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…
I elaborate on this a little more here
I do not know the mechanism of compensation, but I do know the target- CD95. Yes, cd95 is used for the differentiation of t cells and their upregulation of Interferon. CD95 kills terminally differentiated t cells and differentiates Tn and Tmem. Block CD95 and you can temper this
other immunologists are finally saying t cross immunity is not protective. remember, I fought that since it first appeared on a preprint server bc I knew this mechanism. I also knew that reinfection would be worse depending on the differentiation state of the person's t cells.
The gm-csf target is published to modulate the Fas, and it appears like the pathway has been targeted to the proper effect. medrxiv.org/content/10.110…
So it looks like my point in targeting the Fas pathway has been done. This was the answer. Kudos to the group. bbmt.org/article/S1083-…
there is another lesson here- never make assumptions. Had I not assumed that everyone 'could' pulse infected cells that had hidden virus (orf8) with interferon, I would have been on my way to the idea ppl with this deficit would be enriched in the ill
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