ArticlePLoS pathogens2008
Influenza A virus inhibits type I IFN signaling via NF-kappaB-dependent induction of SOCS-3 expression.
Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers, 3 of them syntheses that pooled it.
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Who cites it
176 citing papers in PubMed, 3 syntheses or guidelines pooled it, 278 citations in OpenAlex.
- Influenza A Virus (H1N1) Infection Induces Ferroptosis to Promote Developmental Injury in Fetal Tissues.Cell proliferation · 2026Pooled it
- The multifaceted interactions between Newcastle disease virus proteins and host proteins: a systematic review.Virulence · 2024Pooled it
- 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
- High Expression of IL-36γ in Influenza Patients Regulates Interferon Signaling Pathway and Causes Programmed Cell Death During Influenza Virus Infection.Frontiers in immunology · 2020Trial
- A multicentre, randomised, double-blind, placebo-controlled trial with the interleukin-1 receptor antagonist anakinra in patients with systemic-onset juvenile idiopathic arthritis (ANAJIS trial).Annals of the rheumatic diseases · 2011Trial
- Gene Expression of Suppressor of Cytokine Signaling 3 (SOCS3), Interferons Alpha and Beta (IFN-α and β) in Common Warts.Indian dermatology online journal · 2026Article
- Systems-Level Analysis of HPAI H5N1 Infection in Ducks: Integrating Transcriptomic, Proteomic, and Phosphoproteomic Data.International journal of molecular sciences · 2026Article
- Comprehensive Bioinformatics Analysis the circRNAs of Viral Infection Associated Pathway in HepG2 Expressing ORF3 of Genotype IV Swine Hepatitis E Virus.Microorganisms · 2025Article
- SOCS Proteins: Key Players in Immune Regulation During SARS-CoV-2 Infection.European journal of immunology · 2025Review
- CRISPR screens and quantitative proteomics reveal remodeling of the aryl hydrocarbon receptor-driven proteome through PARP7 activity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Nuclear AGO2 supports influenza A virus replication through type-I interferon regulation.Nucleic acids research · 2025Article
- Positive Regulation of Cellular Proteins by Influenza Virus for Productive Infection.International journal of molecular sciences · 2025Review
- Article
- Innate immune role of IL-6 in influenza a virus pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- Functional Involvement of Signal Transducers and Activators of Transcription in the Pathogenesis of Influenza A Virus.International journal of molecular sciences · 2024Review
- Interferon as an immunoadjuvant to enhance antibodies following influenza B infection and vaccination in ferrets.NPJ vaccines · 2024Article
- Article
- Article
- STAT3 Increases CVB3 Replication and Acute Pancreatitis and Myocarditis Pathology via Impeding Nuclear Translocation of STAT1 and Interferon-Stimulated Gene Expression.International journal of molecular sciences · 2024Article
- An intranasal nanoparticle STING agonist protects against respiratory viruses in animal models.Nature communications · 2024Article
116 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The type I interferon (IFN) system is a first line of defense against viral infections. Viruses have developed various mechanisms to counteract this response. So far, the interferon antagonistic activity of influenza A viruses was mainly observed on the level of IFNbeta gene induction via action of the viral non-structural protein 1 (NS1). Here we present data indicating that influenza A viruses not only suppress IFNbeta gene induction but also inhibit type I IFN signaling through a mechanism involving induction of the suppressor of cytokine signaling-3 (SOCS-3) protein. Our study was based on the observation that in cells that were infected with influenza A virus and subsequently stimulated with IFNalpha/beta, phosphorylation of the signal transducer and activator of transcription protein 1 (STAT1) was strongly reduced. This impaired STAT1 activation was not due to the action of viral proteins but rather appeared to be induced by accumulation of viral 5' triphosphate RNA in the cell. SOCS proteins are potent endogenous inhibitors of Janus kinase (JAK)/STAT signaling. Closer examination revealed that SOCS-3 but not SOCS-1 mRNA levels increase in an RNA- and nuclear factor kappa B (NF-kappaB)-dependent but type I IFN-independent manner early in the viral replication cycle. This direct viral induction of SOCS-3 mRNA and protein expression appears to be relevant for suppression of the antiviral response since in SOCS-3 deficient cells a sustained phosphorylation of STAT1 correlated with elevated expression of type I IFN-dependent genes. As a consequence, progeny virus titers were reduced in SOCS-3 deficient cells or in cells were SOCS-3 expression was knocked-down by siRNA. These data provide the first evidence that influenza A viruses suppress type I IFN signaling on the level of JAK/STAT activation. The inhibitory effect is at least in part due to the induction of SOCS-3 gene expression, which results in an impaired antiviral 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.