The hyperinflammatory and the fibrotic changes observed in COVID-19 clinical complications resemble those associated with diseases of deficiency of the ACE-2 enzyme system.
COVID-19-linked comorbidities can be associated with increased output levels of aldosterone outside of the classical regulatory renin-angiotensin-system (RAS). This increased aldosterone is from the HPAaxis output, the primary and secondary hyper-aldosteronism outputs. Aldosterone has the potential to suppress the ACE-2 enzyme.
It is the suppression of the ACE-2 enzyme system, and the extent thereof, in people with comorbidities, that accounts for the unchecked angiotensin II-mediated hyperinflammation, fibrosis and thrombotic phenomena seen in complicated SARS-CoV-2 infection.