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Immune response may damage ACE2:B0AT1 complex, but not necessarily gut flora (gut endothelia is separate barrier from gut flora). Long covid like symptoms are evident after the vaccination due to B0AT1 disfunction and ACE2:S1:Abs immune complex prolonged presence in the host.

Vaccine designs prescribed dosage that avoids significant damages to the gut ACE2:B0AT1 complex, and any damage is recycled by endosomal cathepsins usually without any systemic evidence. It is harder for immune system to resolve damaged gut ACE2:B0AT1 when bound with S1, then sACE2 (soluble ACE2) bound to S1. Since ADAM17 access to ACE2 is sterically blocked by the presence of B0AT1, ACE2 of the tetramer complex does not release soluble sACE2 ectodomains in the gut (Sharma et al 2020). And clearance of ACE2:B0AT1:S1:Abs complex is delayed in comparison to sACE2:S1 clearance from the circulation.

But it could be argued that long covid is not 100% gut dependent. Mitochondrial dysfunction in other cell lines cause long-term post covid symptoms as well. In stricto sensu mitochondrial damage is regarded as Covid-19 complication and not a form of long covid that is regarded as prolonged activation of immune response. But without mitochondrial homeostasis with JAK-STAT pathway a patient can’t fully recover from Covid-19 complication.

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