Konovalov G V, Dobykin A M
Arkh Patol. 1981;43(11):92-7.
Demyelination processes due to viral infections (encephalomyelitis induced by mouse hepatitis virus, Theiler's encephalomyelitis, canine distemper, and marek's disease) were simulated in laboratory animals to study the corresponding human diseases (multiple sclerosis, multifocal leucoencephalopathy, Guillain-Barre's syndrome). The following mechanisms of tissue injury are discussed: (1) viral damage of myelin-supporting cells, (2) demyelination occurring as a side effect of specific and non-specific inflammatory reactions to the viruses persisting in the nervous system, (3) autoimmune reaction triggered by virus infection. Special attention is paid to the role of virus agents in the development of these processes.
在实验动物中模拟了由病毒感染引起的脱髓鞘过程(小鼠肝炎病毒诱发的脑脊髓炎、泰勒氏脑脊髓炎、犬瘟热和马立克氏病),以研究相应的人类疾病(多发性硬化症、多灶性白质脑病、格林-巴利综合征)。讨论了以下组织损伤机制:(1)髓鞘支持细胞的病毒损伤;(2)作为对持续存在于神经系统中的病毒的特异性和非特异性炎症反应的副作用而发生的脱髓鞘;(3)病毒感染引发的自身免疫反应。特别关注病毒因子在这些过程发展中的作用。