Severe respiratory SARS-CoV2 infection: Does ACE2 receptor matter? - 27/05/20

Doi : 10.1016/j.rmed.2020.105996

Fabio Perrotta ^a, Maria Gabriella Matera ^b, Mario Cazzola ^c,^⁎ , Andrea Bianco ^d,^⁎
^a Department of Medicine and Health Sciences “V. Tiberio”, University of Molise, Campobasso, Italy
^b Department of Experimental Medicine, University of Campania “Luigi Vanvitelli”, Naples, Italy
^c Department of Experimental Medicine, University of Rome “Tor Vergata”, Rome, Italy
^d Department of Translational Medical Sciences, University of Campania “Luigi Vanvitelli"/Hosp. Monaldi, Naples, Italy

^∗Corresponding author. Department of Experimental Medicine, University of Rome “Tor Vergata”, Via Montpellier, 1 – 00133, Rome, Italy.Department of Experimental MedicineUniversity of Rome “Tor Vergata”Via MontpellierRome1 – 00133Italy^∗∗Corresponding author. Department of Translational Medical Sciences University of Campania “L Vanvitelli”, Hosp Monaldi, Via L Bianchi, 80131, Napoli, Italy.Department of Translational Medical Sciences University of Campania “L Vanvitelli”, Hosp MonaldiVia L BianchiNapoli80131Italy

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.

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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.

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

Plan

Introduction

Coronaviruses and ACE2 receptor: molecular interaction and damage associated pathways

ACE and ACE2 expression in pre-existing chronic pulmonary diseases

Role of pharmacological agents in ACE2 modulation

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Vol 168

Article 105996- juillet 2020 Retour au numéro

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Severe respiratory SARS-CoV2 infection: Does ACE2 receptor matter? - 27/05/20

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