Thread by @fitterhappierAJ

@barttels2 @ZiikZiiii @GainOfDystopia @ChristosArgyrop @plakaexeitotoui @greg_travis the furin cleavage site is in such a location where it makes a bacterial superantigen. The amino acids required for that bacterial superantigen are all there on ratg13 except for the furin cleavage site.

@barttels2 @ZiikZiiii @GainOfDystopia @ChristosArgyrop @plakaexeitotoui @greg_travis that kind of makes the furin cleavage site, ratg13, and the superantigen all special. @RogueRad

@barttels2 @ZiikZiiii @GainOfDystopia @ChristosArgyrop @plakaexeitotoui @greg_travis @RogueRad cov2 RaTG13

@barttels2 @ZiikZiiii @GainOfDystopia @ChristosArgyrop @plakaexeitotoui @greg_travis @RogueRad normally, one would expect a superfluous superantigen to be selected out without a function- especially a bacterial one on a virus. But this is partly comprised of an fcs- meaning there is a functional advantage to the retention of its sequence. FCS allows for easy transmission

@barttels2 @ZiikZiiii @GainOfDystopia @ChristosArgyrop @plakaexeitotoui @greg_travis @RogueRad I can't find the publication, but one finds that the amino acids around the fcs are highly conserved as well. probably has to do with favorable conformations. So form has been linked with dual functions.

@barttels2 @ZiikZiiii @GainOfDystopia @ChristosArgyrop @plakaexeitotoui @greg_travis @RogueRad So to spell it out- selection pressure and random mutation to ablate the bacterial superantigen, but since it is partly comprised by a functional FCS there is a very strong pressure/ selection to conserve the conformation. Unlikely we will see ablation of the sag

@barttels2 @ZiikZiiii @GainOfDystopia @ChristosArgyrop @plakaexeitotoui @greg_travis @RogueRad Why is the superantigen important? T cells respond to it- they will become stimulated to kill. many of them, in proportion to the amount of biomass they see. And it will be seen outside of cells that are infected per se so you have indiscriminate killing and stimulation

@barttels2 @ZiikZiiii @GainOfDystopia @ChristosArgyrop @plakaexeitotoui @greg_travis @RogueRad this is a delayed reaction. in fact, one of the most delayed reactions you can have. delayed pathogenesis in cov2 allows for a longer clinical incubation period
You can have people loaded with virus and biomass and their t cells take a while to differentiate to exact autoimmunity

@barttels2 @ZiikZiiii @GainOfDystopia @ChristosArgyrop @plakaexeitotoui @greg_travis @RogueRad this is partly why mis-c takes so long to manifest. young t cells take a while to be pushed so far. older, more differentiated ones will become cytotoxic sooner.

@barttels2 @ZiikZiiii @GainOfDystopia @ChristosArgyrop @plakaexeitotoui @greg_travis @RogueRad meanwhile a delayed clinical manifestation and llonger incubation period afforded by a type 4 hypersensitivity reaction allow for more pathogenic strains to more readily pass onward, as pathology is quite delayed from the beginning of an infectious period.

@barttels2 @ZiikZiiii @GainOfDystopia @ChristosArgyrop @plakaexeitotoui @greg_travis @RogueRad so now you are up to date with the pathogenesis of cov2. without the fcs and the superantigen, it would be as tame as a kitten.

https://twitter.com/fitterhappierAJ/status/1358456426545500161