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Interaction of SARS-CoV-2 and Other Coronavirus With ACE (Angiotensin-Converting Enzyme)-2 as Their Main Receptor: Therapeutic Implications.
Hypertension. 2020 Nov; 76(5):1339-1349.H

Abstract

Severe acute respiratory syndrome coronavirus (SARS-CoV)-2 originated from Wuhan, China, in December 2019 and rapidly spread to other areas worldwide. Since then, coronavirus disease 2019 (COVID-19) has reached pandemic proportions with >570 000 deaths globally by mid-July 2020. The magnitude of the outbreak and the potentially severe clinical course of COVID-19 has led to a burst of scientific research on this novel coronavirus and its host receptor ACE (angiotensin-converting enzyme)-2. ACE2 is a homolog of the ACE that acts on several substrates in the renin-Ang (angiotensin) system. With unprecedented speed, scientific research has solved the structure of SARS-CoV-2 and imaged its binding with the ACE2 receptor. In SARS-CoV-2 infection, the viral S (spike) protein receptor-binding domain binds to ACE2 to enter the host cell. ACE2 expression in the lungs is relatively low, but it is present in type II pneumocytes-a cell type also endowed with TMPRSS2 (transmembrane protease serine 2). This protease is critical for priming the SARS-CoV-2 S protein to complex with ACE2 and enter the cells. Herein, we review the current understanding of the interaction of SARS-CoV-2 with ACE2 as it has rapidly unfolded over the last months. While it should not be assumed that we have a complete picture of SARS-CoV-2 mechanism of infection and its interaction with ACE2, much has been learned with clear therapeutic implications. Potential therapies aimed at intercepting SARS-CoV-2 from reaching the full-length membrane-bound ACE2 receptor using soluble ACE2 protein and other potential approaches are briefly discussed as well.

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Authors+Show Affiliations

Davidson AM
From the Division of Nephrology and Hypertension, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611.
Wysocki J
From the Division of Nephrology and Hypertension, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611.
Batlle D
From the Division of Nephrology and Hypertension, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611.

MeSH

Angiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsBetacoronavirusCOVID-19ChinaCoronavirus InfectionsDisease OutbreaksFemaleHumansMalePandemicsPeptidyl-Dipeptidase APneumonia, ViralProtein BindingRNA, ViralSARS-CoV-2

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

32851855

Citation

Davidson, Anne M., et al. "Interaction of SARS-CoV-2 and Other Coronavirus With ACE (Angiotensin-Converting Enzyme)-2 as Their Main Receptor: Therapeutic Implications." Hypertension (Dallas, Tex. : 1979), vol. 76, no. 5, 2020, pp. 1339-1349.
Davidson AM, Wysocki J, Batlle D. Interaction of SARS-CoV-2 and Other Coronavirus With ACE (Angiotensin-Converting Enzyme)-2 as Their Main Receptor: Therapeutic Implications. Hypertension. 2020;76(5):1339-1349.
Davidson, A. M., Wysocki, J., & Batlle, D. (2020). Interaction of SARS-CoV-2 and Other Coronavirus With ACE (Angiotensin-Converting Enzyme)-2 as Their Main Receptor: Therapeutic Implications. Hypertension (Dallas, Tex. : 1979), 76(5), 1339-1349. https://doi.org/10.1161/HYPERTENSIONAHA.120.15256
Davidson AM, Wysocki J, Batlle D. Interaction of SARS-CoV-2 and Other Coronavirus With ACE (Angiotensin-Converting Enzyme)-2 as Their Main Receptor: Therapeutic Implications. Hypertension. 2020;76(5):1339-1349. PubMed PMID: 32851855.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interaction of SARS-CoV-2 and Other Coronavirus With ACE (Angiotensin-Converting Enzyme)-2 as Their Main Receptor: Therapeutic Implications. AU - Davidson,Anne M, AU - Wysocki,Jan, AU - Batlle,Daniel, Y1 - 2020/08/27/ PY - 2020/8/28/pubmed PY - 2020/10/21/medline PY - 2020/8/28/entrez KW - China KW - coronavirus KW - coronavirus infections KW - renin-angiotensin system KW - serine SP - 1339 EP - 1349 JF - Hypertension (Dallas, Tex. : 1979) JO - Hypertension VL - 76 IS - 5 N2 - Severe acute respiratory syndrome coronavirus (SARS-CoV)-2 originated from Wuhan, China, in December 2019 and rapidly spread to other areas worldwide. Since then, coronavirus disease 2019 (COVID-19) has reached pandemic proportions with >570 000 deaths globally by mid-July 2020. The magnitude of the outbreak and the potentially severe clinical course of COVID-19 has led to a burst of scientific research on this novel coronavirus and its host receptor ACE (angiotensin-converting enzyme)-2. ACE2 is a homolog of the ACE that acts on several substrates in the renin-Ang (angiotensin) system. With unprecedented speed, scientific research has solved the structure of SARS-CoV-2 and imaged its binding with the ACE2 receptor. In SARS-CoV-2 infection, the viral S (spike) protein receptor-binding domain binds to ACE2 to enter the host cell. ACE2 expression in the lungs is relatively low, but it is present in type II pneumocytes-a cell type also endowed with TMPRSS2 (transmembrane protease serine 2). This protease is critical for priming the SARS-CoV-2 S protein to complex with ACE2 and enter the cells. Herein, we review the current understanding of the interaction of SARS-CoV-2 with ACE2 as it has rapidly unfolded over the last months. While it should not be assumed that we have a complete picture of SARS-CoV-2 mechanism of infection and its interaction with ACE2, much has been learned with clear therapeutic implications. Potential therapies aimed at intercepting SARS-CoV-2 from reaching the full-length membrane-bound ACE2 receptor using soluble ACE2 protein and other potential approaches are briefly discussed as well. SN - 1524-4563 UR - https://www.unboundmedicine.com/medline/citation/32851855/Interaction_of_SARS_CoV_2_and_Other_Coronavirus_With_ACE__Angiotensin_Converting_Enzyme__2_as_Their_Main_Receptor:_Therapeutic_Implications_ DB - PRIME DP - Unbound Medicine ER -