PropertyValue
?:abstract
  • Epidemiological studies of the COVID-19 pandemic have revealed evidence of cardiac involvement and documented that myocardial injury and myocarditis are predictors of poor outcomes. Nonetheless, little is understood regarding SARS-CoV-2 tropism within the heart and whether cardiac complications result directly from myocardial infection. Here, we develop a human engineered heart tissue model and demonstrate that SARS-CoV-2 selectively infects cardiomyocytes. Viral infection is dependent on expression of angiotensin-I converting enzyme 2 (ACE2) and endosomal cysteine proteases, suggesting an endosomal mechanism of cell entry. After infection with SARS-CoV-2, engineered tissues display typical features of myocarditis, including cardiomyocyte cell death, impaired cardiac contractility, and innate immune cell activation. Consistent with these findings, autopsy tissue obtained from individuals with COVID-19 myocarditis demonstrated cardiomyocyte infection, cell death, and macrophage-predominate immune cell infiltrate. These findings establish human cardiomyocyte tropism for SARS-CoV-2 and provide an experimental platform for interrogating and mitigating cardiac complications of COVID-19.
is ?:annotates of
?:creator
?:doi
?:doi
  • 10.1101/2020.11.04.364315
?:journal
  • bioRxiv
?:license
  • biorxiv
?:pdf_json_files
  • document_parses/pdf_json/59d5d4b6002f2f20b4c820238bb9e1a346483c87.json
?:pmid
?:pmid
  • 33173875.0
?:publication_isRelatedTo_Disease
?:sha_id
?:source
  • BioRxiv; Medline; WHO
?:title
  • SARS-CoV-2 Infects Human Engineered Heart Tissues and Models COVID-19 Myocarditis
?:type
?:year
  • 2020-11-05

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