[Neuronal apoptosis in the central and peripheral nervous system in HIV infection].

H Adle-Biassette, L Wingertsmann, F J Authier, H Kondo, F Poron, C Héry, J Bell, M Tardieu, R Gherardi, F Gray
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Abstract

Apart from the unique changes characteristic of "HIV encephalitis", the productive infection of central nervous system by HIV, which predominantly involves the white matter and basal ganglia, evidence is accumulating that the cerebral cortex may also be affected in AIDS patients. Neuronal loss, suspected at microscopic examination, has been demonstrated by a number of morphometric studies. However, the cause and mechanism of neuronal damage in HIV infection, are still unclear. In an attempt to look for an apoptotic process at the origin of neuronal loss in AIDS, we examined samples of frontal cortex, temporal cortex and basal ganglia from 12 patients who died from AIDS and 4 asymptomatic HIV-positive cases using in situ end labelling to demonstrate characteristic DNA fragmentation. These were compared with 5 asymptomatic seronegative controls, and 2 seronegative patients with Alzheimer's disease. We demonstrated neuronal apoptosis in all AIDS cases and in the Alzheimer's cases. Positive in situ end labelling was usually associated with morphological changes suggestive of neuronal apoptosis. Semiquantitative assessment of the density of apoptotic neurons showed that neuronal apoptosis was more severe in atrophic brains. In contrast, no correlation was found between the density of apoptotic neurons and the presence of HIV-encephalitis or a history of cognitive disorder. Only occasional apoptotic neurons were found in one asymptomatic, HIV-positive case. Apoptosis was never observed in asymptomatic seronegative cases. We also looked for apoptotic neurons in spinal ganglia of 20 AIDS cases, 5 of whom had a terminal sensory distal neuropathy, and 10 seronegative controls devoid of neuropathy. Apoptotic neurons were found in 6 of the AIDS patients and in none of the seronegative controls. However, no correlation was found between the severity of neuronal apoptosis in the spinal root ganglia and the presence of absence of a terminal distal sensory neuropathy. Experimental studies tend to support our in vivo findings. HIV-infection of primary cultures of human embryonic central nervous system induced frequent apoptosis of neurons. No apoptotic cell was identified in non infected control cultures.

[HIV感染中中枢和周围神经系统的神经元凋亡]。
除了“艾滋病毒脑炎”特有的变化,即主要累及白质和基底神经节的中枢神经系统的艾滋病毒生产性感染外,越来越多的证据表明,艾滋病患者的大脑皮层也可能受到影响。在显微镜检查中怀疑的神经元丢失,已经被许多形态计量学研究证实。然而,HIV感染中神经元损伤的原因和机制尚不清楚。为了寻找艾滋病中神经元丢失起源的凋亡过程,我们使用原位末端标记法检测了12名死于艾滋病的患者和4名无症状hiv阳性患者的额叶皮层、颞叶皮层和基底神经节样本,以证明其特征DNA片段化。这些患者与5名无症状血清阴性对照者和2名血清阴性阿尔茨海默病患者进行比较。我们在所有艾滋病病例和阿尔茨海默病病例中证实了神经元凋亡。原位末端标记阳性通常伴有提示神经元凋亡的形态学改变。凋亡神经元密度的半定量分析表明,萎缩脑组织中神经元凋亡更为严重。相反,凋亡神经元的密度与hiv脑炎的存在或认知障碍史之间没有相关性。在一例无症状的hiv阳性病例中,仅发现偶有凋亡的神经元。在无症状的血清阴性病例中未观察到细胞凋亡。我们还在20例艾滋病患者的脊髓神经节中寻找凋亡神经元,其中5例有终末感觉远端神经病变,10例无神经病变的血清阴性对照。6例艾滋病患者出现神经元凋亡,血清阴性对照组无细胞凋亡。然而,脊髓根神经节中神经元凋亡的严重程度与末端远端感觉神经病变的存在无相关性。实验研究倾向于支持我们在体内的发现。人胚胎中枢神经系统原代培养物感染hiv可引起神经元频繁凋亡。在未感染的对照培养中未发现凋亡细胞。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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