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Renin-Angiotensin-Aldosterone Inhibitors and Susceptibility to and Severity of COVID-19

Educational Objective
To understand renin-angiotensin-aldosterone inhibitors and susceptibility to and severity of COVID-19

The biological mechanisms by which severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the coronavirus that causes coronavirus disease 2019 (COVID-19), enters human cells have been identified in detail.1 The key viral protein involved in cell entry is the spike (S) protein located on the surface of the virus particle. Two host-cell proteins, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine S2 (TMPRSS2), are also critical for cell entry. The viral S protein binds to ACE2, which serves as the cell membrane receptor for SARS-CoV-2, but only after the S protein has been “primed” by the action of the serine protease TMPRSS2. Thus, the host enzymes, ACE2 and TMPRSS2, act in concert to facilitate viral entry, setting the stage for the development of COVID-19.

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Article Information

Published Online: June 19, 2020. doi:10.1001/jama.2020.11401

Corresponding Author: Gregory Curfman, MD, JAMA, 330 N Wabash, Chicago, IL 60611 (gregory.curfman@jamanetwork.org).

Conflict of Interest Disclosures: None reported.

References
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