Key result
SARS-CoV-2 infection cuts hiPSC-CM viability ~28% through direct cytopathogenic effects and inflammation.
Why the study?
SARS-CoV-2 infection is associated with myocardial injury, but there is a paucity of experimental platforms to study this condition.
Answers are grounded in this paper and cite their sources.
Supports hypothesis of direct cardiomyocyte injury by SARS-CoV-2; leaves open clinical relevance pending in vivo and human validation.
BACKGROUND: SARS-CoV-2 infection is associated with myocardial injury, but there is a paucity of experimental platforms for the condition. METHODS AND RESULTS: Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) infected by SARS-CoV-2 for 3 days ceased beating and exhibited cytopathogenic changes with reduced viability. Active viral replication was evidenced by an increase in supernatant SARS-CoV-2 and the presence of SARS-CoV-2 nucleocaspid protein within hiPSC-CMs. Expressions of BNP, CXCL1, CXCL2, IL-6, IL-8 and TNF-α were upregulated, while ACE2 was downregulated. CONCLUSIONS: Our hiPSC-CM-based in-vitro SARS-CoV-2 myocarditis model recapitulated the cytopathogenic effects and cytokine/chemokine response. It could be exploited as a drug screening platform.
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Wong et al. (2020) studied SARS-CoV-2-related myocardial injury. SARS-CoV-2 infection vs. Mock infection was evaluated on hiPSC-CM viability (p=0.008). SARS-CoV-2 infection of human-induced pluripotent stem cell-derived cardiomyocytes induced direct cytopathogenic effects, reducing cell viability at an MOI of 1 and upregulating inflammatory cytokines.
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