Price R W, Brew B, Sidtis J, Rosenblum M, Scheck A C, Cleary P
Department of Neurology, Memorial Hospital, New York, NY 10021.
Science. 1988 Feb 5;239(4840):586-92. doi: 10.1126/science.3277272.
Infection with human immunodeficiency virus type 1 (HIV-1) is frequently complicated in its late stages by the AIDS dementia complex, a neurological syndrome characterized by abnormalities in cognition, motor performance, and behavior. This dementia is due partially or wholly to a direct effect of the virus on the brain rather than to opportunistic infection, but its pathogenesis is not well understood. Productive HIV-1 brain infection is detected only in a subset of patients and is confined largely or exclusively to macrophages, microglia, and derivative multinucleated cells that are formed by virus-induced cell fusion. Absence of cytolytic infection of neurons, oligodentrocytes, and astrocytes has focused attention on the possible role of indirect mechanisms of brain dysfunction related to either virus or cell-coded toxins. Delayed development of the AIDS dementia complex, despite both early exposure of the nervous system to HIV-1 and chronic leptomeningeal infection, indicates that although this virus is "neurotropic," it is relatively nonpathogenic for the brain in the absence of immunosuppression. Within the context of the permissive effect of immunosuppression, genetic changes in HIV-1 may underlie the neuropathological heterogeneity of the AIDS dementia complex and its relatively independent course in relation to the systemic manifestations of AIDS noted in some patients.
1型人类免疫缺陷病毒（HIV-1）感染在晚期常并发艾滋病痴呆综合征，这是一种以认知、运动表现和行为异常为特征的神经综合征。这种痴呆部分或完全归因于病毒对大脑的直接作用，而非机会性感染，但其发病机制尚不清楚。仅在一部分患者中检测到HIV-1在大脑中的有效感染，且主要或仅局限于巨噬细胞、小胶质细胞以及由病毒诱导的细胞融合形成的衍生多核细胞。神经元、少突胶质细胞和星形胶质细胞未出现溶细胞性感染，这使得人们将注意力集中在与病毒或细胞编码毒素相关的脑功能障碍间接机制的可能作用上。尽管神经系统早期接触HIV-1且存在慢性软脑膜感染，但艾滋病痴呆综合征仍发展较晚，这表明尽管这种病毒具有“嗜神经性”，但在没有免疫抑制的情况下，它对大脑相对无致病性。在免疫抑制的允许作用背景下，HIV-1的基因变化可能是艾滋病痴呆综合征神经病理学异质性及其在一些患者中相对于艾滋病全身表现的相对独立病程的基础。
