ArticleScience advances2022
Transient RNA structures cause aberrant influenza virus replication and innate immune activation.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- USP17L13 Enhances Influenza a Virus Replication by Mediating the Degradation of RIG-I and MDA5.Viruses · 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
- A two-step mechanism for RIG-I activation by influenza virus mvRNAs.Science advances · 2025Article
- Febrile temperature activates the innate immune response by promoting aberrant influenza A virus RNA synthesis.bioRxiv : the preprint server for biology · 2025Article
- Analysis of NS2-dependent effects on influenza PB1 segment extends replication requirements beyond the canonical promoter.Nature communications · 2025Article
- Quantification of influenza virus mini viral RNAs using Cas13.RNA (New York, N.Y.) · 2024Article
- The role of structure in regulatory RNA elements.Bioscience reports · 2024Review
- Quantification of influenza virus mini viral RNA dynamics using Cas13.bioRxiv : the preprint server for biology · 2024Article
- Structural Impact of the Interaction of the Influenza A Virus Nucleoprotein with Genomic RNA Segments.Viruses · 2024Article
- Negative and ambisense RNA virus ribonucleocapsids: more than protective armor.Microbiology and molecular biology reviews : MMBR · 2023Review
- Evolution of transient RNA structure-RNA polymerase interactions in respiratory RNA virus genomes.bioRxiv : the preprint server for biology · 2023Article
- Maximal interferon induction by influenza lacking NS1 is infrequent owing to requirements for replication and export.PLoS pathogens · 2023Article
- Evolution of transient RNA structure-RNA polymerase interactions in respiratory RNA virus genomes.Virus evolution · 2023Article
- Levels of Influenza A Virus Defective Viral Genomes Determine Pathogenesis in the BALB/c Mouse Model.Journal of virology · 2022Article
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
During infection, the influenza A virus RNA polymerase produces both full-length and aberrant RNA molecules, such as defective viral genomes (DVGs) and mini viral RNAs (mvRNAs). Subsequent innate immune activation involves the binding of host pathogen receptor retinoic acid-inducible gene I (RIG-I) to viral RNAs. However, it is not clear what factors determine which influenza A virus RNAs are RIG-I agonists. Here, we provide evidence that RNA structures, called template loops (t-loops), stall the viral RNA polymerase and contribute to innate immune activation by mvRNAs during influenza A virus infection. Impairment of replication by t-loops depends on the formation of an RNA duplex near the template entry and exit channels of the RNA polymerase, and this effect is enhanced by mutation of the template exit path from the RNA polymerase active site. Overall, these findings are suggestive of a mechanism involving polymerase stalling that links aberrant viral replication to the activation of the innate immune response.
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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.