SARS-CoV-2 directly infects human cardiomyocytes, resulting in contractile deficits, cytokine production, sarcomere disassembly, and cell death.
SARS-CoV-2 directly infects human cardiomyocytes, causing cell death and contractile deficits, providing a mechanistic basis for direct viral injury in COVID-19 myocarditis.
There is ongoing debate as to whether cardiac complications of coronavirus disease-2019 (COVID-19) result from myocardial viral infection or are secondary to systemic inflammation and/or thrombosis. We provide evidence that cardiomyocytes are infected in patients with COVID-19 myocarditis and are susceptible to severe acute respiratory syndrome coronavirus 2. We establish an engineered heart tissue model of COVID-19 myocardial pathology, define mechanisms of viral pathogenesis, and demonstrate that cardiomyocyte severe acute respiratory syndrome coronavirus 2 infection results in contractile deficits, cytokine production, sarcomere disassembly, and cell death. These findings implicate direct infection of cardiomyocytes in the pathogenesis of COVID-19 myocardial pathology and provides a model system to study this emerging disease.
Bailey et al. (Fri,) conducted a other in COVID-19 myocarditis (n=4). SARS-CoV-2 infection vs. Mock infection was evaluated on Cardiomyocyte infection and contractility. SARS-CoV-2 directly infects human cardiomyocytes, resulting in contractile deficits, cytokine production, sarcomere disassembly, and cell death.