Some immunologists theorize there could be a neural reservoir for cov2
In a chicken coronavirus, a similar Furin Cleavage Site enabled neurotropism which engendered neural symptoms and more illness pubmed.ncbi.nlm.nih.gov/32057769/
Here is a nice review of the neurological/encephalitic models of neurotropic viruses as they relate to cov2
We do not know if there will be a later manifestation
B.1.617 has mutations that may *enhance* pathogenesis
A mutation at P681R in combination with L452R and E484Q significantly increases syncitia formation
This is when the cells fuse together, and it's linked to fatal disease.
2/ The Gupta lab found the mutations L452R/E484Q/P681R together significantly increase Syncitia formation.
This is a function of the polybasic cleavage site. Syncitia formation is linked to fatal diseasehttps://www.biorxiv.org/content/10.1101/2021.05.08.443253v1
3/ Syncitia are a way the virus kills T cells
This paper in Cell Death and Differentiation discusses how Syncitia internalize T cells in order to kill them
3/ Interestingly, a few case reports have emerged of Parkinson's following infection. thelancet.com/journals/laneu…
A worrisome correlate may exist as seen by this preprint: monkeys had precursors of Parkinson's after infection, called Lewy Bodies biorxiv.org/content/10.110…
I've not seen so much power and simplicity in data for a long time.
Cov2 is generating T cell escape epitopes, and there may be a dominant selection for a nucleocapsid site for B*27:05 biorxiv.org/content/10.110…
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2/ The authors show a number of mutated peptides/variants that cause partial or complete loss of T cell reactivity for certain HLAs
3/ In my opinion, there can be a degree of selection against T cell epitopes when T cells are being used to react to virus- the situation where one has T cell memory but no sera. I think I mentioned this exact scenario before @MonicaGandhi9?