Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA.
J Neurovirol. 2011 Feb;17(1):58-62. doi: 10.1007/s13365-010-0004-3. Epub 2010 Nov 30.
In the central nervous system, chemokines are primarily mediators of inflammatory processes. Their receptors, in particular, CXCR4 and CCR5, serve as co-factors along with CD4 that permit Human immunodeficiency virus-1 (HIV) infection. Moreover, experimental evidence has shown that CXCR4 and CCR5 mediate the neurotoxic effects of the HIV envelope protein gp120, suggesting that these receptors could also promote the neuropathogenesis observed in HIV-positive individuals. Therefore, a better understanding of the molecular mechanisms governing the expression of chemokine receptors in the brain may lead to improved therapies that reduce HIV neurotoxicity. This study presents evidence that the expression of chemokine receptors in the brain is modulated by two neurotrophins in an area-specific manner. This new evidence suggests that the neurotrophins may be an adjunct therapy to reduce HIV-mediated neuronal injury evoked by chemokine receptor activation.
在中枢神经系统中，趋化因子主要是炎症过程的介质。趋化因子的受体，特别是 CXCR4 和 CCR5，与 CD4 一起作为辅助因子，允许人类免疫缺陷病毒-1（HIV）感染。此外，实验证据表明，CXCR4 和 CCR5 介导 HIV 包膜蛋白 gp120 的神经毒性作用，这表明这些受体也可能促进 HIV 阳性个体中观察到的神经病变发生。因此，更好地了解控制大脑中趋化因子受体表达的分子机制可能会导致改善治疗方法，减少 HIV 神经毒性。本研究提供的证据表明，两种神经营养因子以特定于区域的方式调节大脑中趋化因子受体的表达。这一新证据表明，神经营养因子可能是一种辅助治疗方法，可减少趋化因子受体激活引起的 HIV 介导的神经元损伤。
