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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。
In order to understand the mechanism of demyelination of the central nervous system (CNS) white matter caused by human herpes simplex virus type 2 (HSV-2), the experiment was conducted to infect mice with the virus vaginally. Intraperitoneal injection of cyclophosphamide was used to inhibit the immunity of mice before infection. On the 8th day after virus infection, the spinal cord of mice was taken to make samples for light and electron microscope respectively. The results showed that under the conditions of immune suppression, the rate of demyelination caused by the virus was higher than that caused by the virus alone. Demyelination is thought to be due to the virus acting directly on oligodendrocytes and the myelin associated with it, rather than autoimmunity. In the discussion, it is believed that the increased frequency of demyelination increases the virus’s ability to attack oligodendrocytes and their associated myelin due to decreased immunity. Electron microscopy in this experiment showed that oligodendrocytes degeneration and myelin edema degeneration, when the axonal nerve fibers are not damaged. Subsequently, the fiber breaks, collapses and is swallowed by phagocytes, which contains a large amount of secondary lysosomes in the cytoplasm. The demyelinating myelin sheaths are in different stages of digestion.