ArticlePloS one2013
Varicella-zoster viruses associated with post-herpetic neuralgia induce sodium current density increases in the ND7-23 Nav-1.8 neuroblastoma cell line.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Ultrasound-Guided Liposomal vs. Conventional Bupivacaine Erector Spinae Plane Block Plus Gabapentin for Postherpetic Neuralgia.The Kaohsiung journal of medical sciences · 2026Trial
- Low-Level Light Therapy in Postherpetic Neuralgia: A Review of Mechanistic Insights and Clinical Implications.Cellular and molecular neurobiology · 2026Review
- Biological relevance ofMicrobiology and molecular biology reviews : MMBR · 2025Review
- A Literature Review: The Mechanisms and Treatment of Neuropathic Pain-A Brief Discussion.Biomedicines · 2024Review
- Comparison of the Severity of Zoster-Associated Pain and Incidence of Postherpetic Neuralgia in Patients with and without Pre-Existing Spinal Disorders at the Same Spinal Nerve Level: A Retrospective Multicenter Study.Journal of personalized medicine · 2023Article
- Review
- Review
- Neurotoxicity of Tityus bahiensis (brown scorpion) venom in sympathetic vas deferens preparations and neuronal cells.Archives of toxicology · 2020Article
- Comparing Gene Expression in the Parabrachial and Amygdala of Diestrus and Proestrus Female Rats after Orofacial Varicella Zoster Injection.International journal of molecular sciences · 2020Article
- Ion Channels as Therapeutic Targets for Viral Infections: Further Discoveries and Future Perspectives.Viruses · 2020Review
- Determinants of neurological syndromes caused by varicella zoster virus (VZV).Journal of neurovirology · 2020Review
- Modulation of Voltage-Gated Sodium Channel Activity in Human Dorsal Root Ganglion Neurons by Herpesvirus Quiescent Infection.Journal of virology · 2020Article
- Pathophysiological roles and therapeutic potential of voltage-gated ion channels (VGICs) in pain associated with herpesvirus infection.Cell & bioscience · 2020Review
- Immortalized Dorsal Root Ganglion Neuron Cell Lines.Frontiers in cellular neuroscience · 2020Review
- Spider Knottin Pharmacology at Voltage-Gated Sodium Channels and Their Potential to Modulate Pain Pathways.Toxins · 2019Review
- Regulation of T-type CaJournal of neurochemistry · 2019Article
- Review
- NaV1.6 and NaV1.7 channels are major endogenous voltage-gated sodium channels in ND7/23 cells.PloS one · 2019Article
- Modeling Varicella Zoster Virus Persistence and Reactivation - Closer to Resolving a Perplexing Persistent State.Frontiers in microbiology · 2019Review
- Regulation of T-type CaJournal of neurovirology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Post-herpetic neuralgia (PHN) is the most significant complication of herpes zoster caused by reactivation of latent Varicella-Zoster virus (VZV). We undertook a heterologous infection in vitro study to determine whether PHN-associated VZV isolates induce changes in sodium ion channel currents known to be associated with neuropathic pain. Twenty VZV isolates were studied blind from 11 PHN and 9 non-PHN subjects. Viruses were propagated in the MeWo cell line from which cell-free virus was harvested and applied to the ND7/23-Nav1.8 rat DRG x mouse neuroblastoma hybrid cell line which showed constitutive expression of the exogenous Nav 1.8, and endogenous expression of Nav 1.6 and Nav 1.7 genes all encoding sodium ion channels the dysregulation of which is associated with a range of neuropathic pain syndromes. After 72 hrs all three classes of VZV gene transcripts were detected in the absence of infectious virus. Single cell sodium ion channel recording was performed after 72 hr by voltage-clamping. PHN-associated VZV significantly increased sodium current amplitude in the cell line when compared with non-PHN VZV, wild-type (Dumas) or vaccine VZV strains ((POka, Merck and GSK). These sodium current increases were unaffected by acyclovir pre-treatment but were abolished by exposure to Tetrodotoxin (TTX) which blocks the TTX-sensitive fast Nav 1.6 and Nav 1.7 channels but not the TTX-resistant slow Nav 1.8 channel. PHN-associated VZV sodium current increases were therefore mediated in part by the Nav 1.6 and Nav 1.7 sodium ion channels. An additional observation was a modest increase in message levels of both Nav1.6 and Nav1.7 mRNA but not Nav 1.8 in PHN virally infected cells.
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