This is the most straightforward explanation for chronic symptoms in at least a subset of #LongCovid patients. Partly b/c if the #virus is still present its activity can directly contribute to other phenomena also being documented in LongCovid
https://twitter.com/fearnley_k/status/1495695480323510276
2/ Persistence of #SARS-CoV-2 in tissue could lead to shedding of spike protein into blood, which can catalyze the ongoing formation of microclots and hyperactivated platelets
3/ Persistence of SARS-CoV-2 can lead to ongoing downregulation of interferon and/or T cell signaling by the virus, creating an optimal atmosphere for activation of EBV or other #pathogens normally controlled by such immunity
4/ Persistence of SARS-CoV-2 can downregulate the immune response in body sites such as the gut/mouth in a manner that exacerbates #microbiome imbalance, barrier integrity + shedding of pro-inflammatory #bacterial products into blood in a manner that activates cytokines
5/ Persistence of SARS-CoV-2 can perpetuate an inflammatory environment where the #immune system fires on a growing number of viral or microbiome #pathogen proteins, leading to autoantibody production via molecular mimicry
6/ Persistence of SARS-CoV-2 can lead to ongoing #inflammation sensed by the vagus nerve and conveyed to the brainstem in a manner that can augment autonomic, sickness, nausea + pain symptoms
7/ Persistence of SARS-CoV-2 can dysregulate brainstem signaling as described above in a manner that causes microglia to activate and drive #neuroinflammation (which may also contribute to “brain fog” symptoms)
8/ Persistence of SARS-CoV-2 in either the vagus #nerve itself and/or directly in brainstem tissue could contribute to severe #LongCovid cases by fully throwing off their respective signaling
9/ Persistence of SARS-CoV-2 may lead to upregulation of matrix metalloproteinase activity, and/of increased translocation of #bacteria into tissue in a manner that can lead to connective #tissue breakdown
10/ Persistence of SARS-CoV-2 would be expected to lead to continual recruitment of mast cells to infected areas, priming such cells for increased activation to other environmental insults (resulting in #MCAS symptoms)
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