ArticleFrontiers in cellular and infection microbiology2022
TRAF3 Positively Regulates Host Innate Immune Resistance to Influenza A Virus Infection.
Article in Frontiers in cellular and infection microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Gga-miR-92-targeted TNFRSF1B inhibits the replication of influenza A virus by degrading TRAF3.Journal of virology · 2026Article
- A Pilot Study on the Role of TRAFs in the Development of SARS-CoV-2 Infection Before and After Immunization with AstraZeneca Chadox1 in Mice.Current issues in molecular biology · 2025Article
- eEF-2K Deficiency Boosts the Virus-Specific Effector CD8Viruses · 2024Article
- Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape.Pathogens (Basel, Switzerland) · 2024Review
- Downregulation of miR-1388 Regulates the Expression of Antiviral Genes via Tumor Necrosis Factor Receptor (Biomolecules · 2024Article
- CD46 inhibits the replication of swine influenza viruses by promoting the production of type I IFNs in PK-15 cells.Veterinary research communications · 2024Article
- TRAF3 gene regulates macrophage migration and activation by lung epithelial cells infected withMicrobiology spectrum · 2024Article
- Analysis of miRNA expression in the trachea of Ri chicken infected with the highly pathogenic avian influenza H5N1 virus.Journal of veterinary science · 2023Article
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- The Roles of TRAF3 in Immune Responses.Disease markers · 2023Review
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor receptor-associated factor 3 (TRAF3) is one of the intracellular adaptor proteins for the innate immune response, which is involved in signaling regulation in various cellular processes, including the immune responses defending against invading pathogens. However, the defense mechanism of TRAF3 against influenza virus infection remains elusive. In this study, we found that TRAF3 could positively regulate innate antiviral response. Overexpression of TRAF3 significantly enhanced virus-induced IRF3 activation, IFN-β production, and antiviral response, while TRAF3 knockdown promoted influenza A virus replication. Moreover, we clarified that inhibiting ubiquitinated degradation of TRAF3 was associated with anti-influenza effect, thereby facilitating antiviral immunity upon influenza A virus infection. We further demonstrated the key domains of TRAF3 involved in anti-influenza effect. Taken together, these results suggested that TRAF3 performs a vital role in host defense against influenza A virus infection by the type-I IFN signaling pathway. Our findings provide insights into the development of drugs to prevent TRAF3 degradation, which could be a novel therapeutic approach for treatment of influenza A virus infection.
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