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Hypothesis Article: Free SARS-CoV-2 spike protein S1 particles may act as a factor of COVID-19 pathogenesis
  • Andrey Letarov,
  • Vladislav Babenko,
  • Eugene Kulikov
Andrey Letarov
Federal Research Center "Fundamentals of Biotechnology", Russian Academy of Sciences

Corresponding Author:[email protected]

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Vladislav Babenko
FSBI Federal Research and Clinical Center of Physical-Chemical Medicine of the Federal Medical Biological Agency of Russia
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Eugene Kulikov
Winogradsky Institute of Microbiology, FRC "Fundamentals of Biotechnology", Russian Academy of Sciences
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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.