Abstract

Although the main vital organ affected by SARS CoV-2 is the lung, more than 20% of hospitalized patients show heart injury, however, the underlying mechanisms are still actively investigated. Inflammation or myocardial ischemia are now well-established pathogenic factors. Direct cardiac damage by the virus is likely and might account for some aspects of cardiac disease in COVID-19 patients. However, precise knowledge on mechanisms of virus entry and progression in host cells and notably in cardiac cells is necessary in order to define the broad spectrum of pathogenicity of SARS-Cov-2 on myocardium and to identify specific therapeutic targets. This review will focus on the intracellular trafficking machinery, the Achilles heel of host cells, which can be used by the virus to infect cells of the cardiovascular system.

Highlights

  • Reviewed by: Margaret Westfall, University of Michigan, United States James W

  • Precise knowledge on mechanisms of virus entry and progression in host cells and notably in cardiac cells is necessary in order to define the broad spectrum of pathogenicity of SARS-Cov-2 on myocardium and to identify specific therapeutic targets

  • This review will focus on the intracellular trafficking machinery, the Achilles heel of host cells, which can be used by the virus to infect cells of the cardiovascular system

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Summary

Introduction

Reviewed by: Margaret Westfall, University of Michigan, United States James W. Cellular Entry Mechanisms of SARS-Cov-2 Affect Myocardial Cells and Contribute to Cardiac Injury in COVID-19 Patients? It seems well established that SARS-CoV-2 can use the intracellular trafficking pathway of the host cell since classical lysosomotropic agents such as ammonium chloride, which increases endosomal pH, and bafilomycin A, a proton pump inhibitor, exert a strong inhibitory effect on viral load in mammalian cells in vitro (Hoffmann et al, 2020; Ou et al, 2020).

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