I'm calling it now. Long term covid-19 disease will be found to be mostly a side effect of abnormal cell-cell fusion due to the membrane fusion mediating properties of the basic terminal of the protease cleaved spike protein in sars-cov-2 particles. There are many studies in lung, heart, and cell culture model tissues showing abnormal cell fusion happens, and happens far more with sars-cov-2 than it does with sars-cov-1 (or other lipid enveloped viruses). The inflammatory effects of these persistent merged cells would cause the weird immune response (ie, parasitic factors being expressed along with viral throwing immune response off) and long term issues in the surrounding tissues of the organ.
Of course there's a lot more going on in long term covid-19 than just this accidental side-effect cell membrane fusion. Stuff with the angeotensin signaling being completely messed up to due competitive binding by sars-cov-2 spike RBD, and the circulatory damage this causes can't be ignored. Or even the normal cytotoxic effects of all viral infection. But the cell fusion bit has it's role to play and I think it's an important one.
<anon>10:42:33, Tue Jan 26, 2021 : /blog/2020-12-06-1.html/, How do you think this cell-to-cell fusion resulting side-effects would be complicated by infection post-vaccination? At least in the mRNA vaccines Moderna and Pfizer, translated "spike" protein would likely competitively bind and further interfere with angeotensin signaling...
<superkuh> 19:53:11, Sat Jan 30, 2021 : If you've already been vaccinated for sars-cov-2 then, probably, you won't have a viral load nearly as high as someone who's immune system has never encountered sars-cov-2 particles before. With lower viral load there'd be less accidental cell-cell fusion events. Additionall, what viral load there is will (probably) have antibodies binding to it's spike proteins and preventing them from attaching to cells and being cleaved. At least within the body proper. Within the surface tissues of the mucosal system (nose, upper respiratory, etc) you'll still get infection and viral replication though. So some accidental cell-cell fusion is likely to still happen there.
As for how this all effects angeotensin signally, well, that's beyond me. Competitive binding of antibodies to the spike will prevent sars-cov-2 particles from binding to ACE2 receptors as much and decrease the angeotensis problems in the body proper. In mucosal tissues, well, less so.
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