Kristensson K, Svennerholm B, Vahlne A, Nilheden E, Persson L, Lycke E
J Neurol Sci. 1982 Feb;53(2):205-16. doi: 10.1016/0022-510x(82)90006-5.
Herpes simplex virus (HSV) infection of the mouse trigeminal ganglia and the brain stem is associated with demyelination of axons in the central part of the trigeminal root and inflammatory cell infiltration and perivascular demyelination in the brain stem. Cyclophosphamide (CPA) treatment prior to or soon after HSV inoculation caused increased axonal spread of infective virus from the peripheral site of inoculation, more widespread and severe demyelination and increased mortality, suggesting that by CPA the virus invasion of the CNS was facilitated. A direct cytocidal effect of HSV on myelinating cells seemed one plausible explanation for the demyelination. Influence on demyelination at late stages of infection by cytotoxic immune reactions are not excluded by the results reported but seemed not to dominate the picture. Schwann cells from the peripheral part of the nerve root invaded demyelinated areas in the brain stem and remyelinated the axons.
单纯疱疹病毒（HSV）感染小鼠三叉神经节和脑干与三叉神经根中部轴突的脱髓鞘、脑干中的炎性细胞浸润及血管周围脱髓鞘有关。在HSV接种之前或之后不久进行环磷酰胺（CPA）治疗，会导致感染性病毒从接种外周部位的轴突传播增加、脱髓鞘更广泛且严重，以及死亡率增加，这表明CPA促进了病毒对中枢神经系统的侵袭。HSV对髓鞘形成细胞的直接杀细胞作用似乎是脱髓鞘的一个合理原因。本研究结果并未排除细胞毒性免疫反应在感染后期对脱髓鞘的影响，但似乎并非主要因素。来自神经根外周部分的施万细胞侵入脑干的脱髓鞘区域并使轴突重新髓鞘化。
