HSV-2感染小鼠导致脊髓白质髓鞘脱失的研究

该实验为了解人类Ⅱ型单纯疮疹病毒（HSV－2）所致中枢神经系统（CNS）白质的脱髓鞘机制，将病毒经阴道感染小鼠。在感染前用环磷酸胺腹腔注射抑制小鼠免疫力，在病毒感染后第8天取小鼠脊髓制作样本分别进行光镜和电镜观察。结果显示，在机体免疫力抑制的条件下，病毒引起的髓鞘脱失率高于单独病毒感染所致。认为髓鞘脱失是由于病毒直接作用于少突胶质细胞及与其有关的髓鞘所致，而非自身免疫所引起。在讨论中认为由于免疫力降低，增加了病毒对少突胶质细胞及与其有关的髓鞘的毒性攻击能力，以致脱髓鞘频率增高。本实验的电镜中观察显示了少突细胞线粒体变性及髓鞘水肿变性，此时神经纤维轴索未受损伤。随后纤维断裂、崩解、被吞噬细胞吞噬，其时胞浆中内含有大量的次级溶酶体，其中的变性髓鞘处于不同的消化阶段。

Study ON Demyelination of Spinal Cord Induced By HSV-2 In Mice

For understanding the mechanism of demyelination induced by HSV-2 in white metter ofCNS, the mice were inoculated vaginally with the virus (V) after one day since intraperitonal injection ofcyclophosphamide (Cy +V) as an immunosuppressor. The mice were sacrified on eighth day after viralinoculation and the spinal cords were taken for light and electron microscopy. The results showed that thefrequency of demyelination in white mettey was higher in group CY + V than that in group V. Theobservation under electron microscope revealed that in patchy areas of demyelination both mitochondria ofoliogodendroglia and the myelin sheath were degenerated simultoneously. Between two ma major dense Linesof myelin sheath presented spaces with different sizes and formes. The axons wrapped by the degenerativemyelin sheath were well preserved, but finally they would be broken, the fragments of myelin sheath wereingested by macrophages and degraded in secondary lysosomes to different extent. According to the studyit suggested that the demyetination induced by HSV-2 resulted from viral damage directly tooliogodendroglia and toxic assault on myelin shenath, while it might not be caused by an autoimmuneresponse.