ArticlePLoS pathogens2013
T-Cell tropism of simian varicella virus during primary infection.
Article in PLoS pathogens, 2013. 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
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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
37 citing papers in PubMed, 45 citations in OpenAlex.
- Varicella zoster virus and the central nervous system.Nature reviews. Microbiology · 2026Review
- Transcriptional and functional remodeling of lung-resident T cells and macrophages by Simian varicella virus infection.Frontiers in immunology · 2024Article
- A Guide to Preclinical Models of Zoster-Associated Pain and Postherpetic Neuralgia.Current topics in microbiology and immunology · 2023Review
- Simian Varicella Virus: Molecular Virology and Mechanisms of Pathogenesis.Current topics in microbiology and immunology · 2023Article
- Article
- The architecture of the simian varicella virus transcriptome.PLoS pathogens · 2021Article
- Brain immune cells undergo cGAS/STING-dependent apoptosis during herpes simplex virus type 1 infection to limit type I IFN production.The Journal of clinical investigation · 2021Article
- Varicella-zoster virus VLT-ORF63 fusion transcript induces broad viral gene expression during reactivation from neuronal latency.Nature communications · 2020Article
- Alveolar barrier disruption in varicella pneumonia is associated with neutrophil extracellular trap formation.JCI insight · 2020Article
- Article
- Measles skin rash: Infection of lymphoid and myeloid cells in the dermis precedes viral dissemination to the epidermis.PLoS pathogens · 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
- Review
- Article
- Simian Varicella Virus DNA in Saliva and Buccal Cells After Experimental Acute Infection in Rhesus Macaques.Frontiers in microbiology · 2019Article
- Immunobiology of Varicella-Zoster Virus Infection.The Journal of infectious diseases · 2018Review
- An alternative pathway of enteric PEDV dissemination from nasal cavity to intestinal mucosa in swine.Nature communications · 2018Article
- Molecular Aspects of Varicella-Zoster Virus Latency.Viruses · 2018Review
- Attenuation of Simian Varicella Virus Infection by Enhanced Green Fluorescent Protein in Rhesus Macaques.Journal of virology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Varicella-zoster virus (VZV) causes varicella, establishes a life-long latent infection of ganglia and reactivates to cause herpes zoster. The cell types that transport VZV from the respiratory tract to skin and ganglia during primary infection are unknown. Clinical, pathological, virological and immunological features of simian varicella virus (SVV) infection of non-human primates parallel those of primary VZV infection in humans. To identify the host cell types involved in virus dissemination and pathology, we infected African green monkeys intratracheally with recombinant SVV expressing enhanced green fluorescent protein (SVV-EGFP) and with wild-type SVV (SVV-wt) as a control. The SVV-infected cell types and virus kinetics were determined by flow cytometry and immunohistochemistry, and virus culture and SVV-specific real-time PCR, respectively. All monkeys developed fever and skin rash. Except for pneumonitis, pathology produced by SVV-EGFP was less compared to SVV-wt. In lungs, SVV infected alveolar myeloid cells and T-cells. During viremia the virus preferentially infected memory T-cells, initially central memory T-cells and subsequently effector memory T-cells. In early non-vesicular stages of varicella, SVV was seen mainly in perivascular skin infiltrates composed of macrophages, dendritic cells, dendrocytes and memory T-cells, implicating hematogenous spread. In ganglia, SVV was found primarily in neurons and occasionally in memory T-cells adjacent to neurons. In conclusion, the data suggest the role of memory T-cells in disseminating SVV to its target organs during primary infection of its natural and immunocompetent host.
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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.