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MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

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    SARS-CoV-2 induces double-stranded RNA-mediated innate immune responses in respiratory epithelial derived cells and cardiomyocytes

    Authors: Yize Li; David Renner; Courtney E Comar; Jillian Whelan; Hanako Reyes; Fabian Leonardo Cardenas-Diaz; Rachel Truitt; Li Hui Tan; Beihua Dong; Konstantinos Dionysios Alysandratose; Jesse Huang; James N Palmer; Nithin D Adappa; Michael A Kohanski; Darrell N Kotton; Robert H Silverman; Wenli Yang; Edward Morrisey; Noam Cohen; Susan R Weiss; David C. Jackson; Nathan W Bartlett; Francesca Mercuri; Miles W Carroll; Sonam T. Nyatsatsang; Alexander L. Greninger; Ansuman T. Satpathy; John S Pauk; Scott D. Boyd; James R. Heath

    doi:10.1101/2020.09.24.312553 Date: 2020-09-25 Source: bioRxiv

    Coronaviruses are adept at evading and/or antagonizing double-stranded RNA-induced host antiviral pathways, including interferon signaling, OAS HGNC- RNase L HGNC and PKR HGNC while robust cytokine responses characterize severe coronavirus disease MESHD. Knowledge of how newly emerged SARS-CoV-2 interacts with these pathways is minimal. SARS-CoV-2 readily infects patient-derived nasal epithelial cells and induced pluripotent stem cell-derived alveolar MESHD type 2 cells (iAT2) and cardiomyocytes (iCM). Robust activation of interferons or RNase L HGNC is not observed, while PKR HGNC activation is evident in iAT2 and iCM. In SARS-CoV-2 infected MESHD Calu-3 and A549ACE2 lung derived cell lines, activation of all pathways is observed, similar to a mutant MERS-CoV lacking innate immune antagonists. Moreover, increased replication in RNASEL HGNC knockout A549ACE2 cells, implicates RNase L HGNC in restricting SARS-CoV-2. Finally, while SARS-CoV-2 is less adept at antagonizing these host defense pathways compared to other coronaviruses, the innate immune response is still generally weak. These host-virus interactions may contribute to the unique pathogenesis of SARS-CoV-2.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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