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Published on: June 16, 2020
SARS-CoV-2 Infects Human Engineered Heart Tissues and Models COVID-19 Myocarditis
Adam L Bailey1, Oleksandr Dmytrenko2, Lina Greenberg3
1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA.
Insights
Direct infection of heart cells by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19 myocarditis. This study demonstrates SARS-CoV-2 infects cardiomyocytes, leading to heart dysfunction and cell death.
Area of Science:
- Cardiology
- Virology
- Pathology
Background:
- Cardiac complications are a concern in COVID-19.
- The role of direct viral infection versus systemic inflammation in COVID-19 myocarditis is debated.
Purpose of the Study:
- To investigate whether cardiomyocytes are infected by SARS-CoV-2 in COVID-19 myocarditis.
- To establish a model for studying COVID-19 myocardial pathology.
- To elucidate the mechanisms of viral pathogenesis in the heart.
Main Methods:
- Utilized an engineered heart tissue model.
- Infected cardiomyocytes with SARS-CoV-2.
- Assessed viral effects on cardiomyocyte function and structure.
Main Results:
- Demonstrated that cardiomyocytes are infected by SARS-CoV-2.
- Observed contractile deficits, cytokine production, sarcomere disassembly, and cell death in infected cardiomyocytes.
- Confirmed cardiomyocyte susceptibility to SARS-CoV-2.
Conclusions:
- Direct infection of cardiomyocytes plays a role in the pathogenesis of COVID-19 myocardial pathology.
- The engineered heart tissue model is effective for studying COVID-19-related heart disease.
- Findings provide insights into the mechanisms of SARS-CoV-2 cardiac involvement.
Abstract:
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.
