Fujiwara Takashi, Matsuda Seiji, Tanaka Junya, Hato Naohito
Kurashiki Central Hospital, Department of Otolaryngology, Kurashiki, Okayama, Japan.
Department of Anatomy and Embryology, Ehime University Graduate School of Medicine, Toon, Ehime, Japan.
Auris Nasus Larynx. 2017 Feb;44(1):58-64. doi: 10.1016/j.anl.2016.04.002. Epub 2016 Apr 17.
Bell's palsy is caused by the reactivation of herpes simplex virus type 1 (HSV-1). Using Balb/c mice inoculated with the KOS strain of HSV-1, we previously developed an animal disease model that simulated mild Bell's palsy. The current study developed an animal disease model of more severe facial palsy than that seen in the mouse model.
Three-week-old female Wister rats weighing 60-80g were inoculated on the auricle with HSV-1 and acyclovir was administered intraperitoneally to deactivate the infected HSV-1. Instead of HSV-1, phosphate-buffered saline was used for inoculation as a negative control. Quantitative polymerase chain reaction (PCR), behavior testing (blink reflex), electroneuronography, histopathology of the peripheral nerve, and immunohistochemistry of the facial nerve nucleus were evaluated.
Facial palsy occurred 3-5 days after virus inoculation, and the severity of the facial palsy progressed for up to 7 days. Quantitative PCR showed an increase in HSV-1 DNA copies in the facial nerve from 24 to 72h, suggesting that HSV-1 infection occurred in the nerve. Electroneuronography values were 33.0±15.3% and 110.0±18.0% in HSV-1-inoculated and control rats, respectively. The histopathology of the peripheral nerve showed demyelination and loss of the facial nerve, and the facial nerve nucleus showed degeneration.
Facial palsy developed in Wister rats following inoculation of the KOS strain of HSV-1 onto the auricles. The behavioral, histopathological, and electroneuronography data suggested that the severity of facial palsy was greater in our rats than in animals in the previous mouse disease model.
贝尔面瘫由1型单纯疱疹病毒（HSV-1）重新激活所致。我们之前利用接种了HSV-1 KOS株的Balb/c小鼠，开发了一种模拟轻度贝尔面瘫的动物疾病模型。当前研究开发了一种比小鼠模型中所见更为严重的面瘫动物疾病模型。
将体重60 - 80g的3周龄雌性Wister大鼠耳廓接种HSV-1，并腹腔注射阿昔洛韦以灭活感染的HSV-1。作为阴性对照，用磷酸盐缓冲盐水代替HSV-1进行接种。评估定量聚合酶链反应（PCR）、行为测试（眨眼反射）、神经电图、周围神经组织病理学以及面神经核免疫组织化学。
病毒接种后3 - 5天出现面瘫，面瘫严重程度持续进展长达7天。定量PCR显示面神经中HSV-1 DNA拷贝数在24至72小时增加，提示神经发生了HSV-1感染。HSV-1接种组和对照组大鼠的神经电图值分别为33.0±15.3%和110.0±18.0%。周围神经组织病理学显示面神经脱髓鞘和缺失，面神经核显示变性。
将HSV-1 KOS株接种到Wister大鼠耳廓后发生了面瘫。行为学、组织病理学和神经电图数据表明，我们实验大鼠的面瘫严重程度高于之前小鼠疾病模型中的动物。
