ArticleJournal of virology2007
Downregulation of class I major histocompatibility complex surface expression by varicella-zoster virus involves open reading frame 66 protein kinase-dependent and -independent mechanisms.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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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
66 citing papers in PubMed, 101 citations in OpenAlex.
- Vaccination Targeting Native Receptors to Enhance the Function and Proliferation of Chimeric Antigen Receptor (CAR)-Modified T Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Trial
- 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
- Recombinant Alphaherpesvirus Vectors in Veterinary Vaccinology: Platforms, Applications, and Translational Challenges.International journal of molecular sciences · 2026Review
- Viral manipulation of the HLA class I antigen processing and presentation pathway.Frontiers in immunology · 2025Review
- VZV IE4 downregulates cellular surface MHC-I via sequestering it to the Golgi complex.Cellular and molecular life sciences : CMLS · 2024Article
- Varicella Zoster Virus Downregulates Expression of the Nonclassical Antigen Presentation Molecule CD1d.The Journal of infectious diseases · 2024Article
- Neurexin 3 Regulates Synaptic Connections Between Central Amygdala Neurons and Excitable Cells of the Lateral Parabrachial Nucleus in Rats with Varicella Zoster Induced Orofacial Pain.Journal of pain research · 2024Article
- Varicella-zoster virus recapitulates its immune evasive behaviour in matured hiPSC-derived neurospheroids.Frontiers in immunology · 2024Article
- Defining the role of natural killer cells in COVID-19.Nature immunology · 2023Review
- Varicella Zoster Virus Impairs Expression of the Nonclassical Major Histocompatibility Complex Class I-Related Gene Protein (MR1).The Journal of infectious diseases · 2023Article
- Modulation of MHC and MHC-Like Molecules by Varicella Zoster Virus.Current topics in microbiology and immunology · 2023Review
- Regulation of alphaherpesvirus protein via post-translational phosphorylation.Veterinary research · 2022Review
- Article
- Review
- 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
- Varicella-Zoster Virus and the Enteric Nervous System.The Journal of infectious diseases · 2018Article
- Attenuation of Simian Varicella Virus Infection by Enhanced Green Fluorescent Protein in Rhesus Macaques.Journal of virology · 2018Article
- Simian varicella virus inhibits the interferon gamma signalling pathway.The Journal of general virology · 2017Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
Abstract
We show here that the varicella-zoster virus (VZV) open reading frame 66 (ORF66) protein kinase is one mechanism employed to reduce class I major histocompatibility complex (MHC-I) surface expression in VZV-infected cells. Cells expressing enhanced green fluorescent protein-tagged functional and inactivated ORF66 (GFP-66 and GFP-66kd) from replication-defective adenovirus vectors revealed that ORF66 reduced MHC-I surface levels in a manner dependent on kinase activity. Cells infected with recombinant VZV expressing GFP-66 exhibited a significantly greater reduction in MHC-I surface expression than that observed in cells infected with VZV disrupted in GFP-66 expression. MHC-I maturation was delayed in its transport from the endoplasmic reticulum through the Golgi in both adenovirus-transduced cells expressing only GFP-66 and in VZV-infected cells expressing high levels of GFP-66, and this was predominantly kinase dependent. MHC-I levels were reduced in VZV-infected cells, and analyses of intracellular MHC-I revealed accumulation of folded MHC-I in the Golgi region, irrespective of ORF66 expression. Thus, the ORF66 kinase is important for VZV-mediated MHC-I downregulation, but additional mechanisms also may be involved. Analyses of the VZV ORF9a protein, the ortholog of the bovine herpesvirus 1 transporter associated with antigen processing inhibitor UL49.5 revealed no effects on MHC-I. These results establish a new role for viral protein kinases in immune evasion and suggest that VZV utilizes unique mechanisms to inhibit antigen presentation.
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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.