🧵on serotonin, SSRIs, 5HT2 receptor antagonism, bromhexine, and niclosamide mechanisms of action in COVID as it pertains to our recently published RCT

This will be detailed. References in parentheses and listed in the last tweet.

https://x.com/farid__jalali/status/1768418776998158600?s=20

Clinical deterioration in COVID-19 typically occurs during the second week of illness, marked by a severe immune reaction and excessive production of pro-inflammatory cytokines such as IL-6, IL-8, TNF-α, and IL-1β. (2)

🧵on our RCT published in Lancet’s @eClinicalMed led by @dr_leshan, where we show

Early treatment with 2-drug combos of fluvoxamine, bromhexine, cyproheptadine, niclosamide in COVID

✅completely prevented deterioration
⬇️viral load
⬇️inflammatory cytokines
⬇️#LongCovid risk This publication is the culmination of 3 years of work, led by @dr_leshan and his team.

Please follow thru to below thread for further description of the study.

🔗sciencedirect.com/science/articl…

🧵 on our preprint with @ZaidYounes9 and team

In this study, we delve deep into COVID pathophysiology to show that:

SARS-CoV-2 infects the human bone marrow megakaryocytes, and this shapes the trajectory and severity of the illness by triggering ...

🔗biorxiv.org/content/10.110… ... the production of pathogenic afucosylated antibodies against the spike protein.

First, some introduction in order to better understand the premise and the findings of this work:

SARS-CoV-2 most definitely infects the bone marrow.

Not only in the acute infection.

But also chronically, the spike protein is found present in the bone marrow on autopsies of patients who died for other reasons.

I wish I could share more, but ... ... we are actively investigating and have some very intriguing findings on how the infection of the bone marrow by SARS-CoV-2 brings about the gear shift from early mild disease -> to severe COVID.

This ties the various parts of disease pathophysiology in a convincing manner.