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. 2021 Nov 11;12:749291. doi: 10.3389/fimmu.2021.749291

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Copyright © 2021 Al-kuraishy, Al-Gareeb, Mostafa-Hedeab, Kasozi, Zirintunda, Aslam, Allahyani, Welburn and Batiha

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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SARS-CoV-2 and release of pro-inflammatory cytokines: SARS-CoV-2 activates the sympathetic center, increases activity of the sympathetic nervous system (SNS), the release of catecholamine, which activates the expression of CD147 that increase viral entry. SARS-CoV-2 downregulates ACE2 which increases circulating angiotensin II (AngII). SARS-CoV-2 inhibits anti-inflammatory nicotinic acetylcholine receptor (nAChR) with reduced activity of the parasympathetic nervous system (PSNS). These changes together trigger the release of pro-inflammatory cytokines.