-19.



Therefore, this is no longer a theory, but rather an established fact about the disease process.
@coolnidal @farid__jalali Second:

Because the excess plasma serotonin has obvious and serious ramifications for clinical symptoms and management.

It is a miserable condition to be in for even hours, much less weeks.



People thrashing, hallucinating, clawing at tubes: here's why.
@coolnidal @farid__jalali Journalists like videos and media, right?

Here's what it looks like.

Click this post, scroll up by one for the video.



Imagine if this were your father or uncle or grandfather.

Just weeks like that.

We can do something about this. It can be blocked.
Read 7 tweets
3 Jan
Excessive plasma serotonin levels contribute to lymphopenia.

This may partly explain the relative lymphopenia seen in some severe COVID-19 cases and its poor prognostic implications.

H2 antagonists (e.g. famotidine) and cyproheptadine block the effect.

sciencedirect.com/science/articl…
More on the effect of excessive plasma serotonin levels in suppressing T cell activity:

tandfonline.com/doi/abs/10.310…

@farid__jalali
Elevated plasma serotonin also promotes B cell activation and antibody secretion.

nature.com/articles/s4159…

ncbi.nlm.nih.gov/pmc/articles/P…

Severe COVID-19 often includes useless or harmful antibody production-- against the viral N protein, other CoVs, other viruses, human tissue, etc.
Read 6 tweets
3 Jan
@ianbirrell Comprehensive.

Only a few flaws.

The first is the 'missing researcher'-- she left years earlier, irrelevant.

The second is that you missed the EcoHealth Alliance grant, and Daszak explicitly confirmed recombinant CoV testing in humanized mice Nov 2019.

Read 4 tweets
3 Jan
What to expect in a COVID-19 case that progresses to the severe phase and ICU admission-- in terms of typical patient experiences.

Note this thread is 14 posts long.
The things we are discussing about 5-HT2 antagonists and plasma serotonin, about attempting to halt progression in the early severe stage, are relevant *during* these events.

Rates of PTSD following survival from severe COVID-19 exceed 30%, ditto anxiety and depression.
The ventilator settings required to keep these patients alive tend to permit blood CO2 levels to rise somewhat, in avoiding excessive mechanical damage to the lungs.

This has been repeatedly demonstrated to cause severe anxiety and promote PTSD.

Read 5 tweets
2 Jan
Cyproheptadine prevents pulmonary platelet trapping in endotoxin shocked or severely beaten dogs.

osti.gov/biblio/5502933…

Further evidence for potential efficacy against development of ARDS via pulmonary microthrombosis-- explicitly discussed.

@farid__jalali ImageImageImageImage
@cameronks @pathdoc3 @icedoc61 @Jopo_dr @Acute_Pulmo_Med @ZaidYounes9 @Geurys7 @MARYau_MCU_PH @DrBrandon55 @VectorSting @Crashcart

Interesting earlier result on cyproheptadine and pulmonary platelets.
Just found this one for pulmonary fibrosis as well-- another success for cyproheptadine in earlier animal experiments:

Read 4 tweets
30 Dec 20
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

Read 4 tweets

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