ArticleJournal of virology2016
The P Protein of Spring Viremia of Carp Virus Negatively Regulates the Fish Interferon Response by Inhibiting the Kinase Activity of TANK-Binding Kinase 1.
Article in Journal of virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 88 citations in OpenAlex.
- Lactylation of its phosphoprotein interferes with the replication of the spring viremia of carp virus.Microbiology spectrum · 2026Article
- TANK potentiates antiviral innate immunity by recruiting deubiquitinase USP46 to activate IKKε.PLoS pathogens · 2026Article
- SVCV phosphoprotein hijacks phase separation to immobilize the IRF3-TBK1 signaling axis and suppress interferon antiviral immunity.Journal of virology · 2026Article
- Insertion of the P gene of spring viremia of carp virus into the snakehead rhabdovirus genome increases virulence.Archives of virology · 2025Article
- HnRNPC triggers the degradation of MITA to suppress the interferon-mediated antiviral response.Veterinary research · 2025Article
- Spring viremia of carp virus infection induces hypoxia response in zebrafish by stabilizing hif1α.Journal of virology · 2025Article
- Tripartite motif 2b (Journal of virology · 2024Article
- Zebrafish mylipb attenuates antiviral innate immunity through two synergistic mechanisms targeting transcription factor irf3.PLoS pathogens · 2024Article
- Generation of Recombinant Snakehead Rhabdovirus (SHRV) Expressing Artificial MicroRNA Targeting Spring Viremia of Carp Virus (SVCV) P Gene and In Vivo Therapeutic Use Against SVCV Infection.Marine biotechnology (New York, N.Y.) · 2023Article
- Zebrafish MAP2K7 Simultaneously Enhances Host IRF7 Stability and Degrades Spring Viremia of Carp Virus P Protein via Ubiquitination Pathway.Journal of virology · 2023Article
- ZebrafishJournal of virology · 2023Article
- GCRV NS38 counteracts SVCV proliferation by intracellular antagonization during co-infection.Virologica Sinica · 2023Article
- Cytokine Receptor-Like Factor 3 Negatively Regulates Antiviral Immunity by Promoting the Degradation of TBK1 in Teleost Fish.Journal of virology · 2023Article
- IRF2 Cooperates with Phosphoprotein of Spring Viremia of Carp Virus to Suppress Antiviral Response in Zebrafish.Journal of virology · 2022Article
- Singapore Grouper Iridovirus VP131 Drives Degradation of STING-TBK1 Pathway Proteins and Negatively Regulates Antiviral Innate Immunity.Journal of virology · 2022Article
- Negative Regulatory Role of the Spring Viremia of Carp Virus Matrix Protein in the Host Interferon Response by Targeting the MAVS/TRAF3 Signaling Axis.Journal of virology · 2022Article
- Fish Innate Immune Response to Viral Infection-An Overview of Five Major Antiviral Genes.Viruses · 2022Review
- PLAAT1 inhibits type I interferon responseFrontiers in immunology · 2022Article
- Structural and Functional Analyses of Type I IFNa Shed Light Into Its Interaction With Multiple Receptors in Fish.Frontiers in immunology · 2022Article
- Grass Carp Reovirus VP35 Degrades MAVS Through the Autophagy Pathway to Inhibit Fish Interferon Production.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spring viremia of carp virus (SVCV) is an efficient pathogen causing high mortality in the common carp. Fish interferon (IFN) is a powerful cytokine enabling host cells to establish an antiviral response; therefore, the strategies that SVCV uses to avoid the cellular IFN response were investigated. Here, we report that the SVCV P protein is phosphorylated by cellular TANK-binding kinase 1 (TBK1), which decreases IFN regulatory factor 3 (IRF3) phosphorylation and suppresses IFN production. First, overexpression of P protein inhibited the IFN promoter activation induced by SVCV and the IFN activity activated by the mitochondrial antiviral signaling protein (MAVS) although TBK1 activity was not blocked by P protein. Second, P protein colocalized and interacted with TBK1. Dominant negative experiments suggested that the TBK1 N-terminal kinase domain interacted with P protein and was essential for P protein and IRF3 phosphorylation. Finally, P protein overexpression reduced the IRF3 phosphorylation activated by TBK1 and reduced host cellular ifn transcription. Collectively, our data demonstrated that the SVCV P protein is a decoy substrate for the host phosphokinase TBK1, preventing IFN production and facilitating SVCV replication. IMPORTANCE: TBK1 is a pivotal phosphokinase that activates host IFN production to defend against viral infection; thus, it is a potential target for viruses to negatively regulate IFN response and facilitate viral evasion. We report that the SVCV P protein functions as a decoy substrate for cellular TBK1, leading to the reduction of IRF3 phosphorylation and suppression of IFN expression. These findings reveal a novel immune evasion mechanism of SVCV.
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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.