Pierre Little, in reply:"Look, it’s really quite simple. Does the cov2 genome have HIV inclusions on the s protein or not? If it does, the theory of immunosuppression from Cov2 has plausibility, thereby motivating other teams worldwide to study T and B cell impacts."
Alexander Dent, in reply: "It doesn't have HIV inclusions. That's disinformation. I checked the sequence alignment myself."
>These results suggest that SARS-CoV-2 may enter MT-2 cells at 6 h post infection, but does not replicate, and then the viral RNA degrade.
So it infects the cells but it's a dead end for the virus.
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I can't believe the journal published the article with that clickbait title, without mentioning that it's non-productive infection. I was about to dig up the transcriptomics paper (cited by this paper) and the pre-print about the virus decimating the spleen/lymphoid organs which show that T cells aren't infected (I guess they are technically infected, but not in the way most people think).
To a complete layperson (myself) it seems that anything entering a cell it's not supposed to isn't going to help that cell out much. I would appreciate some expert commentary though if anyone has some!
This is a question out of ignorance, but couldn't this be a precursor of a potential strain (one that, through a mutation, can start replicating on MT-2 cells?). Like this could be a dead end for the virus, until it's not?
Or this potential is irrelevant, because tracking all potential mutations/strains simply makes no sense?
Alexander Dent, in reply: "It doesn't have HIV inclusions. That's disinformation. I checked the sequence alignment myself."
thread: https://twitter.com/CurlyJungleJake/status/12488112666357514...