ArticlePLoS pathogens2011
The influenza virus protein PB1-F2 inhibits the induction of type I interferon at the level of the MAVS adaptor protein.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers, 1 of them a synthesis that pooled it.
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Who cites it
166 citing papers in PubMed, 1 synthesis or guideline pooled it, 251 citations in OpenAlex.
- Pooled it
- Detection of Highly Pathogenic Avian Influenza A(H5N1) Clade 2.3.4.4b Genotype D1.2 Virus in Swine after Experimental Inoculation.Emerging infectious diseases · 2026Article
- Temporal Dynamics of Innate Immune Activation and Viral Interference During Sequential Co-Infection with Influenza A Virus and SARS-CoV-2: Molecular Mechanisms, Clinical Evidence, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Distinct infectivity, pathogenicity, and adaptive evolution of clade 2.3.4.4 H5N2 avian influenza viruses in chickens in Taiwan.Poultry science · 2026Article
- Emerging threats of H5N1 clade 2.3.4.4b: cross-species transmission, pathogenesis, and pandemic risk.Frontiers in cellular and infection microbiology · 2025Review
- Influenza Virus Genomic Mutations, Host Barrier and Cross-species Transmission.Current genomics · 2025Review
- Viral strategies to antagonize the host antiviral innate immunity: an indispensable research direction for emerging virus-host interactions.Emerging microbes & infections · 2024Review
- Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape.Pathogens (Basel, Switzerland) · 2024Review
- Influenza A virus NS1 effector domain is required for PA-X-mediated host shutoff in infected cells.Journal of virology · 2024Article
- Triggering Degradation of Host Cellular Proteins for Robust Propagation of Influenza Viruses.International journal of molecular sciences · 2024Review
- Genomic characterization of equine influenza A subtype H3N8 viruses by long read sequencing and functional analyses of the PB1-F2 virulence factor of A/equine/Paris/1/2018.Veterinary research · 2024Article
- Color-Flu Fluorescent Reporter Influenza A Viruses Allow for In Vivo Studies of Innate Immune Function in Zebrafish.Viruses · 2024Article
- ORF3c is expressed in SARS-CoV-2-infected cells and inhibits innate sensing by targeting MAVS.EMBO reports · 2023Article
- Deep mutational scanning reveals the functional constraints and evolutionary potential of the influenza A virus PB1 protein.Journal of virology · 2023Article
- Multi-spectral Fluorescent Reporter Influenza A Viruses Allow forbioRxiv : the preprint server for biology · 2023Article
- The neuropathogenesis of highly pathogenic avian influenza H5Nx viruses in mammalian species including humans.Trends in neurosciences · 2023Review
- Proteomic and genetic analyses of influenza A viruses identify pan-viral host targets.Nature communications · 2023Article
- Review
- Interferons-Implications in the Immune Response to Respiratory Viruses.Microorganisms · 2023Review
- Maximal interferon induction by influenza lacking NS1 is infrequent owing to requirements for replication and export.PLoS pathogens · 2023Article
106 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
PB1-F2 is a 90 amino acid protein that is expressed from the +1 open reading frame in the PB1 gene of some influenza A viruses and has been shown to contribute to viral pathogenicity. Notably, a serine at position 66 (66S) in PB1-F2 is known to increase virulence compared to an isogenic virus with an asparagine (66N) at this position. Recently, we found that an influenza virus expressing PB1-F2 N66S suppresses interferon (IFN)-stimulated genes in mice. To characterize this phenomenon, we employed several in vitro assays. Overexpression of the A/Puerto Rico/8/1934 (PR8) PB1-F2 protein in 293T cells decreased RIG-I mediated activation of an IFN-β reporter and secretion of IFN as determined by bioassay. Of note, the PB1-F2 N66S protein showed enhanced IFN antagonism activity compared to PB1-F2 wildtype. Similar observations were found in the context of viral infection with a PR8 PB1-F2 N66S virus. To understand the relationship between NS1, a previously described influenza virus protein involved in suppression of IFN synthesis, and PB1-F2, we investigated the induction of IFN when NS1 and PB1-F2 were co-expressed in an in vitro transfection system. In this assay we found that PB1-F2 N66S further reduced IFN induction in the presence of NS1. By inducing the IFN-β reporter at different levels in the signaling cascade, we found that PB1-F2 inhibited IFN production at the level of the mitochondrial antiviral signaling protein (MAVS). Furthermore, immunofluorescence studies revealed that PB1-F2 co-localizes with MAVS. In summary, we have characterized the anti-interferon function of PB1-F2 and we suggest that this activity contributes to the enhanced pathogenicity seen with PB1-F2 N66S- expressing influenza viruses.
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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.