Herpesvirus is ranked as one of the grand old members of all pathogens. Of all the viruses in the superfamily, Herpes simplex virus type 1 (HSV-1) is considered as a model virus for a variety of reasons. In a permissive non-neuronal cell culture, HSV-1 concludes the entire life cycle in approximately 18–20 h, encoding approximately 90 unique transcriptional units. In latency, the robust viral gene expression is suppressed in neurons by a group of noncoding RNA. Historically the lesions caused by the virus can date back to centuries ago. As a neurotropic pathogen, HSV-1 is associated with painful oral lesions, severe keratitis and lethal encephalitis. Transmission of pain signals is dependent on the generation and propagation of action potential in sensory neurons. T-type Ca2+ channels serve as a preamplifier of action potential generation. Voltage-gated Na+ channels are the main components for action potential production. This review summarizes not only the voltage-gated ion channels in neuropathic disorders but also provides the new insights into HSV-1 induced pain.

中文翻译：

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电压门控离子通道（VGIC）在疱疹病毒感染相关疼痛中的病理生理作用和治疗潜力。

疱疹病毒被列为所有病原体的重要成员之一。在超家族的所有病毒中，出于多种原因，单纯疱疹病毒1型（HSV-1）被视为模型病毒。在允许的非神经元细胞培养中，HSV-1在大约18–20 h内结束了整个生命周期，编码大约90个独特的转录单位。在潜伏期中，一组非编码RNA抑制神经元中强大的病毒基因表达。从历史上看，由病毒引起的病变可以追溯到几个世纪以前。HSV-1是一种神经致病性病原，与口腔疼痛，严重的角膜炎和致命性脑炎有关。疼痛信号的传递取决于感觉神经元中动作电位的产生和传播。T型Ca2 +通道充当动作电位生成的前置放大器。电压门控的Na +通道是产生动作电位的主要组件。这篇综述不仅总结了神经病性疾病中的电压门控离子通道，而且还提供了对HSV-1诱发疼痛的新见解。