The HIV envelope protein gp120 in the nervous system -: Interactions with nitric oxide, interleukin-1β and nerve growth factor signalling, with pathological implications in vivo and in vitro
The HIV envelope protein gp120 in the nervous system -: Interactions with nitric oxide, interleukin-1β and nerve growth factor signalling, with pathological implications in vivo and in vitro
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DOI：
10.1016/s0006-2952(98)00044-6
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发表时间：
1998-07-15
影响因子：
5.8
通讯作者：
Nisticò, G
中科院分区：
文献类型：
--
作者：
Corasaniti, MT;Bagetta, G;Nisticò, G
通常描述的神经元损失在死后在患有艾滋病的患者的大脑新皮层已被提出负责艾滋病痴呆综合症的发展。HIV病毒的神经侵袭性毒株感染巨噬细胞、小胶质细胞和多核巨细胞，但不感染神经元;骨髓单核细胞谱系的细胞对病毒的加工产生病毒产物，已知其启动复杂的事件网络，可能导致神经元死亡和AIDS相关神经综合征的发展。特别是HIV-1外壳蛋白gp 120，已被认为阿萨所述神经元缺失的可能病原体，因为它导致培养中神经元的死亡。最近，已经表明，脑室内注射gp 120引起的大鼠脑皮质细胞死亡通过细胞凋亡发生。这一观察结果拓宽了我们对所报道的神经元细胞损失的病理生理学的了解，并为开发治疗患有艾滋病相关神经综合征的患者的新治疗策略开辟了实验研究的新途径。(C)1998年爱思唯尔科学公司
The neuronal loss often described at post-mortem in the brain neocortex of patients suffering from AIDS has been proposed to be responsible for the development of the AIDS dementia complex. Neuroinvasive strains of the HIV virus infect macrophages, microglial cells, and multinucleated giant cells, but not neurones; Processing of the virus by cells of the myelomonocytic lineage yields viral produces known to initiate a complex network of events that may lead to the death of neurones and to the development of AIDS-associated neurological syndrome. The HIV-1 coat protein gp120, in particular, has been proposed asa likely etiologic agent of the described neuronal loss because it causes the death of neurones in culture. More recently, it has been shown that brain cortical cell death caused in rats by intracerebroventricular injection of gp120 occurs via apoptosis. This observation broadens our knowledge of the pathophysiology of the reported neuronal cell loss and opens a new avenue of experimental research for the development of novel therapeutic strategies for the treatment of patients suffering from AIDS-associated neurological syndrome. (C) 1998 Elsevier Science Inc.