Journal
CELL REPORTS
Volume 39, Issue 4, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2022.110744
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Funding
- French government's Investissement d'Avenir program, Laboratoire d'Excellence Integrative Biology of Emerging Infectious Diseases [ANR-10-LABX-62-IBEID]
- Fondation pour la Recherche Medicale [FRM-EQU202003010193]
- Agence Nationale de la Recherche (ANR/FRM Flash COVID project IDISCOVR)
- Agence Nationale de la Recherche (project FISHBP) [ANR-20-CO11-0004]
- University Paris Cite [RACPL20FIR01-COVID-SOUL]
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This study identifies 107 cellular factors that interact with the SARS-CoV-2 genome during infection and demonstrates that HNRNPA2B1, ILF3, QKI, and SFPQ promote viral RNA amplification. These findings provide valuable resources for future investigations into SARS-CoV-2 replication mechanisms and the development of host-centered antiviral therapies.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the COVID-19 pandemic, which has led to a devastating global health crisis. The emergence of variants that escape neutralizing responses emphasizes the urgent need to deepen our understanding of SARS-CoV-2 biology. Using a comprehensive identification of RNA-binding proteins (RBPs) by mass spectrometry (ChIRP-MS) approach, we identify 107 high-confidence cellular factors that interact with the SARS-CoV-2 genome during infection. By systematically knocking down their expression in human lung epithelial cells, we find that the majority of the identified RBPs are SARS-CoV-2 proviral factors. In particular, we show that HNRNPA2B1, ILF3, QKI, and SFPQ interact with the SARS-CoV-2 genome and promote viral RNA amplification. Our study provides valuable resources for future investigations into the mechanisms of SARS-CoV-2 replication and the identification of host-centered antiviral therapies.
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