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. 2020 Jul 29;8:383. doi: 10.3389/fpubh.2020.00383

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Copyright © 2020 Chams, Chams, Badran, Shams, Araji, Raad, Mukhopadhyay, Stroberg, Duval, Barton and Hajj Hussein.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The association between SARS-CoV-2 and the Renin-Angiotensin-Aldosterone System (RAAS). SARS-CoV-2 binds to ACE2 receptor and enters into the cell. It has been hypothesized that this process leads to down-regulation of surface ACE2, resulting in unopposed angiotensin II buildup and activity, leading to a pro-inflammatory cascade. Alternative hypotheses are further described in the text. The uncertainties regarding the role of ACE-Is and ARBs in COVID-19 are also discussed. Ang, angiotensin; ACE, angiotensin-converting enzyme; AT1, angiotensin II type 1 receptor.