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

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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.