1型单纯疱疹病毒三叉神经节潜伏感染再激活对大鼠三叉神经痛阈的影响

目的:建立SD大鼠1型单纯疱疹病毒(HSV-1)三叉神经节潜伏感染和再激活的动物模型,利用痛阈检测观察HSV-1神经节感染和再激活对三叉神经痛阈的影响。方法:SD大鼠随机分为实验组和对照组,实验组角膜划痕滴加HSV-1接种病毒,建立神经节潜伏感染模型;对照组仅滴加生理盐水。8周后,再将实验组大鼠分为紫外照射组和非紫外照射组,实施紫外线照射,干预诱导潜伏感染再激活。利用Von Frey纤维丝测痛仪检测各组大鼠触须垫机械痛阈。提取大鼠三叉神经节组织,RT-PCR检测HSV-GD、LAT、ICP27的表达水平,验证HSV-1神经节潜伏感染和再激活是否成功。结果:大鼠HSV-1神经节潜伏感染和再激活成功;实验组大鼠在HSV-1潜伏感染状态下和再激活状态下,发生疼痛刺激样反应,痛阈有降低趋势,尤其在再激活后更加明显。结论:三叉神经节HSV-1潜伏感染再激活可以诱发动物三叉神经痛阈降低,提示HSV-1可能是三叉神经痛的病因。

Decrease of pain threshold of trigeminal nerve induced by reactivation of latent trigeminal ganglia infection of herpes simplex virus type 1 in SD rats

PURPOSE: To establish an animal model of latent infection and reactivation of trigeminal ganglia caused by herpes simplex virus type 1 (HSV-1) in SD rats. The effect of HSV-1 infection and reactivation of ganglion on pain threshold of trigeminal nerve was observed by pain threshold test. METHODS: SD rats were randomly divided into the experimental group and the control group. Rats in the experimental group were treated by corneal scratch with HSV-1 to establish latent infection model of ganglion, while rats in the control group were treated by corneal scratch with normal saline. After 8 weeks, the rats in the experimental group were divided into ultraviolet irradiation group and non ultraviolet irradiation group, ultraviolet irradiation was used to induce reactivation of HSV-1. The mechanical pain threshold of each group of rats was measured by von Frey filament pain threshold detector. The expression levels of HSV-gD, LAT and ICP27 were detected by RT-PCR to verify the success of latent infection and reactivation of HSV-1 in ganglion. RESULTS: Latency and reactivation of HSV-1 in ganglion were successful fulfilled in rats; pain like stimulation reaction occurred in rats of the experimental group and pain threshold decreased both in latency and reactivation,especially in reactivation. CONCLUSIONS: Reactivation of latent infection of HSV-1 in trigeminal ganglia can induce the decrease of trigeminal neuralgia threshold, which suggests that HSV-1 may be the cause of trigeminal neuralgia.