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

单纯疱疹病毒1型（HSV-1）是一种嗜神经病毒原发感染，恢复后会在感觉神经节潜伏。潜伏的HSV-1感染及其在面神经膝状神经节中的再激活已被强烈认为是特发性面神经麻痹（称为贝尔麻痹）的原因。应用聚合酶链反应（PCR）技术成功检测了贝尔麻痹患者减压手术中获得的神经内膜液或耳廓后肌临床样本中的HSV-1基因组。然而，面神经麻痹的发病机制尚不清楚。本实验研究的目的是在小鼠模型系统中阐明HSV-1感染引起面神经麻痹的免疫学方面。在接种HSV-1 3小时后，将抗HSV-1抗体或HSV-1免疫的脾T细胞被动转移到4周龄小鼠体内，可防止面神经麻痹的发生和死亡，而在接种HSV-1 48小时或96小时后，这种转移不能预防或加重面神经麻痹。这些结果表明，小鼠的年龄和免疫能力与面神经麻痹的发病机制密切相关。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。

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.