ArticleJournal of virology2013
Herpes simplex virus 1-encoded tegument protein VP16 abrogates the production of beta interferon (IFN) by inhibiting NF-κB activation and blocking IFN regulatory factor 3 to recruit its coactivator CBP.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
102 citing papers in PubMed, 147 citations in OpenAlex.
- Associations of viral infections and antiviral vaccinations with anti-NMDAR and other forms of autoimmune encephalitis.Brain, behavior, & immunity - health · 2026Review
- Axonal entry and retrograde transport define HSV-1 latency establishment and reactivation potential in neurons.bioRxiv : the preprint server for biology · 2026Article
- Efficient clustered, regularly interspaced short palindromic repeats-based gene activation using combinatorial human transcription activation domains.Protein & cell · 2026Article
- The cell-mediated adaptive immune response to herpes simplex virus type 1 encephalitis: mechanisms and clinical implications.Frontiers in immunology · 2026Review
- The Antiviral Activity of Polyphenols.Molecular nutrition & food research · 2025Review
- Immunological Control of Herpes Simplex Virus Type 1 Infection: A Non-Thermal Plasma-Based Approach.Viruses · 2025Review
- HHV-6B ribonucleotide reductase sequesters NF-κB subunit p65 to inhibit innate immune responses.iScience · 2025Article
- TRIM29 controls enteric RNA virus-induced intestinal inflammation by targeting NLRP6 and NLRP9b signaling pathways.Mucosal immunology · 2025Article
- Tug of war: innate immunity and herpes simplex keratitis.Frontiers in immunology · 2025Review
- Complement Suppresses the Initial Type 1 Interferon Response to Ocular Herpes Simplex Virus Type 1 Infection in Mice.Pathogens (Basel, Switzerland) · 2024Article
- Cell Intrinsic Determinants of Alpha Herpesvirus Latency and Pathogenesis in the Nervous System.Viruses · 2023Review
- Several Alphaherpesviruses Interact Similarly with the NF-κB Pathway and Suppress NF-κB-Dependent Gene Expression.Microbiology spectrum · 2023Article
- Role of IL-27 in HSV-1-Induced Herpetic Stromal Keratitis.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Epstein-Barr Virus Envelope Glycoprotein gp110 Inhibits IKKi-Mediated Activation of NF-κB and Promotes the Degradation of β-Catenin.Microbiology spectrum · 2023Article
- Role of Innate Interferon Responses at the Ocular Surface in Herpes Simplex Virus-1-Induced Herpetic Stromal Keratitis.Pathogens (Basel, Switzerland) · 2023Review
- HSV-1 selectively packs the transcription factor Oct-1 into EVs to facilitate its infection.Frontiers in microbiology · 2023Article
- Host factors associated with either VP16 or VP16-induced complex differentially affect HSV-1 lytic infection.Reviews in medical virology · 2022Review
- Inhibition of USP14 influences alphaherpesvirus proliferation by degrading viral VP16 protein via ER stress-triggered selective autophagy.Autophagy · 2022Article
- TRIM18 is a critical regulator of viral myocarditis and organ inflammation.Journal of biomedical science · 2022Article
- The Molecular Mechanism of Herpes Simplex Virus 1 UL31 in Antagonizing the Activity of IFN-β.Microbiology spectrum · 2022Article
42 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Host cells activate innate immune signaling pathways to defend against invading pathogens. To survive within an infected host, viruses have evolved intricate strategies to counteract host immune responses. Herpesviruses, including herpes simplex virus type 1 (HSV-1), have large genomes and therefore have the capacity to encode numerous proteins that modulate host innate immune responses. Here we define the contribution of HSV-1 tegument protein VP16 in the inhibition of beta interferon (IFN-β) production. VP16 was demonstrated to significantly inhibit Sendai virus (SeV)-induced IFN-β production, and its transcriptional activation domain was not responsible for this inhibition activity. Additionally, VP16 blocked the activation of the NF-κB promoter induced by SeV or tumor necrosis factor alpha treatment and expression of NF-κB-dependent genes through interaction with p65. Coexpression analysis revealed that VP16 selectively blocked IFN regulatory factor 3 (IRF-3)-mediated but not IRF-7-mediated transactivation. VP16 was able to bind to IRF-3 but not IRF-7 in vivo, based on coimmunoprecipitation analysis, but it did not affect IRF-3 dimerization, nuclear translocation, or DNA binding activity. Rather, VP16 interacted with the CREB binding protein (CBP) coactivator and efficiently inhibited the formation of the transcriptional complexes IRF-3-CBP in the context of HSV-1 infection. These results illustrate that VP16 is able to block the production of IFN-β by inhibiting NF-κB activation and interfering with IRF-3 to recruit its coactivator CBP, which may be important to the early events leading to HSV-1 infection.
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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.