Hypothesis Article: Free SARS-CoV-2 spike protein S1 particles may act
as a factor of COVID-19 pathogenesis
Abstract
The disbalance of the renin-angiotensin system was suggested to play an
important role in the pathogenesis of the COVID-19 disease. Previously
it has been shown that ACE2 expression in downregulated in the murine
model in response to SARS-CoV infection and may be also induced by the
recombinant spike protein alone. We hypothesize that the soluble
SARS-CoV-2 spike protein S1 subunits shed from the infected cells and
from the virions in vivo may bind to the ACE2 receptor and trigger ACE2
downregulation. Decreased ACE2 activity on the background of the
constant or increased ACE activity in the lungs may lead to the
prevalence of angiotensin II effects over angiotensin(1-7) connected to
increased thrombosis, inflammation and pulmonary damage.