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A role of herpes simplex virus infection in the pathogenesis of Bell's palsy

单纯疱疹病毒感染在贝尔麻痹发病机制中的作用

基本信息

批准号：
06454488
负责人：
YANAGIHARA Naoaki
金额：
$ 4.35万
依托单位：
Ehime University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06454488/
关键词：
Bell's palsy facial nerve paralysis herpes simplex virus PCR mouse immunological aspects 顔面神経潜伏感染中和抗体

项目摘要

Herpes simplex virus type 1 (HSV-1) is a neurotropic virus primary infection with which subsides to latency in the sensory ganglia after recovery. Latent HSV-1 infection and its reactivation in the geniculate ganglion of the facial nerve have been strongly suggested as a cause of the idiopathic facial nerve paralysis known as Bell's palsy. We have succeeded in detecting HSV-1 genomes in the clinical samples of endoneurial fluid or posterior auricle muscle obtained during decompression surgery of Bell's palsy patients used by polymerase chain reaction (PCR). However, the pathomechanism of facial nerve paralysis remains unclear.The purpose of this experimantal study was to clarify the immunological aspects to facial nerve paralysis due to HSV-1 infection in a mouse model system. Passive transfer of either anti-HSV-1 antibody or HSV-1 immunized splenic T cells into 4-week-old mice 3 hr after HSV-1 inoculation prevented development of facial nerve paralysis and death, whereas such transfers 48 hr or 96 hr after HSV-1 inoculation did not prevent or exacerbate facial nerve paralysis. These results demonstrated that the age and the immunological potency of mice are closely related to the pathogenesis of facial nerve paralysis. The results of T cell passive immunization tests suggested that autoimmune demyelination is unlikely as a cause of facial nerve paralysis in this model.

单纯疱疹病毒1型（HSV-1）是一种嗜神经病毒原发性感染，恢复后在感觉神经节中潜伏。潜伏性HSV-1感染及其在面神经膝状神经节中的再激活已被强烈建议为被称为贝尔麻痹的特发性面神经麻痹的原因。我们已经成功地检测HSV-1基因组中的临床样本的神经内膜液或耳后肌贝尔麻痹患者减压手术中使用的聚合酶链反应（PCR）。本实验的目的是在小鼠模型系统中阐明HSV-1感染引起的面神经麻痹的免疫学方面。抗HSV-1抗体或HSV-1免疫的脾T细胞在HSV-1接种后3小时被动转移到4周龄小鼠中防止了面神经麻痹和死亡的发展，而在HSV-1接种后48小时或96小时这样的转移没有防止或加重面神经麻痹。提示小鼠的年龄和免疫功能与面神经麻痹的发病密切相关。T细胞被动免疫试验的结果表明，自身免疫性脱髓鞘不太可能是该模型中面神经麻痹的原因。