For initial entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into cells, the large viral Spike (S) protein needs to be primed by host proteases. For SARS-CoV-2 that is the serine protease TMPRSS2. After binding to its functional receptor, angiotensin-converting enzyme 2 (ACE2), the virus undergoes endocytosis. After endocytosis of the viral complex, surface ACE2 is further down-regulated, resulting in unopposed angiotensin 2 accumulation. Local activation of the angiotensin pathway system may mediate lung injury responses to viral insults.
ACE denotes angiotensin-converting enzyme and ARB angiotensin-receptor blocker.
Comments
Literature curation of biological processes involved in the COVID-19 disease after SARS-Cov-2 infection and molecular mechanism and potential therapeutic target
Muthiah Vaduganathan, M.D., M.P.H., Orly Vardeny, Pharm.D., Thomas Michel, M.D., Ph.D., John J.V. McMurray, M.D., Marc A. Pfeffer, M.D., Ph.D., and Scott D. Solomon, M.D.; ''Renin–Angiotensin–Aldosterone System Inhibitors in Patients with Covid-19''; DOI: 10.1056/NEJMsr2005760, 2020 PubMedEurope PMCScholia
Zhang H, Penninger JM, Li Y, Zhong N, Slutsky AS; ''Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target.''; Intensive Care Med, 2020 PubMedEurope PMCScholia
Hoffmann M, Kleine-Weber H, Schroeder S, Krüger N, Herrler T, Erichsen S, Schiergens TS, Herrler G, Wu NH, Nitsche A, Müller MA, Drosten C, Pöhlmann S; ''SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor.''; Cell, 2020 PubMedEurope PMCScholia
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