Atkins G J, Sheahan B J, Mooney D A
Department of Microbiology, Moyne Institute, Trinity College, Dublin, Ireland.
Neuropathol Appl Neurobiol. 1990 Feb;16(1):57-68. doi: 10.1111/j.1365-2990.1990.tb00932.x.
The neurovirulent L10 strain of Semliki Forest virus (SFV) causes extensive neuronal damage in the central nervous system (CNS) of infected rats, and is probably the cause of death. The avirulent A7 and M9 strains do not cause extensive neuronal damage, but do induce immune-mediated CNS demyelination. In primary CNS cell cultures derived from rats, L10 multiplies more rapidly in neurons than avirulent strains, but infection with both virulent and avirulent strains causes depletion of oligodendrocytes from mixed glial cell cultures. It is proposed that the immune-mediated demyelination, which follows infection with avirulent strains, is induced by phagocytosis of myelin debris from infected oligodendrocytes, and the presentation of antigens derived from such debris to T-helper lymphocytes. Based on these and previous results, a scheme for the pathogenicity of defined strains of SFV is proposed. The applicability of this scheme to the understanding of human demyelinating disease such as multiple sclerosis is discussed.
塞姆利基森林病毒（SFV）的神经毒力L10株可在受感染大鼠的中枢神经系统（CNS）中造成广泛的神经元损伤，这可能是导致死亡的原因。无毒力的A7和M9株不会造成广泛的神经元损伤，但会引发免疫介导的中枢神经系统脱髓鞘。在源自大鼠的原代中枢神经系统细胞培养物中，L10在神经元中的增殖速度比无毒力株更快，但强毒株和无毒力株的感染都会导致混合神经胶质细胞培养物中的少突胶质细胞耗竭。有人提出，无毒力株感染后发生的免疫介导脱髓鞘是由受感染少突胶质细胞的髓鞘碎片被吞噬，以及此类碎片衍生的抗原呈递给辅助性T淋巴细胞所诱导的。基于这些及先前的结果，提出了一个关于特定SFV毒株致病性的方案。讨论了该方案在理解人类脱髓鞘疾病如多发性硬化症方面的适用性。
