Coronavirus could attack T lymphocytes like HIV [pdf](nature.com)
nature.com
Coronavirus could attack T lymphocytes like HIV [pdf]
https://www.nature.com/articles/s41423-020-0424-9.pdf
12 comments
>theory of immunosuppression from Cov2
A lot of the people it kills seem to be getting attacked by their own immune system though, can both these things happen at the same time?
A lot of the people it kills seem to be getting attacked by their own immune system though, can both these things happen at the same time?
>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).
(Quick CP from Reddit)
So it infects the cells but it's a dead end for the virus.
====
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).
(Quick CP from Reddit)
If it does not replicate, does that mean it doesn't harm the cell it enters?
I also wondered that. Even if it doesn't replicate inside a T lymphocyte could it damage it thereby weakening the immune response as a side effect?
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?
Or this potential is irrelevant, because tracking all potential mutations/strains simply makes no sense?
Nature publisher group is corrupted as many other main publication journals.
Don't bother, instead check the publishing researching team and their credentials to evaluate the authenticity of the claims.
I would also not trust any materials Chinese publishing teams provide.
Also pointing out, as today, 80% of the result published online are not reproducible solely following the "material and methods" section of the paper.
So yeah, welcome to biological sciences!!
"Repost since flagged for no reason, i'm a god damn biologist for the god sake"
Don't bother, instead check the publishing researching team and their credentials to evaluate the authenticity of the claims.
I would also not trust any materials Chinese publishing teams provide.
Also pointing out, as today, 80% of the result published online are not reproducible solely following the "material and methods" section of the paper.
So yeah, welcome to biological sciences!!
"Repost since flagged for no reason, i'm a god damn biologist for the god sake"
The data is of interest, but the editorializing is a bit heavy-handed.
"SARS-CoV-2 infects T lymphocytes" would do if one feels a need to shorten the title.
"SARS-CoV-2 infects T lymphocytes" would do if one feels a need to shorten the title.
I found in the news media anything with the words 'could' or 'may' in it is sensational and typically turns out to be false.
It's not like HIV at all...
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...