ArticleJournal of virology2021
Nectin-1 Is an Entry Mediator for Varicella-Zoster Virus Infection of Human Neurons.
Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The trial behind it
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Knowledge of Herpes Zoster and Attitudes Toward Vaccination: A Questionnaire-Based Study in Outpatient and Online Settings.Vaccines · 2026Article
- Varicella zoster virus and the central nervous system.Nature reviews. Microbiology · 2026Review
- Reactivation and Management of Endogenous Latent Herpesviruses in the Spaceflight Environment.Current microbiology · 2026Review
- Herpes Zoster: Risk Factors for Occurrence, Complications, and Recurrence with a Focus on Immunocompromised Patients.Diseases (Basel, Switzerland) · 2025Review
- Article
- Review
- Atypical Presentation of Disseminated Varicella Zoster Virus Infection Mimicking Bullous Pemphigoid.Cureus · 2024Article
- Nectin1 is a pivotal host factor involved in attachment and entry of red-spotted grouper nervous necrosis virus in the early stages of the viral life cycle.Journal of virology · 2024Article
- Article
- CNS Viral Infections-What to Consider for Improving Drug Treatment: A Plea for Using Mathematical Modeling Approaches.CNS drugs · 2024Review
- Single amino acid mutation of nectin-1 provides remarkable resistance against lethal pseudorabies virus infection in mice.The Journal of veterinary medical science · 2024Article
- Herpes zoster in lupus nephritis: experience on 292 patients followed up for 15 years.Frontiers in immunology · 2023Article
- Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Varicella-zoster virus (VZV) maintains lifelong latency in neurons following initial infection and can subsequently be reactivated to result in herpes zoster or severe neurological manifestations such as encephalitis. Mechanisms of VZV neuropathogenesis have been challenging to study due to the strict human tropism of the virus. Although neuronal entry mediators of other herpesviruses, including herpes simplex virus, have been identified, little is known regarding how VZV enters neurons. Here, we utilize a human stem cell-based neuronal model to characterize cellular factors that mediate entry. Through transcriptional profiling of infected cells, we identify the cell adhesion molecule nectin-1 as a candidate mediator of VZV entry. Nectin-1 is highly expressed in the cell bodies and axons of neurons. Either knockdown of endogenous nectin-1 or incubation with soluble forms of nectin-1 produced in mammalian cells results in a marked decrease in infectivity of neurons. Notably, while addition of soluble nectin-1 during viral infection inhibits infectivity, addition after infection has no effect on infectivity. Ectopic expression of human nectin-1 in a cell line resistant to productive VZV infection confers susceptibility to infection. In summary, we have identified nectin-1 as a neuronal entry mediator of VZV.
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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.