ArticleJournal of virology2020
Modulation of Voltage-Gated Sodium Channel Activity in Human Dorsal Root Ganglion Neurons by Herpesvirus Quiescent Infection.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Efficacy and Security of Tetrodotoxin in the Treatment of Cancer-Related Pain: Systematic Review and Meta-Analysis.Marine drugs · 2023Pooled it
- Ultrasound-Guided Liposomal vs. Conventional Bupivacaine Erector Spinae Plane Block Plus Gabapentin for Postherpetic Neuralgia.The Kaohsiung journal of medical sciences · 2026Trial
- Herpes simplex virus pUL56 abolishes neuronal activity by removing voltage-gated ion channels from the plasma membrane.Science advances · 2026Article
- Human Dorsal Root Ganglia Neuronal Cell Line to Study Nociceptive Signaling: A New Pipeline for Pain Therapy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- In vitro modeling of human dorsal root ganglion neurons for GCaMP6-based calcium imaging of sensory responses to HSV-1 infection.Journal of virological methods · 2026Article
- A human sensory neuron model for varicella-zoster virus latency and reactivationbioRxiv : the preprint server for biology · 2025Article
- Expression Profiles of lncRNAs and mRNAs in the Mouse Brain Infected with Pseudorabies Virus: A Bioinformatic Analysis.Viruses · 2025Article
- Neuroimmune Pain and Its Manipulation by Pathogens.Evolutionary applications · 2025Article
- Single-Cell Transcriptomic Analysis of Kaposi Sarcoma.PLoS pathogens · 2025Article
- Regulation of voltage-gated sodium channels by TNF-α during herpes simplex virus latency establishment.Journal of neurovirology · 2024Article
- Article
- Trigeminal Postherpetic Neuralgia: From Pathophysiology to Treatment.Current pain and headache reports · 2024Review
- Alpha herpesvirus exocytosis from neuron cell bodies uses constitutive secretory mechanisms, and egress and spread from axons is independent of neuronal firing activity.PLoS pathogens · 2024Article
- Varicella Zoster Virus Neuronal Latency and Reactivation Modeled in Vitro.Current topics in microbiology and immunology · 2023Review
- Establishing a Herpesvirus Quiescent Infection in Differentiated Human Dorsal Root Ganglion Neuronal Cell Line Mediated by Micro-RNA Overexpression.Pathogens (Basel, Switzerland) · 2022Article
- Recent Issues in Varicella-Zoster Virus Latency.Viruses · 2021Review
- Review
- Ion Channels as Therapeutic Targets for Viral Infections: Further Discoveries and Future Perspectives.Viruses · 2020Review
- Immortalized Dorsal Root Ganglion Neuron Cell Lines.Frontiers in cellular neuroscience · 2020Review
- Bioinformatics Analysis of Genes and Mechanisms in Postherpetic Neuralgia.Pain research & management · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The molecular mechanisms of pain associated with alphaherpesvirus latency are not clear. We hypothesize that the voltage-gated sodium channels (VGSC) on the dorsal root ganglion (DRG) neurons controlling electrical impulses may have abnormal activity during latent viral infection and reactivation. We used herpes simplex virus 1 (HSV-1) to infect the human DRG-derived neuronal cell line HD10.6 in order to study the establishment and maintenance of viral latency, viral reactivation, and changes in the functional expression of VGSCs. Differentiated cells exhibited robust tetrodotoxin (TTX)-sensitive sodium currents, and acute infection significantly reduced the functional expression of VGSCs within 24 h and completely abolished VGSC activity within 3 days. A quiescent state of infection mimicking latency can be achieved in the presence of acyclovir (ACV) for 7 days followed by 5 days of ACV washout, and then the viruses can remain dormant for another 3 weeks. It was noted that during the establishment of HSV-1 latency, the loss of VGSC activity caused by HSV-1 infection could not be blocked by ACV treatment. However, neurons with continued ACV treatment for another 4 days showed a gradual recovery of VGSC functional expression. Furthermore, the latently infected neurons exhibited higher VGSC activity than controls. The overall regulation of VGSCs by HSV-1 during quiescent infection was proved by increased transcription and possible translation of Nav1.7. Together, these observations demonstrated a very complex pattern of electrophysiological changes during HSV infection of DRG neurons, which may have implications for understanding of the mechanisms of virus-mediated pain linked to latency and reactivation.
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