ArticleProceedings of the National Academy of Sciences of the United States of America2024
A CRISPR-Cas9 knockout screening identifies IRF2 as a key driver of OAS3/RNase L-mediated RNA decay during viral infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Histopathological Alterations and Dysregulation of Type I Interferon Signaling in the Human Cerebral Cortex During Severe Dengue.Journal of medical virology · 2025Article
- Condensation of human OAS proteins initiates diverse antiviral activities in response to West Nile virus.Genes & development · 2025Article
- Discovery and mechanistic insights of dibenzoylmethane as a broad spectrum inhibitor of coronavirus.PLoS pathogens · 2025Article
- Cooperative role of PACT and ADAR1 in preventing aberrant PKR activation by self-derived double-stranded RNA.Nature communications · 2025Article
- Metabolic regulation of interferon-mediated innate antiviral immunity.Frontiers in immunology · 2025Review
- A CRISPR-Cas9 knockout screening identifies IRF2 as a key driver of OAS3/RNase L-mediated RNA decay during viral infection.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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Authors and funding
7 authors.
Funding
Abstract
OAS-RNase L is a double-stranded RNA-induced antiviral pathway triggered in response to diverse viral infections. Upon activation, OAS-RNase L suppresses virus replication by promoting the decay of host and viral RNAs and inducing translational shutdown. However, whether OASs and RNase L are the only factors involved in this pathway remains unclear. Here, we develop CRISPR-Translate, a FACS-based genome-wide CRISPR-Cas9 knockout screening method that uses translation levels as a readout and identifies IRF2 as a key regulator of OAS3. Mechanistically, we demonstrate that IRF2 promotes basal expression of OAS3 in unstressed cells, allowing a rapid activation of RNase L following viral infection. Furthermore, IRF2 works in concert with the interferon response through STAT2 to further enhance OAS3 expression. We propose that IRF2-induced RNase L is critical in enabling cells to mount a rapid antiviral response immediately after viral infection, serving as the initial line of defense. This rapid response provides host cells the necessary time to activate additional antiviral signaling pathways, forming secondary defense waves.
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