tetano
Editor, Senior Moderator
Sci Transl Med
. 2021 Mar 15;eabf7872.
doi: 10.1126/scitranslmed.abf7872. Online ahead of print.
SARS-CoV-2 infection of human iPSC-derived cardiac cells reflects cytopathic features in hearts of patients with COVID-19
Juan A Perez-Bermejo[SUP] #[/SUP][SUP] 1 [/SUP], Serah Kang[SUP] #[/SUP][SUP] 1 [/SUP], Sarah J Rockwood[SUP] #[/SUP][SUP] 1 [/SUP], Camille R Simoneau[SUP] #[/SUP][SUP] 1 2 [/SUP], David A Joy[SUP] 1 3 [/SUP], Ana C Silva[SUP] 1 [/SUP], Gokul N Ramadoss[SUP] 1 2 [/SUP], Will R Flanigan[SUP] 1 3 [/SUP], Parinaz Fozouni[SUP] 1 2 [/SUP], Huihui Li[SUP] 1 [/SUP], Pei-Yi Chen[SUP] 1 [/SUP], Ken Nakamura[SUP] 1 4 [/SUP], Jeffrey D Whitman[SUP] 5 [/SUP], Paul J Hanson[SUP] 6 [/SUP], Bruce M McManus[SUP] 6 [/SUP], Melanie Ott[SUP] 7 8 [/SUP], Bruce R Conklin[SUP] 7 9 10 8 [/SUP], Todd C McDevitt[SUP] 7 11 [/SUP]
Affiliations
Abstract
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 striking 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 as well as severe cases.
. 2021 Mar 15;eabf7872.
doi: 10.1126/scitranslmed.abf7872. Online ahead of print.
SARS-CoV-2 infection of human iPSC-derived cardiac cells reflects cytopathic features in hearts of patients with COVID-19
Juan A Perez-Bermejo[SUP] #[/SUP][SUP] 1 [/SUP], Serah Kang[SUP] #[/SUP][SUP] 1 [/SUP], Sarah J Rockwood[SUP] #[/SUP][SUP] 1 [/SUP], Camille R Simoneau[SUP] #[/SUP][SUP] 1 2 [/SUP], David A Joy[SUP] 1 3 [/SUP], Ana C Silva[SUP] 1 [/SUP], Gokul N Ramadoss[SUP] 1 2 [/SUP], Will R Flanigan[SUP] 1 3 [/SUP], Parinaz Fozouni[SUP] 1 2 [/SUP], Huihui Li[SUP] 1 [/SUP], Pei-Yi Chen[SUP] 1 [/SUP], Ken Nakamura[SUP] 1 4 [/SUP], Jeffrey D Whitman[SUP] 5 [/SUP], Paul J Hanson[SUP] 6 [/SUP], Bruce M McManus[SUP] 6 [/SUP], Melanie Ott[SUP] 7 8 [/SUP], Bruce R Conklin[SUP] 7 9 10 8 [/SUP], Todd C McDevitt[SUP] 7 11 [/SUP]
Affiliations
- PMID: 33723017
- DOI: 10.1126/scitranslmed.abf7872
Abstract
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 striking 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 as well as severe cases.