ArticleMedical microbiology and immunology2013
Herpes simplex virus 1 DNA polymerase processivity factor UL42 inhibits TNF-α-induced NF-κB activation by interacting with p65/RelA and p50/NF-κB1.
Article in Medical microbiology and immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 72 citations in OpenAlex.
- Associations of viral infections and antiviral vaccinations with anti-NMDAR and other forms of autoimmune encephalitis.Brain, behavior, & immunity - health · 2026Review
- Viral microRNA inhibition enhances antiviral immunity by modulating corneal inflammatory and resolution pathways in HSV-1 induced keratitis.Experimental eye research · 2026Article
- Divergent Strategies in Innate Immune Evasion: A Comparative Review of Three Alphaherpesvirus Subfamily Members-PRV, HSV-1, and VZV.Transboundary and emerging diseases · 2026Review
- The producer cell type of HSV-1 alters the proteomic contents and infectious capacity of virions.Journal of virology · 2025Article
- Antagonizing Viral MicroRNAs Reduces Ocular HSV-1 Pathogenesis and Enhances Mucosal Immune Homeostasis.Investigative ophthalmology & visual science · 2025Article
- HHV-6B ribonucleotide reductase sequesters NF-κB subunit p65 to inhibit innate immune responses.iScience · 2025Article
- Article
- Epstein-Barr Virus Envelope Glycoprotein gp110 Inhibits IKKi-Mediated Activation of NF-κB and Promotes the Degradation of β-Catenin.Microbiology spectrum · 2023Article
- Review
- Herpes simplex virus type I glycoprotein L evades host antiviral innate immunity by abrogating the nuclear translocation of phosphorylated NF-κB sub-unit p65.Frontiers in microbiology · 2023Article
- Herpes simplex virus type 2 inhibits TNF-α-induced NF-κB activation through viral protein ICP22-mediated interaction with p65.Frontiers in immunology · 2022Article
- Research advances in cGAS-stimulator of interferon genes pathway and central nervous system diseases: Focus on new therapeutic approaches.Frontiers in molecular neuroscience · 2022Review
- Human Herpesvirus 6A Tegument Protein U14 Induces NF-κB Signaling by Interacting with p65.Journal of virology · 2021Article
- Advancing Our Understanding of Corneal Herpes Simplex Virus-1 Immune Evasion Mechanisms and Future Therapeutics.Viruses · 2021Review
- Porcine epidemic diarrhea virus nsp14 inhibits NF-κB pathway activation by targeting the IKK complex and p65.Animal diseases · 2021Article
- Evasion of I Interferon-Mediated Innate Immunity by Pseudorabies Virus.Frontiers in microbiology · 2021Review
- Inhibitory Effects ofEvidence-based complementary and alternative medicine : eCAM · 2021Article
- Herpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction.Scientific reports · 2020Article
- The Race between Host Antiviral Innate Immunity and the Immune Evasion Strategies of Herpes Simplex Virus 1.Microbiology and molecular biology reviews : MMBR · 2020Review
- Review
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus 1 (HSV-1) is the archetypal member of the alphaherpesvirus with a large genome encoding over 80 viral proteins, many of which are involved in virus-host interactions and show immune modulatory capabilities. In this study, we demonstrated that the HSV-1 UL42 protein, a DNA polymerase processivity factor, was a novel antagonism of the canonical NF-κB signaling pathway. UL42 was shown to significantly suppress TNF-α mediated NF-κB activation. Co-immunoprecipitation experiment revealed that UL42 bound to the NF-κB subunits p65 and p50. Fluorescence microscopy demonstrated that UL42 abolished nuclear translocation of p65 and p50 upon TNF-α-stimulation. But the inhibiting capacity of UL42 2R/2A (R279A, R280A) and UL42 3R/3A (R113A, R279A and R280A) mutants were less than wild type UL42. Also UL42 bound to the Rel homology domain of the NF-κB subunit p65 and p50. Notably, the N-terminal of UL42 was sufficient to interact with p65 and p50 and abolished NF-κB reporter gene activity. Thus, it was first time we demonstrated that HSV-1 UL42 appeared to prevent NF-κB-dependent gene expression by retaining p65 and p50 in the cytoplasm, and UL42-dependent transcriptional activation were inherently coupled to promote HSV-1 lytic replication, which also may contribute to immune evasion and pathogenesis of HSV-1.
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