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首页> 外文期刊>AIDS Research and Human Retroviruses >Differential induction of rat neuronal excitotoxic cell death by human immunodeficiency virus type 1 clade B and C tat proteins.
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Differential induction of rat neuronal excitotoxic cell death by human immunodeficiency virus type 1 clade B and C tat proteins.

机译：人免疫缺陷病毒1型进化枝B和C tat蛋白差异诱导大鼠神经元兴奋性毒性细胞死亡。

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In the absence of effective antiretroviral therapy, infection with clade B human immunodeficiency virus (HIV-1) infection commonly progresses to AIDS dementia. However, in India, where clade C infection is most prevalent, severe cognitive impairment due to HIV-1 is reported to be less prevalent. The Tat protein of HIV-1, which is released from HIV-1-infected macrophages, is thought to play a major role in the disruption of neuronal function as well as in the infiltration of macrophages associated with advanced neuropathogenesis. Clade B Tat is excitotoxic to hippocampal neurons by potentiating N-methyl-d-aspartate-induced currents of the zinc-sensitive NR1/NR2A N-methyl-d-aspartate receptor in a zinc-binding-dependent mechanism. This study characterizes the zinc-binding properties of clade C Tat protein. Using ultraviolet spectroscopy and the Ellman reaction, we show that clade C Tat protein binds just one zinc ion per monomer. We then investigated the ability of clade C Tat to block the inhibition of N-methyl-d-aspartate receptors from zinc antagonism through ion chelation. Although clade C Tat enhanced N-methyl-d-aspartate-mediated rat hippocampus neuronal toxicity in the presence of zinc, the increase was significantly less than that observed with clade B Tat. These findings suggest that the observed differences in neuropathogenesis found with HIV-1 clade C infection compared to clade B may, in part, be due to a decrease in Tat-mediated neurotoxicity.
机译：在缺乏有效的抗逆转录病毒疗法的情况下，进化枝B型人免疫缺陷病毒（HIV-1）感染通常会发展为AIDS痴呆症。但是，在印度，进化枝C感染最为普遍，据报道，由HIV-1引起的严重认知障碍的发生率较低。从感染HIV-1的巨噬细胞释放的HIV-1的Tat蛋白被认为在破坏神经元功能以及巨噬细胞浸润相关的主要神经病中起主要作用。 Clade B Tat通过以锌结合依赖性机制增强锌敏感的NR1 / NR2A N-甲基-d-天冬氨酸受体的N-甲基-d-天冬氨酸诱导的电流，对海马神经元具有兴奋性毒性。这项研究的特点是进化枝C Tat蛋白的锌结合特性。使用紫外光谱和Ellman反应，我们显示进化枝C Tat蛋白每个单体仅结合一个锌离子。然后，我们研究了进化枝C Tat通过离子螯合阻止N-甲基-d-天冬氨酸受体对锌拮抗作用的抑制作用。尽管在存在锌的情况下，进化枝C Tat增强了N-甲基-d-天冬氨酸介导的大鼠海马神经元毒性，但其增加量明显小于进化枝B Tat所观察到的。这些发现表明，与进化枝B相比，HIV-1进化枝C感染所发现的神经病理学差异可能部分归因于Tat介导的神经毒性的降低。

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