Yoshioka M, Itoyama Y
Neurology Service, National Iwate Hospital.
Nihon Rinsho. 1994 Nov;52(11):2912-8.
Impairment of the central nervous system (CNS) and peripheral nervous system (PNS) is common during the human immunodeficiency virus type 1 (HIV-1) infection. There are evidences of activated immune reactions in the CNS and PNS of patients with acquired immunodeficiency syndrome (AIDS). The expression of HIV-1 predominantly in monocyte/macrophage lineage cells strongly suggests immunopathogenetic mechanisms. Possible mechanisms of neuronal and glial cell damage include calcium dependent excitotoxicity by HIV-1 envelope protein, N-methyl-D-aspartate (NMDA) receptor-mediated neurotoxicity of quinolinic acid, injury of oligodendrocytes by tumor necrosis factor--alpha, cell injury by HIV-1-specific cytotoxic T cells, and apoptosis of oligodendrocytes or neurons. These mechanisms are not mutually exclusive. Multiple factors may be involved in the pathogenesis of HIV-1-associated neurological diseases.
在人类免疫缺陷病毒1型（HIV-1）感染期间，中枢神经系统（CNS）和周围神经系统（PNS）受损很常见。有证据表明，获得性免疫缺陷综合征（AIDS）患者的中枢神经系统和周围神经系统存在免疫反应激活。HIV-1主要在单核细胞/巨噬细胞谱系细胞中表达，这强烈提示了免疫发病机制。神经元和神经胶质细胞损伤的可能机制包括HIV-1包膜蛋白引起的钙依赖性兴奋性毒性、喹啉酸的N-甲基-D-天冬氨酸（NMDA）受体介导的神经毒性、肿瘤坏死因子-α对少突胶质细胞的损伤、HIV-1特异性细胞毒性T细胞引起的细胞损伤以及少突胶质细胞或神经元的凋亡。这些机制并非相互排斥。多种因素可能参与HIV-1相关神经疾病的发病机制。
