AIDS DEMENTIA COMPLEX AND HIV-1 BRAIN INFECTION - CLINICAL-VIROLOGICAL CORRELATIONS
AIDS DEMENTIA COMPLEX AND HIV-1 BRAIN INFECTION - CLINICAL-VIROLOGICAL CORRELATIONS
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DOI：
10.1002/ana.410380404
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发表时间：
1995-10-01
影响因子：
11.2
通讯作者：
PRICE, RW
中科院分区：
文献类型：
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作者：
BREW, BJ;ROSENBLUM, M;PRICE, RW
为了评估人类免疫缺陷病毒 1 型 (HIV-1) 中枢神经系统感染的存在和分布，我们使用免疫组织化学方法绘制了 55 名获得性免疫缺陷综合征 (AIDS) 尸检患者大脑中的 HIV-1 p24 核心蛋白图谱。在其中 40 名接受过艾滋病痴呆综合征 (ADC) 生前神经学评估的患者中，我们分析了病毒感染的严重程度与临床功能障碍之间的关系。在巨噬细胞和具有小胶质细胞以及多核细胞形态和免疫组织化学特征的细胞中检测到病毒抗原。抗原阳性细胞的分布优先涉及某些深部脑结构，特别是苍白球、其他基底节核和中央白质。总体而言，感染细胞的存在和频率与多核细胞脑炎的组织学结果高度相关，并且一般与临床 ADC 分期高度相关。然而，感染往往比患者临床功能障碍严重程度“预期”的更为有限：只有 61% 至少患有 ADC 1 期的患者具有可检测到的抗原，其中只有大约 30% 的脑切片呈抗原阳性。这些结果表明 ADC 的发病模型中，病毒或细胞编码的毒素会放大有限的脑部感染的影响。
To evaluate the presence and distribution of central nervous system infection by human immunodeficiency virus type 1 (HIV-1), we used immunohistochemical methods to map the HIV-1 p24 core protein in the brains of 55 autopsied patients with acquired immunodeficiency syndrome (AIDS). In a subset of 40 of these patients who had undergone antemortem neurological evaluation of the AIDS dementia complex (ADC), we analyzed the relation between the severities of the viral infection and clinical dysfunction. Viral antigen was detected in macrophages and cells with morphological and immunohistochemical characteristics of microglia as well as multinucleated cells. The distribution of antigen-positive cells preferentially involved certain deep brain structures, especially the globus pallidus, other basal ganglia nuclei, and the central white matter. Overall, the presence and frequency of infected cells were highly correlated with the histological findings of multinucleated-cell encephalitis and in general with the clinical ADC stage, However, infection was often more limited than might be ''anticipated'' from the severity of patients' clinical dysfunction: Only 61% of patients with at least ADC stage 1 had detectable antigen and of these only approximately 30% of the brain sections were antigen positive, These results suggest a pathogenetic model of ADC where virus- or cell-coded toxins amplify the effect of limited brain infection.