ArticleScience advances2025
A two-step mechanism for RIG-I activation by influenza virus mvRNAs.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Histone Demethylase JMJD2D Suppresses Influenza A Virus Infection by Promoting RIG-I Expression.Biomolecules · 2026Article
- Spatio-temporal modelling of in vitro influenza A virus infection: The impact of defective interfering particles on the type I interferon response.PLoS computational biology · 2026Article
- DS96432529 enhances osteogenic differentiation and mitigates inflammatory damage in periodontal ligament stem cells involving mitophagy-related processes.Stem cell research & therapy · 2026Article
- Polymerase trapping as the mechanism of H5 highly pathogenic avian influenza virus genesis.Science (New York, N.Y.) · 2026Article
- Febrile temperature activates the innate immune response by promoting aberrant influenza A virus RNA synthesis.Science advances · 2026Article
- Structural and functional perspectives on DEAD-box RNA helicases in the rubber tree cold stress response.Frontiers in plant science · 2026Review
- Comparative progress on the mechanisms of airway mucosal injury induced by different pathogens: SARS-CoV-2, influenza A virus, and Mycoplasma pneumoniae.Frontiers in cellular and infection microbiology · 2026Review
- Spatio-temporal modelling ofbioRxiv : the preprint server for biology · 2025Article
- The RIG-I-like receptor family of immune proteins.Molecular cell · 2025Review
- Febrile temperature activates the innate immune response by promoting aberrant influenza A virus RNA synthesis.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Influenza A virus (IAV) noncanonical RNAs are bound by retinoic acid-inducible gene I (RIG-I). However, innate immune activation is infrequent and it is not understood why noncanonical IAV RNAs activate RIG-I in a sequence- or RNA structure-dependent manner. We hypothesized that multiple events need to occur before IAV RNA synthesis activates RIG-I and investigated whether RIG-I activation is stimulated by the noncanonical or aberrant transcription of mini viral RNAs (mvRNA), an RNA that is overexpressed in highly pathogenic IAV infections. We find that mvRNAs can cause noncanonical transcription termination through a truncated 5' polyadenylation signal or a 5' transient RNA structure that interrupts polyadenylation. The resulting capped complementary RNAs stimulate the release of an mvRNA and complement RIG-I activation in trans. Overall, our findings indicate that sequential rounds of noncanonical or aberrant viral replication and transcription are needed for innate immune signaling by IAV RNA synthesis.
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Registered trials
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.