Key result
SARS-CoV-2 productively infects cardiomyocytes, causing myofibrillar fragmentation in ~20% of cells.
Why the study?
COVID-19 causes cardiac dysfunction in up to 25% of patients, but its pathogenesis remains unclear.
SARS-CoV-2 directly infects cardiomyocytes to cause highly specific disruption of the contractile machinery, providing a mechanistic explanation for cardiac dysfunction observed in patients with COVID-19.
May explain COVID-19 cardiac injury via direct infection; hypothesis-generating from in vitro model and should not change practice.
Although coronavirus disease 2019 (COVID-19) causes cardiac dysfunction in up to 25% of patients, its pathogenesis remains unclear. Exposure of human induced pluripotent stem cell (iPSC)-derived heart cells to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) revealed productive infection and robust transcriptomic and morphological signatures of damage, particularly in cardiomyocytes. Transcriptomic disruption of structural genes corroborates adverse morphologic features, which included a distinct pattern of myofibrillar fragmentation and nuclear disruption. Human autopsy specimens from patients with COVID-19 reflected similar alterations, particularly sarcomeric fragmentation. These notable cytopathic features in cardiomyocytes provide insights into SARS-CoV-2-induced cardiac damage, offer a platform for discovery of potential therapeutics, and raise concerns about the long-term consequences of COVID-19 in asymptomatic and severe cases.
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Pérez-Bermejo et al. (2021) studied COVID-19 associated cardiac damage. SARS-CoV-2 vs. Mock-treated or heat-inactivated SARS-CoV-2 was evaluated on Viral infectivity, transcriptomic disruption, and cytopathic morphological features (specifically myofibrillar fragmentation). Exposure of human iPSC-derived cardiomyocytes to SARS-CoV-2 resulted in productive infection and marked myofibrillar fragmentation in up to 20% of cells, mirroring structural damage observed in autopsy hearts of patients with COVID-19.
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