SARS-CoV-2 induces double-stranded RNA-mediated innate immune responses in respiratory epithelial derived cells and cardiomyocytes.
Yize LiDavid M RennerCourtney E ComarJillian N WhelanHanako M ReyesFabian Leonardo Cardenas-DiazRachel TruittLi Hui TanBeihua DongKonstantinos Dionysios AlysandratosJessie HuangJames N PalmerNithin D AdappaMichael A KohanskiDarrell N KottonRobert H SilvermanWenli YangEdward MorriseyNoam A CohenSusan R WeissPublished in: bioRxiv : the preprint server for biology (2020)
SARS-CoV-2 emergence in late 2019 led to the COVID-19 pandemic that has had devastating effects on human health and the economy. Early innate immune responses are essential for protection against virus invasion. While inadequate innate immune responses are associated with severe COVID-19 diseases, understanding of the interaction of SARS-CoV-2 with host antiviral pathways is minimal. We have characterized the innate immune response to SARS-CoV-2 infections in relevant respiratory tract derived cells and cardiomyocytes and found that SARS-CoV-2 activates two antiviral pathways, oligoadenylate synthetase-ribonuclease L (OAS-RNase L), and protein kinase R (PKR), while inducing minimal levels of interferon. This in contrast to MERS-CoV which inhibits all three pathways. Activation of these pathways may contribute to the distinctive pathogenesis of SARS-CoV-2.
Keyphrases
- sars cov
- immune response
- respiratory syndrome coronavirus
- innate immune
- respiratory tract
- human health
- induced apoptosis
- risk assessment
- dendritic cells
- cell cycle arrest
- magnetic resonance
- coronavirus disease
- climate change
- toll like receptor
- endoplasmic reticulum stress
- cell proliferation
- computed tomography
- early onset
- cell migration
- oxidative stress
- endothelial cells