慢性可卡因会增强大鼠暴露于HIV-1反式激活因子（Tat）后的皮质影响。
Cortical consequences of HIV-1 Tat exposure in rats are enhanced by chronic cocaine.
作者信息
Wayman Wesley N, Chen Lihua, Persons Amanda L, Napier T Celeste
机构信息
Department of Pharmacology, Rush University Medical Center, 1735 W. Harrison Street, Cohn Research Building, Rm. 463, Chicago, IL 60612, USA.
出版信息
Curr HIV Res. 2015;13(1):80-7. doi: 10.2174/0929867322666150311164504.
Abstract
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 HIVassociated 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.
摘要
人类免疫缺陷病毒（HIV）血清呈阳性个体的寿命已大幅延长；然而，涉及中枢神经系统（CNS）的并发症仍然令人担忧。虽然HIV不会直接感染神经元，但病毒产生的蛋白质，包括HIV转录激活因子（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HIV相关神经损伤的病理过程。可卡因滥用在HIV感染者中很常见，这种滥用会加剧HIV相关的神经缺陷。慢性可卡因和Tat共同导致失调的脑区和病理生理机制是本综述的重点。
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