ArticlePLoS pathogens2017
Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Cancer viroimmunotherapy platforms based on varicella-zoster virus and cytomegalovirus.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Review
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
- Biological relevance ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- Differentiation of Human Neurons and Neuron-Like Cells to Study VZV Neuronal Infection.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Decoding VZV's evolutionary arsenal: how Beijing strains use recombination and adaptive mutations to thrive.Virus evolution · 2025Article
- Viral modulation of type II interferon increases T cell adhesion and virus spread.Nature communications · 2024Article
- Oncolytic varicella-zoster virus engineered with ORF8 deletion and armed with drug-controllable interleukin-12.Journal for immunotherapy of cancer · 2024Article
- The Structures and Functions of VZV Glycoproteins.Current topics in microbiology and immunology · 2023Article
- G-quadruplexes formed by Varicella-Zoster virus reiteration sequences suppress expression of glycoprotein C and regulate viral cell-to-cell spread.PLoS pathogens · 2023Article
- Viral G Protein-Coupled Receptors Encoded by β- and γ-Herpesviruses.Annual review of virology · 2022Review
- A CMV-induced adaptive human Vδ1+ γδ T cell clone recognizes HLA-DR.The Journal of experimental medicine · 2022Article
- The requirement of glycoprotein C (gC) for interindividual spread is a conserved function of gC for avian herpesviruses.Scientific reports · 2021Article
- The Tegument Protein pUL47 of Marek's Disease Virus Is Necessary for Horizontal Transmission and Is Important for Expression of Glycoprotein gC.Journal of virology · 2020Article
- Increase in the genetic polymorphism of varicella-zoster virus after passaging in in vitro cell culture.Journal of microbiology (Seoul, Korea) · 2019Article
- Identification of differentially expressed genes and enriched pathways in lung cancer using bioinformatics analysis.Molecular medicine reports · 2019Article
- Chemokine Subversion by Human Herpesviruses.Journal of innate immunity · 2018Review
- Chemokines encoded by herpesviruses.Journal of leukocyte biology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 7 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Varicella zoster virus (VZV) is a highly prevalent human pathogen that establishes latency in neurons of the peripheral nervous system. Primary infection causes varicella whereas reactivation results in zoster, which is often followed by chronic pain in adults. Following infection of epithelial cells in the respiratory tract, VZV spreads within the host by hijacking leukocytes, including T cells, in the tonsils and other regional lymph nodes, and modifying their activity. In spite of its importance in pathogenesis, the mechanism of dissemination remains poorly understood. Here we addressed the influence of VZV on leukocyte migration and found that the purified recombinant soluble ectodomain of VZV glycoprotein C (rSgC) binds chemokines with high affinity. Functional experiments show that VZV rSgC potentiates chemokine activity, enhancing the migration of monocyte and T cell lines and, most importantly, human tonsillar leukocytes at low chemokine concentrations. Binding and potentiation of chemokine activity occurs through the C-terminal part of gC ectodomain, containing predicted immunoglobulin-like domains. The mechanism of action of VZV rSgC requires interaction with the chemokine and signalling through the chemokine receptor. Finally, we show that VZV viral particles enhance chemokine-dependent T cell migration and that gC is partially required for this activity. We propose that VZV gC activity facilitates the recruitment and subsequent infection of leukocytes and thereby enhances VZV systemic dissemination in humans.
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.