SARS-CoV-2 infection of human iPSC-derived heart cells and COVID-19 autopsy specimens caused productive infection and robust transcriptomic and morphological damage, including sarcomeric fragmentation.
Does SARS-CoV-2 infection cause direct cytopathic damage in human iPSC-derived cardiac cells and COVID-19 patient hearts?
SARS-CoV-2 directly infects human cardiomyocytes and causes distinct cytopathic features like myofibrillar and sarcomeric fragmentation, providing a mechanistic basis for COVID-19-related cardiac dysfunction.
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.
Pérez-Bermejo et al. (Mon,) conducted a other in COVID-19. SARS-CoV-2 was evaluated on Transcriptomic and morphological signatures of damage. SARS-CoV-2 infection of human iPSC-derived heart cells and COVID-19 autopsy specimens caused productive infection and robust transcriptomic and morphological damage, including sarcomeric fragmentation.