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. 2020 Oct 31;11(1):1482–1500. doi: 10.1080/21505594.2020.1836904

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© 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — Schematic representation of the effects of positive single-stranded RNA viruses on HIF-1α and (possible) mechanisms of action

From left to right: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes hypoxemia. The accumulation of HIF-1α increase the levels of angiotensin II and decreases ACE2 expression; Hepatitis E virus (HEV) increases AKT/protein B and stabilizes HIF-1α; HIF-1α regulates genome replication of Dengue virus (DENV); Hepatitis C virus (HCV) stabilizes and promotes the overexpression of HIF-1α via NF-κB, STAT-3, PI3-K/AKT, p22/p44 MAPKs and the HCV core protein.