Yoshioka M, Itoyama Y
Neurology Service, Mizusawa City Hospital.
Nihon Rinsho. 1997 Apr;55(4):897-903.
The neurologic disease most frequently seen during acquired immunodeficiency syndrome (AIDS) is AIDS dementia complex (ADC) or HIV encephalopathy, which is a direct consequence of HIV-1 infection of the central nervous system (CNS). A limited expression of HIV-1 in CNS and peripheral nervous system (PNS) tissue of AIDS patients in contrast to widespread functional and pathologic abnormalities suggests indirect or immunopathogenetic mechanisms of ADC and HIV-1-associated predominantly sensory neuropathy. Proposed mechanisms include injury of oligodendrocytes by tumor necrosis factor-alpha (TNF-alpha) released from macrophages, calcium dependent excitoneurotoxicity induced by gp120 HIV-1 envelope protein, N-methyl-D-aspartate (NMDA) receptor-mediated neurotoxicity by quinolinic acid, cell injury by HIV-1-specific cytotoxic T cells, and apoptosis of oligodendrocytes or neurons. The amplification of cellular activation by cytokine network and cell-to-cell contact between activated macrophages and neural cells by upregulation of adhesion molecules dramatically enhance toxic effect of macrophage products.
获得性免疫缺陷综合征（AIDS）期间最常出现的神经系统疾病是艾滋病痴呆综合征（ADC）或HIV脑病，这是HIV-1感染中枢神经系统（CNS）的直接后果。与广泛的功能和病理异常形成对比的是，AIDS患者的中枢神经系统和周围神经系统（PNS）组织中HIV-1表达有限，这提示了ADC和HIV-1相关的主要为感觉性神经病变的间接或免疫发病机制。提出的机制包括巨噬细胞释放的肿瘤坏死因子-α（TNF-α）对少突胶质细胞的损伤、gp120 HIV-1包膜蛋白诱导的钙依赖性兴奋性神经毒性、喹啉酸介导的N-甲基-D-天冬氨酸（NMDA）受体介导的神经毒性、HIV-1特异性细胞毒性T细胞导致的细胞损伤，以及少突胶质细胞或神经元的凋亡。细胞因子网络对细胞活化的放大作用，以及通过上调黏附分子使活化巨噬细胞与神经细胞之间的细胞间接触，显著增强了巨噬细胞产物的毒性作用。
