There's always good news about T cells and Cov2, but now it's time for Fascinating news.

We see lots of articles about conserved T cell recognition of variants, but we must include Cov2 is a 🤓 genius only getting more learnéd.

Cov2 has a protein that takes down MHC 1! 🧵
MHC 1 is how T cells 'see' infected cells. Orf8 is a protein that 'takes down' MHC 1, meaning it helps cov2 'hide.'

You can upregulate interferon to fight this, but guess what... pnas.org/content/118/2/…
...the next genius way to hide from T cells is by inducing an interferon antibody!

Interferon is important for upregulating MHC for T cell recognition. Somehow, Cov2 is able to cause your body to block its own process! Brilliant! nature.com/articles/d4158…
There's more friends. I told you Cov2 is a real bookworm 🤓
The next genius way Cov2 hides from the T cells is by causing the cell to replicate the virus in a fury with it's gene Nsp-1. The cell becomes a zombie and preferentially forgoes synthesizing MHC! pubmed.ncbi.nlm.nih.gov/33188728/
And guess what? It's only getting more smart because it's been hitting the books 📙 hard in open schools.

Many of the virologists characterization of t cell epitopes fail to account for this brilliant, evolving, sneaky, physiology (excpt Iwasaki & co).

tandfonline.com/doi/full/10.10…
From hitting the books 📙📙 alongside kids, Cov2 is growing up fast and smart. The variants are getting even better!

Those T cells and the IFN/ MHC axis involved in control? The physiology will be mutated against and selected for! Amazing! biorxiv.org/content/10.110…

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More from @fitterhappierAJ

29 Jan
I've been comparing cov2 to ebola ever since I saw the lymphopenia in Jan in the Lancet. Nasty damn bug. Confuses the hell out of the immune system. theguardian.com/society/2021/j…
I really enjoy looking into Ebola, because when I started out at the NCI we had a phenomenon where we did not know the mechanism
Basically, a talented Physician before I arrived noticed memory T cells in a stimulation would differentiate pools of t cells further pubmed.ncbi.nlm.nih.gov/20971955/
Read 16 tweets
28 Jan
The propaganda is ramping up to pressure admin to open schools. It's based on an interpretation where they look at an exceptional single case in rural wisconsin and ignore the preponderance of evidence about the ability of spread in schools elsewhere.
It's not safe or just to put people in classrooms where they risk long covid, variants, and do not have vaccine protection. If you want kids in classrooms fund the trials and get kids a vaccine. China is doing it. Get with the program! reuters.com/article/us-hea…
putting children in situations where 1/X of them have reactions like this is unfair. We can judge a society by how they treat the infirm, yes, but how about the society which also protects the so called 'least vulnerable?' Covid-19 is not only an acute huffingtonpost.co.uk/entry/long-cov…
Read 8 tweets
17 Nov 20
I'm going to briefly touch upon one of my favorite subjects: immunological memory. nytimes.com/2020/11/17/hea…
2/ First the B cells: I think for Covid-19 these are the most important to prevent infection and reinfection severity. In this large study on B cell memory, the authors see B cells turning into what we can presume is long-lived memory while continually (for the majorit of people)
3/ shedding Antibodies. Antibody shedding is great because it can control virus that rears its ugly head, and prevent virus from going into a new cell. So that's good. I am worried, though, that there may be cells with a reservoir of competent virus that is influencing this. We
Read 11 tweets
15 Nov 20
@stanleyqilab I think your Crispr package would be well delivered by B cells. They traverse all organs and bone marrow and even play a part in neuroregeneration. Shedding vesicles all the while that can be loaded with RNA. @AnImmunologist @ExcisionBiotx pnas.org/content/117/9/…
Read 4 tweets
24 Sep 20
Back in May I said this paper suggested that orf8 was making it hard for the immune system to clear the virus due to the downregulation of MHC I, and that it forced it to age and compensate for this effect. Compensation can occur with ↑ interferon, the cytokine for inflammation
Recently there was a mutated virus in the wild that showed when the orf8 was nonfunctional, it only caused light illness. I believe that it's light illness bc the immune system no longer has to age and produce interferon so much in order to rec. and clear thelancet.com/journals/lance…
Read 8 tweets
19 Sep 20
After infection you lose A LOT of your naive T cells. Then, not having naive t cells predisposes you to baad outcomes the second go around. I've been saying it. cell.com/cell/fulltext/… Image
Read 5 tweets

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