ArticleJournal of virology2017
Japanese Encephalitis Virus NS5 Inhibits Type I Interferon (IFN) Production by Blocking the Nuclear Translocation of IFN Regulatory Factor 3 and NF-κB.
Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 109 citations in OpenAlex.
- The Battle Between Japanese Encephalitis Virus and Host Innate Immune System: Evasion and Response.Viruses · 2026Review
- Japanese Encephalitis Virus and Host Innate Immunity: Insights Into TLR Signaling, PRR Crosstalk, and Viral Immune Evasion.Cell biochemistry and function · 2026Review
- Article
- Japanese encephalitis virus degrades TRAF3 to suppress type I interferon and promote viral replication through NS5 and host TUFM proteins.Veterinary research · 2026Article
- Entry, replication and innate immunity evasion of BANAL-236, a SARS-CoV-2-related bat virus, in Rhinolophus and human cells.PLoS pathogens · 2026Article
- Article
- Foot-and-mouth disease virus VP4 interferes with host interferon response by targeting the nuclear translocation of interferon regulatory factor 3 (IRF3).Veterinary research · 2026Article
- Tembusu virus neuroinvasion and neuropathogenesis: lessons from blood-brain barrier dysfunction in neurotropic flaviviruses.Frontiers in veterinary science · 2026Review
- Interplay between flaviviruses and the interferon response: mechanisms of immune evasion and therapeutic implications.Frontiers in pharmacology · 2026Review
- Importin α1 contributes to Venezuelan equine encephalitis virus-induced cell death, but is not required for the capsid-mediated blockage of nucleocytoplasmic trafficking.Frontiers in microbiology · 2026Article
- DEAD-box helicase gcDDX56 disrupts IRF3 nuclear import complex and promotes nuclear IRF3 degradation for enhancing GCRV replication.Journal of virology · 2025Article
- African swine fever virus L11L interferes with antiviral responses by targeting the IRF3 and PKR.Cellular and molecular life sciences : CMLS · 2025Article
- Advances and Challenges in Vaccination and Therapeutic Strategies Against Japanese Encephalitis Virus.Pathogens (Basel, Switzerland) · 2025Review
- Identifying a novel region in the Tembusu virus NS5 protein antagonizing type I interferon signaling.Journal of virology · 2025Article
- Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025Review
- Lumpy skin disease virus 001/156 protein is a virulence factor that suppresses interferon production through impairing IRF3 dimerization.PLoS pathogens · 2025Article
- Getah virus nonstructural protein 2 suppresses interferon-beta production by interrupting interferon regulatory factor 3 activation.Veterinary research · 2025Article
- Review
- Coronavirus nucleocapsid protein enhances the binding of p-PKCα to RACK1: Implications for inhibition of nucleocytoplasmic trafficking and suppression of the innate immune response.PLoS pathogens · 2024Article
- MERS-CoV-nsp5 expression in human epithelial BEAS 2b cells attenuates type I interferon production by inhibiting IRF3 nuclear translocation.Cellular and molecular life sciences : CMLS · 2024Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The type I interferon (IFN) response is part of the first-line defense against viral infection. To initiate replication, viruses have developed powerful evasion strategies to counteract host IFN responses. In the present study, we found that the Japanese encephalitis virus (JEV) NS5 protein could inhibit double-stranded RNA (dsRNA)-induced IFN-β expression in a dose-dependent manner. Our data further demonstrated that JEV NS5 suppressed the activation of the IFN transcriptional factors IFN regulatory factor 3 (IRF3) and NF-κB. However, there was no defect in the phosphorylation of IRF3 and degradation of IκB, an upstream inhibitor of NF-κB, upon NS5 expression, indicating a direct inhibition of the nuclear localization of IRF3 and NF-κB by NS5. Mechanistically, NS5 was shown to interact with the nuclear transport proteins KPNA2, KPNA3, and KPNA4, which competitively blocked the interaction of KPNA3 and KPNA4 with their cargo molecules, IRF3 and p65, a subunit of NF-κB, and thus inhibited the nuclear translocation of IRF3 and NF-κB. Furthermore, overexpression of KPNA3 and KPNA4 restored the activity of IRF3 and NF-κB and increased the production of IFN-β in NS5-expressing or JEV-infected cells. Additionally, an upregulated replication level of JEV was shown upon KPNA3 or KPNA4 overexpression. These results suggest that JEV NS5 inhibits the induction of type I IFN by targeting KPNA3 and KPNA4.
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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.