Ljungdahl A, Kristensson K, Lundberg J M, Lycke E, Svennerholm B, Ziegler R
J Neurol Sci. 1986 Feb;72(2-3):223-30. doi: 10.1016/0022-510x(86)90010-9.
Following inoculation into the snout herpes simplex virus (HSV) spread to neurons in mouse trigeminal ganglion and subsequently to the brain. Capsaicin treatment of neonatal mice, which causes a loss of unmyelinated sensory neurons, some of which contain substance P, reduced the mortality rate of HSV-infected mice. Moreover, a lower percentage of mice survived the infection with reactivatable virus. There was also an extensive infection of glial cells proximal to the transitional zone in the trigeminal root between the peripheral and central nervous system. Distal to this zone there was an accumulation of substance P immunoreactivity in centrally directed fibres. This amplified degenerative effect on central branches of the substance P containing sensory nerves by glial infection may contribute to the deafferentiation pain syndrome following HSV infection.
将单纯疱疹病毒（HSV）接种到小鼠口鼻部后，病毒扩散至三叉神经节中的神经元，随后扩散至大脑。用辣椒素处理新生小鼠会导致无髓鞘感觉神经元丧失，其中一些含有P物质，这降低了HSV感染小鼠的死亡率。此外，感染可再激活病毒的小鼠存活百分比更低。在周围神经系统和中枢神经系统之间的三叉神经根过渡区近端，神经胶质细胞也受到广泛感染。在该区域远端，向中枢方向的纤维中存在P物质免疫反应性积聚。神经胶质感染对含有P物质的感觉神经中枢分支的这种放大的退化作用，可能导致HSV感染后的去传入性疼痛综合征。
