Journal
MOLECULAR CELL
Volume 81, Issue 13, Pages 2838-+Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2021.04.022
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Funding
- National Culture Collection for Pathogens, Korea National Institute of Health [NCCP43326]
- Korea Bank for Pathogenic Viruses, Korea University Medical Center for HCoV-OC43 [KBPV-VR-8]
- Institute for Basic Science from the Ministry of Science and ICT of Korea [IBS-R008-D1]
- BK21 Research Fellowship from the Ministry of Education of Korea
- Ministry of Science & ICT (MSIT), Republic of Korea [IBS-R008-D1-2021-A00] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [4199990314450, 4199990914370] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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The study reveals the interactions between SARS-CoV-2 and host RNA-binding proteins, provides a comprehensive list of RBPs regulating coronaviral replication, and opens new avenues for therapeutic interventions.
SARS-CoV-2 is an RNA virus whose success as a pathogen relies on its abilities to repurpose host RNA -binding proteins (RBPs) and to evade antiviral RBPs. To uncover the SARS-CoV-2 RNA interactome, we here develop a robust ribonucleoprotein (RNP) capture protocol and identify 109 host factors that directly bind to SARS-CoV-2 RNAs. Applying RNP capture on another coronavirus, HCoV-OC43, revealed evolutionarily conserved interactions between coronaviral RNAs and host proteins. Transcriptome analyses and knockdown experiments delineated 17 antiviral RBPs, including ZC3HAV1, TRIM25, PARP12, and SHFL, and 8 pro viral RBPs, such as EIF3D and CSDE1, which are responsible for co-opting multiple steps of the mRNA life cycle. This also led to the identification of LARP1, a downstream target of the mTOR signaling pathway, as an antiviral host factor that interacts with the SARS-CoV-2 RNAs. Overall, this study provides a comprehensive list of RBPs regulating coronaviral replication and opens new avenues for therapeutic interventions.
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