Fazakerley J K, Webb H E
J Gen Virol. 1987 Feb;68 ( Pt 2):377-85. doi: 10.1099/0022-1317-68-2-377.
Adoptive transfer experiments in athymic nude mice demonstrated that the demyelination seen in the central nervous system (CNS) following Semliki Forest virus (SFV) infection was directly dependent upon sensitized T lymphocytes. Antibodies generated during the infection did not seem to be involved in the demyelination, but thymus-dependent antibodies (IgG) were responsible for the reduction of brain virus titres. In the absence of a T cell response and T cell-dependent antibody production, virus persisted in the CNS for several months. Despite persistence of high virus titres for this time, only mice eventually developing a CNS inflammatory response developed lesions of demyelination. In the absence of an inflammatory response no demyelination was apparent even after several months of persistent infection. Administration of anti-SFV hyperimmune serum intracerebrally to both infected and control mice did not produce demyelination but resulted in CNS tissue degeneration with marked pycnosis.
在无胸腺裸鼠身上进行的过继转移实验表明，感染Semliki森林病毒（SFV）后中枢神经系统（CNS）出现的脱髓鞘直接依赖于致敏T淋巴细胞。感染期间产生的抗体似乎与脱髓鞘无关，但胸腺依赖性抗体（IgG）负责降低脑病毒滴度。在没有T细胞反应和T细胞依赖性抗体产生的情况下，病毒在中枢神经系统中持续存在数月。尽管在此期间病毒滴度一直很高，但只有最终出现中枢神经系统炎症反应的小鼠才会发生脱髓鞘病变。在没有炎症反应的情况下，即使经过数月的持续感染，也没有明显的脱髓鞘现象。向感染和对照小鼠脑内注射抗SFV超免疫血清不会产生脱髓鞘，但会导致中枢神经系统组织变性并伴有明显的核固缩。
