ArticleJournal of virology2012
Varicella-zoster virus inhibition of the NF-κB pathway during infection of human dendritic cells: role for open reading frame 61 as a modulator of NF-κB activity.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Varicella zoster virus infection.Nature reviews. Disease primers · 2026Review
- Biological relevance ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Varicella Zoster Virus disrupts MAIT cell polyfunctional effector responses.PLoS pathogens · 2024Article
- Modulation of MHC and MHC-Like Molecules by Varicella Zoster Virus.Current topics in microbiology and immunology · 2023Review
- Pseudorabies Virus Infection Triggers NF-κB Activation via the DNA Damage Response but Actively Inhibits NF-κB-Dependent Gene Expression.Journal of virology · 2021Article
- Varicella zoster virus encodes a viral decoy RHIM to inhibit cell death.PLoS pathogens · 2020Article
- Pseudorabies Virus UL24 Abrogates Tumor Necrosis Factor Alpha-Induced NF-κB Activation by Degrading P65.Viruses · 2020Article
- Manipulation of the Innate Immune Response by Varicella Zoster Virus.Frontiers in immunology · 2020Review
- Insights into the pathogenesis of varicella viruses.Current clinical microbiology reports · 2019Article
- Innate Immune Evasion of Alphaherpesvirus Tegument Proteins.Frontiers in immunology · 2019Review
- Modulation of the NFκb Signalling Pathway by Human Cytomegalovirus.Virology (Hyderabad) · 2017Article
- Attenuated Nuclear Factor Kappa B Activity by E7 Protein of Human Papillomavirus Type 2 in Human Epidermal Keratinocytes.Annals of dermatology · 2017Article
- TLR9 stability and signaling are regulated by phosphorylation and cell stress.Journal of leukocyte biology · 2016Article
- Recent advances on viral manipulation of NF-κB signaling pathway.Current opinion in virology · 2015Review
- The ORF61 Protein Encoded by Simian Varicella Virus and Varicella-Zoster Virus Inhibits NF-κB Signaling by Interfering with IκBα Degradation.Journal of virology · 2015Article
- Varicella Viruses Inhibit Interferon-Stimulated JAK-STAT Signaling through Multiple Mechanisms.PLoS pathogens · 2015Article
- Microbial strategies for antagonizing Toll-like-receptor signal transduction.Current opinion in immunology · 2015Review
- Dendritic cells as Achilles' heel and Trojan horse during varicella zoster virus infection.Frontiers in microbiology · 2015Article
- Herpes simplex virus 1 protein kinase US3 hyperphosphorylates p65/RelA and dampens NF-κB activation.Journal of virology · 2014Article
- Enforced expression of microRNA-21 influences the replication of varicella-zoster virus by triggering signal transducer and activator of transcription 3.Experimental and therapeutic medicine · 2014Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Dendritic cells (DC) are antigen-presenting cells essential for initiating primary immune responses and therefore an ideal target for viral immune evasion. Varicella-zoster virus (VZV) can productively infect immature human DCs and impair their function as immune effectors by inhibiting their maturation, as evidenced by the expression modulation of functionally important cell surface immune molecules CD80, CD86, CD83, and major histocompatibility complex I. The NF-κB pathway largely regulates the expression of these immune molecules, and therefore we sought to determine whether VZV infection of DCs modulates the NF-κB pathway. Nuclear localization of NF-κB p50 and p65 indicates pathway activation; however, immunofluorescence studies revealed cytoplasmic retention of these NF-κB subunits in VZV-infected DCs. Western blotting revealed phosphorylation of the inhibitor of κBα (IκBα) in VZV-infected DCs, indicating that the pathway is active at this point. We conclude that VZV infection of DC inhibits the NF-κB pathway following protein phosphorylation but before the translocation of NF-κB subunits into the nucleus. An NF-κB reporter assay identified VZV open reading frame 61 (ORF61) as an inhibitor of tumor necrosis factor alpha-induced NF-κB reporter activity. Mutational analysis of ORF61 identified the E3 ubiquitin ligase domain as a region required for NF-κB pathway inhibition. In summary, we provide evidence that VZV inhibits the NF-κB signaling pathway in human DCs and that the E3 ubiquitin ligase domain of ORF61 is required to modulate this pathway. Thus, this work identifies a mechanism by which VZV modulates host immune function.
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