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COVID-19 elicits a wide range of cardiovascular-related complications. Whether these problems are due to viral presence in the heart tissue, or they’re driven by the body’s systemic inflammatory response to the virus has remained unknown. Findings from a new study demonstrate that the SARS-CoV-2 virus targets the cardiomyocytes of the heart in the setting of COVID-19, causing myocarditis.

SARS-CoV-2, the virus that causes COVID-19, exploits the ACE2 receptor to gain entry into cells. A specific region of the virus called a spike protein binds to a cell’s ACE2 receptor, and the virus injects its genetic material – RNA – into the cytosol. Once inside, the virus hijacks the body’s natural replicating processes to promote viral reproduction.

Myocarditis is a condition characterized by inflammation of the heart muscle (myocardium). It typically manifests as chest pain, heart failure, or sudden death. Myocarditis commonly occurs after a viral infection.

Using stem cells, the authors of the study developed an engineered heart tissue system that mimicked many aspects of SARS-CoV-2-induced inflammation of the heart muscle. Their model demonstrated that SARS-CoV-2 infects the heart’s muscle cells, driving many deleterious effects, including reduced expression of genes related to metabolism and contraction, and promoting inflammation and cell death. The model confirmed that SARS-CoV-2 entered the cells via ACE2 and quickly replicated, produced viral particles, and activated the interferon response – classic features of viral infection.

These findings demonstrate that myocarditis in the setting of COVID-19 occurs due to SARS-CoV-2 infection of heart muscle cells and provide a unique model by which to study the disease. Learn more about COVID-19 in this new episode featuring Dr. Roger Seheult.

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