Jiang Tao, Wang Hai-bo, Fan Zhao-min, Han Yue-chen, Xu Lei
Department of Otorhinolaryngology Head and Neck Surgery, Shandong Provencal Hospital, Ji'nan 250021, China.
Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2007 Sep;42(9):683-6.
To establish an animal model of Bell's palsy induced by the reactivation of latent herpes simplex virus type 1 (HSV-1), and observe the effect of interferon and IgG on the facial nerve paralysis induced by HSV-1 infection. METHODS Totally 64 four-week-old female Balb/c mice weighted 16-18 gram were selected. Using scratching the surface of bilateral auricles by a 26-gauge needle, 25 microl HSV-1 with a titer of 6.7 x 10(8) PFU/ml was inoculated into the left auricle and the same volume of PBS was placed in the right in order to develop a mouse model of latent HSV-1. In this study, interferon and IgG administration were performed before and after facial nerve paralysis and continued for 3 days. Controls were given normal sodium instead of interferon and IgG, and the incidence and duration of facial nerve paralysis were compared in the groups interferon and IgG and control. Ciclosporin was given to the mice eight weeks after recovery from facial nerve paralysis caused by inoculation with HSV-1. The HSV-1 DNA in bilateral facial nerve and bilateral trigeminal ganglion after the treatment were examined with polymerase chain reaction (PCR) analysis. RESULTS There were 10 mice of facial nerve paralysis in the first group. The incidence of facial nerve paralysis was 50% and the duration of facial nerve paralysis was (7.2 +/- 2.2) days. There were 6 mice of facial nerve paralysis in the second group. The incidence of facial nerve paralysis was 30% and the duration of facial nerve paralysis was (4.5 +/- 1.8) days. There were 16 mice of facial nerve paralysis in the control group. The incidence of facial nerve paralysis was 67% and the duration of facial nerve paralysis was (8.9 +/-2.6) days. IgG didn't reduce the incidence and duration of facial nerve paralysis by statistics analysis (P > 0.05), but interferon reduced the incidence and duration of facial nerve paralysis (P < 0.05). After administration of ciclosporin, 3/28 of mice developed facial nerve paralysis. The HSV-1 DNA was detected from facial nerve of all the mice of facial palsy. No facial palsy was observed in mice in which no HSV-1 DNA was detected from facial nerve.
Facial nerve paralysis might be caused by reactivation of latent HSV-1, and the reactivation might be related with immunosuppression. Administration of interferon reduces the incidence and duration of facial nerve paralysis. Administration of IgG can't reduced the incidence and duration of facial nerve paralysis.
建立潜伏的单纯疱疹病毒1型（HSV-1）激活诱导的贝尔麻痹动物模型，观察干扰素和IgG对HSV-1感染所致面神经麻痹的影响。方法 选取64只4周龄、体重16～18克的雌性Balb/c小鼠。用26号针头刮擦双侧耳廓表面，将25微升滴度为6.7×10⁸ PFU/ml的HSV-1接种到左耳廓，右耳廓注射等量PBS，以建立潜伏HSV-1小鼠模型。本研究在面神经麻痹前后给予干扰素和IgG，并持续3天。对照组给予生理盐水而非干扰素和IgG，比较干扰素组、IgG组和对照组面神经麻痹的发生率和持续时间。在接种HSV-1所致面神经麻痹恢复8周后给小鼠环孢素。用聚合酶链反应（PCR）分析检测治疗后双侧面神经和双侧三叉神经节中的HSV-1 DNA。结果 第一组有10只小鼠发生面神经麻痹。面神经麻痹发生率为50%，面神经麻痹持续时间为（7.2±2.2）天。第二组有6只小鼠发生面神经麻痹。面神经麻痹发生率为30%，面神经麻痹持续时间为（4.5±1.8）天。对照组有16只小鼠发生面神经麻痹。面神经麻痹发生率为67%，面神经麻痹持续时间为（8.9±2.6）天。经统计学分析，IgG未降低面神经麻痹的发生率和持续时间（P＞0.05），但干扰素降低了面神经麻痹的发生率和持续时间（P＜0.05）。给予环孢素后，28只小鼠中有3只发生面神经麻痹。所有面神经麻痹小鼠的面神经均检测到HSV-1 DNA。面神经未检测到HSV-1 DNA的小鼠未观察到面神经麻痹。结论：面神经麻痹可能由潜伏HSV-1的激活引起，且该激活可能与免疫抑制有关。给予干扰素可降低面神经麻痹的发生率和持续时间。给予IgG不能降低面神经麻痹的发生率和持续时间。
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