Cortical consequences of HIV-1 Tat exposure in rats are enhanced by chronic cocaine.
Cortical consequences of HIV-1 Tat exposure in rats are enhanced by chronic cocaine.
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DOI：
10.2174/0929867322666150311164504
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发表时间：
2015
影响因子：
1
通讯作者：
Napier TC
中科院分区：
文献类型：
--
作者：
Wayman WN;Chen L;Persons AL;Napier TC
人类免疫缺陷病毒（HIV）血清阳性个体的寿命大大延长；然而，涉及中枢神经系统（CNS）的并发症仍然令人担忧。虽然 HIV 不直接感染神经元，但病毒产生的蛋白质，包括 HIV 转录反式激活因子 (Tat)，会从受感染的神经胶质细胞中释放出来；这些蛋白质可能具有神经毒性。这种神经毒性被认为介导了艾滋病毒相关神经损伤的病理学。可卡因滥用在艾滋病毒感染者中很常见，这种滥用会加剧与艾滋病毒相关的神经功能缺陷。慢性可卡因和 Tat 失调的大脑区域和病理生理机制是当前综述的重点。
The life span of individuals that are sero-positive for human immunodeficiency virus (HIV) has greatly improved; however, complications involving the central nervous system (CNS) remain a concern. While HIV does not directly infect neurons, the proteins produced by the virus, including HIV transactivator of transcription (Tat), are released from infected glia; these proteins can be neurotoxic. This neurotoxicity is thought to mediate the pathology underlying HIV-associated neurological impairments. Cocaine abuse is common among HIV infected individuals, and this abuse augments HIV-associated neurological deficits. The brain regions and pathophysiological mechanisms that are dysregulated by both chronic cocaine and Tat are the focus of the current review.