ArticleProceedings of the National Academy of Sciences of the United States of America2005
Rotavirus nonstructural protein 1 subverts innate immune response by inducing degradation of IFN regulatory factor 3.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.
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Who cites it
140 citing papers in PubMed, 252 citations in OpenAlex.
- Whole-genome characterization and pathogenicity of novel human-porcine reassortant rotavirus strains G9P[7] and G1P[7] in China.Veterinary research · 2026Article
- Reprogramming innate immunity through viral interference: A double-edged strategy for enhancing and containing gene therapies.Molecular therapy. Nucleic acids · 2026Review
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- Experimental adaptation of pigeon rotavirus A (pRVA) in human colorectal cancer cells reveals interferon-driven host responses and immune checkpoint modulation.New microbes and new infections · 2026Article
- Prefoldin complex promotes interferon-stimulated gene expression and is inhibited by rotavirus VP3.Nature communications · 2025Article
- M6A Demethylase ALKBH5 in Human Diseases: From Structure to Mechanisms.Biomolecules · 2025Review
- Rhesus rotavirus NSP1 mediates extra-intestinal infection and is a contributing factor for biliary obstruction.PLoS pathogens · 2024Article
- The protective role of prebiotics and probiotics on diarrhea and gut damage in the rotavirus-infected piglets.Journal of animal science and biotechnology · 2024Review
- Isolation and identification of BRV G6P[1] strain in Heilongjiang province, Northeast China.Frontiers in veterinary science · 2024Article
- Recombinant rotavirus expressing the glycosylated S1 protein of SARS-CoV-2.The Journal of general virology · 2023Article
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- Type III and Not Type I Interferons Efficiently Prevent the Spread of Rotavirus in Human Intestinal Epithelial Cells.Journal of virology · 2022Article
- Rotavirus Spike Protein VP4 Mediates Viroplasm Assembly by Association to Actin Filaments.Journal of virology · 2022Article
- Re-Examining Rotavirus Innate Immune Evasion: Potential Applications of the Reverse Genetics System.mBio · 2022Review
- High-Content Screening and Computational Prediction Reveal Viral Genes That Suppress the Innate Immune Response.mSystems · 2022Article
- Article
- Opposite Effects of Apoptotic and Necroptotic Cellular Pathways on Rotavirus Replication.Journal of virology · 2022Article
- Treading a HOSTile path: Mapping the dynamic landscape of host cell-rotavirus interactions to explore novel host-directed curative dimensions.Virulence · 2021Review
- Dynamic, but Not Necessarily Disordered, Human-Virus Interactions Mediated through SLiMs in Viral Proteins.Viruses · 2021Review
- Regulation of antiviral innate immune signaling and viral evasion following viral genome sensing.Experimental & molecular medicine · 2021Review
80 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
IFN regulatory factor 3 (IRF3), a constitutively expressed protein localizing largely to the cytoplasm, is a primary effector of the innate immune response. Infection can trigger the phosphorylation, dimerization, and nuclear translocation of IRF3, where the factor stimulates the expression and release of IFN. In this study, we determined that the rotavirus gene 5 product, nonstructural protein 1 (NSP1), interacts with IRF3 in the infected cell. To understand the importance of the interaction, we compared IRF3 activation by rotaviruses expressing wild-type and C-truncated forms of NSP1. The analysis showed that IRF3 underwent dimerization and nuclear translocation and stimulated IFN promoter activity in infected cells expressing truncated NSP1. In contrast, infected cells expressing wild-type NSP1 were characterized by the rapid degradation of IRF3 during the replication cycle, severe decreases in IRF3 dimerization and nuclear translocation, and lack of IFN promoter activity. The implication of these results, that wild-type NSP1 is an antagonist of the IFN-signaling pathway, was confirmed in transient expression assays, which showed that wild-type NSP1, but not the C-truncated protein, induced the degradation of IRF3 fusion proteins. Related experiments indicated that NSP1 mediates IRF3 degradation through a proteasome-dependent pathway. The critical role of NSP1 in promoting cell-to-cell spread of rotavirus was demonstrated by using gene 5-specific short interfering RNAs in plaque assays. Although several viruses have been described that subvert the innate immune response by preventing IRF3 activation, rotavirus is identified as one that accomplishes this task by inducing the degradation of IRF3.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.