Severe respiratory SARS-CoV2 infection: Does ACE2 receptor matter? - 27/05/20
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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.
Le texte complet de cet article est disponible en PDF.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. |
Keywords : SARS-CoV-2, ACE2 receptor, ACE inhibitors, Renin-angiotensin inhibitors
Plan
Vol 168
Article 105996- juillet 2020 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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