Envelope Protein of SARS-CoV-2 Inhibits Viral Protein Synthesis and Infectivity of HIV-1

Bruh…

This paper just blew my mind in more ways than one.

The findings are two fold. Authors tested the Envelope Protein (from here on, E Protein) from different SARS viruses, including SARS-CoV-2, and see how it affected the infectivity of HIV-1. Both SARS-CoV-1 and 2 impacted the infectivity by a lot, up to 100 fold in reduction. As the abstract itself states, this is the first time a research team finds that one virus impact the infection of other viruses, with an actual proposed mechanism, and not merely a blanket statement (viral interference).

The second part, I will go back to it soon enough, and it is AS BIG as this one (if not more from my perspective.

So the authors went to great lengths to demonstrate the mechanism which SARS-CoV-2 E protein hinders HIV viral replication. Sadly, it does NOT stop infectivity, just substantially lowers the viral load. Therefore, it doesn’t stop it from creating reservoirs, which is what HIV is well known for, slowly chipping away your immune system (CD4 cells). Significant finding.

So what is BST-2 ?

And now we finally have, mechanistically, a clue why forms of B3, and its metabolites help to rescue, and recover people so much, so fast.

Exposing yourself to the large quantities of Spike protein, specially being produced endogenously (inside you, you produce it) wasn’t the best idea huh.

And now we have a possible explanation why the immune system of so many people take nose dive, can barely control subsequent infections after a Covid one. The modulation of Toll Like Receptors alone couldn’t account for all that, it was a little disproportional.

Alongside all the mitochondria papers I covered, and this entire series of posts, we now have a decent picture of what is going on.

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