Study of facial nerve paralysis in mice model by using virus vector

为了探讨贝尔麻痹的发病机制，我们建立了单纯疱疹病毒1型（HSV-1）再激活诱导面神经麻痹的动物模型。接种1型单纯疱疹病毒引起的面神经麻痹恢复8周后，采用前一次接种部位耳廓皮肤抓伤或腹腔注射抗cd3单克隆抗体（mAb），或两种方法联合治疗。当小鼠单独接受耳穴抓伤或单抗注射治疗时，没有小鼠出现面神经麻痹。相比之下，20%的小鼠在联合治疗后出现了面神经麻痹。除了一个例外，接受耳穴抓伤或单抗注射治疗的小鼠面神经组织中没有出现HSV-1 DNA，而接受两种治疗的6只小鼠中有4只在治疗后第10天出现HSV-1 DNA。组织病理学结果显示瘫痪小鼠膝状神经节神经元变性，面神经脱髓鞘。这些发现表明，局部皮肤刺激和一般免疫抑制的组合对于成功诱导潜伏HSV-1感染小鼠的面神经麻痹是必不可少的。

In order to investigate the mechanism of Bell's palsy, we developed an animal model of facial nerve paralysis induced by the reactivation of herpes simplex virus type 1 (HSV-1). Eight weeks after recovery from facial nerve paralysis caused by inoculation with HSV-1, the mice were treated with auricular skin scratch at the site of the previous inoculation, or with intraperitoneal injection of anti-CD3 monoclonal antibody (mAb), or combination of both procedures. No mice developed facial nerve paralysis when they were treated with either auricular scratch or mAb injection alone. In contrast, 20% of mice developed facial nerve paralysis with the combined treatment. With one exception, no mouse treated with either auricular scratch or mAb injection showed HSV-1 DNA in their facial nerve tissue, whereas 4 out of 6 mice receiving both treatments showed HSV-1 DNA on day 10 after treatment. Histopathological findings showed the neuron degeneration in the geniculate ganglion and demyelination of the facial motor nerve in paralyzed mice. These findings suggest that a combination of stimuli, local skin irritation and general immunosuppression, is essential for successfully inducing facial nerve paralysis in mice with latent HSV-1 infection.