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Review
. 2020 Aug 6:18:2100-2106.
doi: 10.1016/j.csbj.2020.08.002. eCollection 2020.

ACE2 enhance viral infection or viral infection aggravate the underlying diseases

Shaolei Teng  1 , Qiyi Tang  2
Affiliations
Review

ACE2 enhance viral infection or viral infection aggravate the underlying diseases

Shaolei Teng et al. Comput Struct Biotechnol J. .

Abstract

ACE2 plays a critical role in SARS-CoV-2 infection to cause COVID-19 and SARS-CoV-2 spike protein binds to ACE2 and probably functionally inhibits ACE2 to aggravate the underlying diseases of COVID-19. The important factors that affect the severity and fatality of COVID-19 include patients' underlying diseases and ages. Therefore, particular care to the patients with underlying diseases is needed during the treatment of COVID-19 patients.

Keywords: ACE2, Angiotensin converting enzyme 2; ACEI, ACE inhibitor; Angiotensin converting enzyme 2; COVID-19, Coronavirus Infectious Disease-19; CVD, cardiovascular disease; Coronavirus Infectious Disease-19; Health disparity; PAH, pulmonary artery hypertension; R0, Reproductive number; RAS, Renin-angiotensin system; RBD, Receptor binding domain; S, Spike: TMPRSS2, Transmembrane protease, serine 2; SARS-CoV-2, Severe Acute Respiratory Syndrome Coronavirus −2 SARS-CoV-2, Middle East Respiratory Syndrome 2: MERS-2; SNP, Single Nucleotide Polymorphism; Severe Acute Respiratory Syndrome Coronavirus −2; Single Nucleotide Polymorphism; Underlying diseases.

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Conflict of interest statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1
Fig. 1
Two theories to explain the severity of COVID-19: 1. ACE2 enhancing viral infection, and 2. Viral aggravating existing diseases. ACE catalyzes the conversion of angiotensin I to angiotensin II, a vasoconstrictor. Angiotensin II is converted by ACE2 to Angiotensin-(1–7), a vasodilator. Theory 1 suggests that using ACEI/ARB increases ACE2, which further enhances viral infection. Theory 2 suggests that ACE2 can be either exhausted or functionally inhibited by S1 so that more angiotensin II and less Angiotensin-(1–7) are produced, which would aggravate underlying diseases.
Fig. 2
Fig. 2
The structure of human ACE2 with SARS-Cov-2 Spike RBD: Human receptor ACE2 (green), SARS-CoV-2 spike receptor-binding domain (RBD, yellow orange) and receptor-binding motif (RBM: brown) were shown as cartoons. ACE2 contacted residues, including S19 (purple), T27 (red), E35 and E27 (magenta), M82 (orange) and D355 (hot pink), were displayed as sticks. The image was generated using PyMOL (http://www.pymol.org/) based on PDB ID: 6LZG. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
See this image and copyright information in PMC

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