Elsevier

Respiratory Medicine

Volume 168, July 2020, 105996
Respiratory Medicine

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

https://doi.org/10.1016/j.rmed.2020.105996 Get rights and content
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Highlights

  • The tropism of SARS-CoV-2 for the respiratory system is sustained by the attachment to ACE2 highly expressed by lung epithelial cells.

  • ACE2 deficit is linked to change in tissue repair and vascular permeability, fluid accumulation in extra-alveolar spaces and oxidative stress.

  • In chronic respiratory conditions, ACE2 down-regulation may prevent SARS-CoV-2 host cell interaction.

  • ACE-I or ARBs might favour severe disease progression but it is recommended against ACE-I or sartans discontinuation.

  • Manipulation of ACE2 receptor expression and its implication on viral cell entry a major target for therapy.

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

SARS-CoV-2
ACE2 receptor
ACE inhibitors
Renin-angiotensin inhibitors

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