Key result
SARS-CoV-2 utilizes host cell intracellular trafficking machinery and proteases to enter myocardial cells, which may contribute to the cardiac injury observed in approximately 20% of COVID-19 patients.
Why the study?
More than 20% of hospitalized COVID-19 patients show heart injury, but the underlying mechanisms of viral entry and intracellular trafficking in cardiac cells remain under active investigation.
Understanding SARS-CoV-2 cellular entry mechanisms in myocardial cells is crucial for identifying therapeutic targets to prevent direct cardiac damage in COVID-19.
Direct cardiac damage by SARS-CoV-2 is likely; leaves open precise cardiomyocyte entry mechanisms for targeted study.
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.
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Balse et al. (2021) conducted a review in COVID-19 with cardiac injury. SARS-CoV-2 cellular entry mechanisms was evaluated. SARS-CoV-2 utilizes host cell intracellular trafficking machinery and proteases to enter myocardial cells, which may contribute to the cardiac injury observed in approximately 20% of COVID-19 patients.
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