Severe respiratory SARS-CoV2 infection: Does ACE2 receptor matter?

Respir Med. 2020 Jul;168:105996. doi: 10.1016/j.rmed.2020.105996. Epub 2020 Apr 25.

Abstract

SARS-CoV-2 is a novel virus of the Coronaviridiae family that represents a major global health issue. Mechanisms implicated in virus/host cells interaction are central for cell infection and replication that in turn lead to disease onset and local damage. To enter airway and lung epithelia, SARS-CoV-2 attaches to ACE2 receptors by spike (S) glycoproteins. Molecular mechanisms that promote interaction between SARS-CoV-2 virus and host with particular focus on virus cell entry receptor ACE2 are described. We further explore the impact of underlying medical conditions and therapies including renin-angiotensin inhibitors on modulating ACE 2, which is the major SARS-CoV-2 cell entry receptor.

Keywords: ACE inhibitors; ACE2 receptor; Renin-angiotensin inhibitors; SARS-CoV-2.

Publication types

  • Review

MeSH terms

  • Angiotensin Receptor Antagonists / pharmacology*
  • Angiotensin-Converting Enzyme 2
  • Angiotensin-Converting Enzyme Inhibitors / pharmacology*
  • Betacoronavirus* / drug effects
  • Betacoronavirus* / physiology
  • COVID-19
  • Coronavirus Infections / virology*
  • Host Microbial Interactions / drug effects
  • Host Microbial Interactions / physiology
  • Humans
  • Pandemics
  • Peptidyl-Dipeptidase A*
  • Pneumonia, Viral / virology*
  • Receptors, Virus*
  • Respiratory Mucosa / metabolism
  • SARS-CoV-2
  • Virus Internalization / drug effects*

Substances

  • Angiotensin Receptor Antagonists
  • Angiotensin-Converting Enzyme Inhibitors
  • Receptors, Virus
  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2