Abstract
As we deal with the COVID-19 pandemic we face a controversy concerning
its pathophysiology and how to integrate available knowledge into
practice while awaiting study outcomes. COVID-19’s pathophysiology
remains elusive, as reflected in putative mechanisms that remain
unsupported by robust evidence. Some models draw on clinical
observations without reference to supporting data from genomic,
proteomic, molecular, physiological, and other data pertaining to human
coronaviruses. Consequently, some proposed models for COVID-19
pathophysiology and their corresponding treatment options remain highly
divergent. To provide a pathophysiological model that better describes
the different phenotypic presentations of the disease in concordance
with existing research on the renin-angiotensin system, previously
described pathophysiological processes for other human coronavirus
infections and the genomic similarities between the SARS and SARS-CoV-2
viruses, we developed a conceptual model,“epithelial-endothelial
crosstalk at alveolar-capillary membrane” that we believe can help
explain the pathogenesis of COVID-19.