ArticlePloS one2011
The varicella-zoster virus ORF47 kinase interferes with host innate immune response by inhibiting the activation of IRF3.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 66 citations in OpenAlex.
- Varicella zoster virus infection.Nature reviews. Disease primers · 2026Review
- HSV-1 and VZV co-reactivation: implications for worsening neurological and neurodegenerative diseases.Journal of neurovirology · 2026Review
- Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis, Treatment, and Prevention.MedComm · 2026Review
- Identification of viral activators of the HSV-2 UL13 protein kinase.Journal of virology · 2025Article
- Biological relevance ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Kinases Associated with Herpes Zoster Virus Infection Unveiled by Phosphoromics Profiling.Infection and drug resistance · 2025Article
- Suppression of the host antiviral response by non-infectious varicella zoster virus extracellular vesicles.Journal of virology · 2024Article
- Varicella-zoster virus recapitulates its immune evasive behaviour in matured hiPSC-derived neurospheroids.Frontiers in immunology · 2024Article
- Article
- Post-Translational Modifications of cGAS-STING: A Critical Switch for Immune Regulation.Cells · 2022Review
- Mechanism of herpesvirus protein kinase UL13 in immune escape and viral replication.Frontiers in immunology · 2022Review
- Regulation of antiviral innate immune signaling and viral evasion following viral genome sensing.Experimental & molecular medicine · 2021Review
- Pseudorabies Virus US3 Protein Inhibits IFN-β Production by Interacting With IRF3 to Block Its Activation.Frontiers in microbiology · 2021Article
- Host Innate Immune Response and Viral Immune Evasion During Alphaherpesvirus Infection.Current issues in molecular biology · 2021Review
- PRV UL13 inhibits cGAS-STING-mediated IFN-β production by phosphorylating IRF3.Veterinary research · 2020Article
- Manipulation of the Innate Immune Response by Varicella Zoster Virus.Frontiers in immunology · 2020Review
- JAK inhibitors and infections risk: focus on herpes zoster.Therapeutic advances in musculoskeletal disease · 2020Article
- Insights into the pathogenesis of varicella viruses.Current clinical microbiology reports · 2019Article
- Coevolution pays off: Herpesviruses have the license to escape the DNA sensing pathway.Medical microbiology and immunology · 2019Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The innate immune response constitutes the first line of host defence that limits viral spread and plays an important role in the activation of adaptive immune response. Viral components are recognized by specific host pathogen recognition receptors triggering the activation of IRF3. IRF3, along with NF-κB, is a key regulator of IFN-β expression. Until now, the role of IRF3 in the activation of the innate immune response during Varicella-Zoster Virus (VZV) infection has been poorly studied. In this work, we demonstrated for the first time that VZV rapidly induces an atypical phosphorylation of IRF3 that is inhibitory since it prevents subsequent IRF3 homodimerization and induction of target genes. Using a mutant virus unable to express the viral kinase ORF47p, we demonstrated that (i) IRF3 slower-migrating form disappears; (ii) IRF3 is phosphorylated on serine 396 again and recovers the ability to form homodimers; (iii) amounts of IRF3 target genes such as IFN-β and ISG15 mRNA are greater than in cells infected with the wild-type virus; and (iv) IRF3 physically interacts with ORF47p. These data led us to hypothesize that the viral kinase ORF47p is involved in the atypical phosphorylation of IRF3 during VZV infection, which prevents its homodimerization and subsequent induction of target genes such as IFN-β and ISG15.
Indexed as
Identifiers
What OpenQuestion holds
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.