ArticleFrontiers in immunology2017
The C-Terminal Effector Domain of Non-Structural Protein 1 of Influenza A Virus Blocks IFN-β Production by Targeting TNF Receptor-Associated Factor 3.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- Synthetic Biology Strategies for the Development of Live Attenuated Influenza Viruses: Recent Advances and Applications.Viruses · 2026Review
- The intricate interplay among microbiota, mucosal immunity, and viral infection in the respiratory tract.Journal of translational medicine · 2025Review
- Probing the functional constraints of influenza A virus NEP by deep mutational scanning.Cell reports · 2025Article
- Viral strategies to antagonize the host antiviral innate immunity: an indispensable research direction for emerging virus-host interactions.Emerging microbes & infections · 2024Review
- Targeting PRMT7-mediated monomethylation of MAVS enhances antiviral innate immune responses and inhibits RNA virus replication.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Hemagglutinin of Influenza A Virus Induces Ferroptosis to Facilitate Viral Replication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape.Pathogens (Basel, Switzerland) · 2024Review
- Exploring type I interferon pathway: virulent vs. attenuated strain of African swine fever virus revealing a novel function carried by MGF505-4R.Frontiers in immunology · 2024Article
- The Roles of TRAF3 in Immune Responses.Disease markers · 2023Review
- The Contribution of Viral Proteins to the Synergy of Influenza and Bacterial Co-Infection.Viruses · 2022Review
- Peste des Petits Ruminants Virus Exhibits Cell-Dependent Interferon Active Response.Frontiers in cellular and infection microbiology · 2022Article
- Review
- Influenza a virus NS1 resembles a TRAF3-interacting motif to target the RNA sensing-TRAF3-type I IFN axis and impair antiviral innate immunity.Journal of biomedical science · 2021Article
- Inhibition of Antiviral Innate Immunity bymSystems · 2021Article
- NLRP3 Inflammasome Activation Enhanced by TRIM25 is Targeted by the NS1 Protein of 2009 Pandemic Influenza A Virus.Frontiers in microbiology · 2021Article
- Review
- TRIM35 mediates protection against influenza infection by activating TRAF3 and degrading viral PB2.Protein & cell · 2020Article
- The Nucleoprotein of H7N9 Influenza Virus Positively Regulates TRAF3-Mediated Innate Signaling and Attenuates Viral Virulence in Mice.Journal of virology · 2020Article
- Role of Post-translational Modifications in Influenza A Virus Life Cycle and Host Innate Immune Response.Frontiers in microbiology · 2020Review
- Regulation of MAVS Expression and Signaling Function in the Antiviral Innate Immune Response.Frontiers in immunology · 2020Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus non-structural protein 1 (NS1) antagonizes interferon response through diverse strategies, particularly by inhibiting the activation of interferon regulatory factor 3 (IRF3) and IFN-β transcription. However, the underlying mechanisms used by the NS1 C-terminal effector domain (ED) to inhibit the activation of IFN-β pathway are not well understood. In this study, we used influenza virus subtype of H5N1 to demonstrate that the NS1 C-terminal ED but not the N-terminal RNA-binding domain, binds TNF receptor-associated factor 3 (TRAF3). This results in an attenuation of the type I IFN signaling pathway. We found that the NS1 C-terminal ED (named NS1/126-225) inhibits the active caspase activation and recruitment domain-containing form of RIG-I [RIG-I(N)]-induced IFN-β reporter activity, the phosphorylation of IRF3, and the induction of IFN-β. Further analysis showed that NS1/126-225 binds to TRAF3 through the TRAF domain, subsequently decreasing TRAF3 K63-linked ubiquitination. NS1/126-225 binding also disrupted the formation of the mitochondrial antiviral signaling (MAVS)-TRAF3 complex, increasing the recruitment of IKKε to MAVS; ultimately shutting down the RIG-I(N)-mediated signal transduction and cellular antiviral responses. This attenuation of cellular antiviral responses leads to evasion of the innate immune response. Taken together, our findings offer an important insight into the interplay between the influenza virus and host innate immunity.
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