Hoffman P M, Pitts O M, Bilello J A, Cimino E F
Research Service, Veterans Administration Medical Center, Baltimore, MD 21218.
Rev Neurol (Paris). 1988;144(11):676-9.
Neurotropic retroviruses are capable of infecting and altering the function of dividing populations of neuron-like cells such as the PC-12 cell line. However, histological, immunohistochemical, and ultrastructural studies have failed to implicate direct infection of neurons by MuLV as the etiologic mechanism responsible for MuLV induced neurodegenerative disease. Indirect mechanisms such as the physical or biochemical disruption of endothelial cell basement membranes or the production of toxic cytokines by virus infected cells may play a role in the development of retrovirus induced neurodegeneration.
嗜神经逆转录病毒能够感染并改变诸如PC - 12细胞系等神经元样细胞分裂群体的功能。然而，组织学、免疫组织化学及超微结构研究未能证实莫洛尼鼠白血病病毒（MuLV）对神经元的直接感染是MuLV诱导神经退行性疾病的病因机制。诸如内皮细胞基底膜的物理或生化破坏，或病毒感染细胞产生毒性细胞因子等间接机制，可能在逆转录病毒诱导的神经退行性变的发展过程中发挥作用。
