Very interesting. UAMS has a long and proud history of nephrology, having been led in the 90s by Thomas E Andreoli who theorized or discovered ( I forget ) the ENaC (epithelial sodium channel) in the kidney.<p>Link to open access journal article: <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0257016" rel="nofollow">https://journals.plos.org/plosone/article?id=10.1371/journal...</a><p>The short of it is that they appear to have found anti-ACE2 autoantibodies appear with latent onset in patients who experience "long covid" and this could fit with an angiotensin driven model.
I am wondering if this other results are related, of the article<p><i>Autoantibodies against ACE2 and angiotensin type-1 receptors increase severity of COVID-19</i><p><a href="https://www.sciencedirect.com/science/article/pii/S0896841121000913" rel="nofollow">https://www.sciencedirect.com/science/article/pii/S089684112...</a><p>(Journal of Autoimmunity)<p>or, COVID19 is worse when an autoimmune response against ACE2 occurs, and the same autoimmune response is at the root of "long COVID".<p>> <i>Severity of several inflammation-related diseases has been associated with autoantibodies against RAS [renin-angiotensin system], particularly agonistic autoantibodies for angiotensin type-1 receptors (AA-AT1) and autoantibodies against ACE2 (AA-ACE2). ... The present results suggest that both AA-AT1 and AA-ACE2 contribute to increase in severity of COVID-19 outcome and could be used as an index of probable progression of COVID-19 towards severity. ... the results encourage further studies on the possible protective treatment with AT1 receptor blockers in COVID-19</i>
> <i>Activation of the immune system is implicated in the Post-Acute Sequelae after SARS-CoV-2 infection (PASC) but the mechanisms remain unknown. Angiotensin-converting enzyme 2 (ACE2) cleaves angiotensin II (Ang II) resulting in decreased activation of the AT1 receptor and decreased immune system activation. We hypothesized that autoantibodies against ACE2 may develop after SARS-CoV-2 infection, as anti-idiotypic antibodies to anti-spike protein antibodies.</i><p>> <i>Many patients with a history of SARS-CoV-2 infection have antibodies specific for ACE2. Patients with ACE2 antibodies have lower activity of soluble ACE2 in plasma. Plasma from these patients also inhibits exogenous ACE2 activity. These findings are consistent with the hypothesis that ACE2 antibodies develop after SARS-CoV-2 infection and decrease ACE2 activity. This could lead to an increase in the abundance of Ang II, which causes a proinflammatory state that triggers symptoms of PASC.</i>