ArticleNature microbiology2020
Influenza virus repurposes the antiviral protein IFIT2 to promote translation of viral mRNAs.
Article in Nature microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- Systematic review and meta-analysis of genome-wide pooled CRISPR screens to identify host factors involved in influenza A virus infection.Journal of virology · 2024Pooled it
- A CRISPR activation screen identifies CH25H as a restriction factor against influenza viruses by targeting accessible cholesterol.Emerging microbes & infections · 2026Article
- TRIM62 facilitates influenza A virus entry by regulating WASH-dependent endosomal trafficking.EMBO reports · 2026Article
- A functional genomics-pharmacotranscriptomics framework identifies host-directed anti-influenza agents.iScience · 2026Article
- Cellular hnRNP D promotes influenza A virus replication by inhibiting TBK1-IRF3-mediated innate immune response.Journal of virology · 2026Article
- The capping arms race: evolutionary interplay between IFIT proteins and viral molecular mimicry.Molecular biology reports · 2026Review
- Proximity proteomics reveals a role for IFI16 during human coronavirus infection.bioRxiv : the preprint server for biology · 2026Article
- SPIB suppresses protective autophagy via the IFIT2/PINK1/Parkin axis to promote anoikis in colorectal cancer.Cancer cell international · 2026Article
- Intrinsic OASL expression governs heterogeneity in interferon induction during influenza A virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- CRISPR-based screening of host factors in veterinary viral infections: from target discovery to host-directed antiviral strategies.Frontiers in veterinary science · 2026Review
- The ribosomal landscape in influenza A virus infection: from molecular mechanisms to clinical relevance.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Review
- Global remodeling of ADP-ribosylation by PARP1 suppresses influenza A virus infection.Nature communications · 2025Article
- The IFIT2-IFIT3 antiviral complex targets short 5' untranslated regions on viral mRNAs for translation inhibition.Nature microbiology · 2025Article
- Nanchangmycin suppresses influenza A virus infection by blocking endosomal acidification.Acta biochimica et biophysica Sinica · 2025Article
- IFIT3 RNA-binding activity promotes influenza A virus infection and translation efficiency.Journal of virology · 2025Article
- Genetic resilience or resistance in poultry against avian influenza virus: mirage or reality?Journal of virology · 2025Review
- Robust antiviral innate immune response and miRNA regulatory network were identified in ZIKV-infected cells: implications in the pathogenesis of ZIKV infection.Virus genes · 2025Article
- Polysaccharide synthesis operon modulates Rickettsia-endothelial cell interactions.PLoS pathogens · 2025Article
- Metabolism-associated protein network constructing and host-directed anti-influenza drug repurposing.Briefings in bioinformatics · 2025Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Cells infected by influenza virus mount a large-scale antiviral response and most cells ultimately initiate cell-death pathways in an attempt to suppress viral replication. We performed a CRISPR-Cas9-knockout selection designed to identify host factors required for replication after viral entry. We identified a large class of presumptive antiviral factors that unexpectedly act as important proviral enhancers during influenza virus infection. One of these, IFIT2, is an interferon-stimulated gene with well-established antiviral activity but limited mechanistic understanding. As opposed to suppressing infection, we show in the present study that IFIT2 is instead repurposed by influenza virus to promote viral gene expression. CLIP-seq demonstrated that IFIT2 binds directly to viral and cellular messenger RNAs in AU-rich regions, with bound cellular transcripts enriched in interferon-stimulated mRNAs. Polysome and ribosome profiling revealed that IFIT2 prevents ribosome pausing on bound mRNAs. Together, the data link IFIT2 binding to enhanced translational efficiency for viral and cellular mRNAs and ultimately viral replication. Our findings establish a model for the normal function of IFIT2 as a protein that increases translation of cellular mRNAs to support antiviral responses and explain how influenza virus uses this same activity to redirect a classically antiviral protein into a proviral effector.
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