Dhillon Navneet Kaur, Williams Rachel, Callen Shannon, Zien Chris, Narayan Opendra, Buch Shilpa
Molecular and Integrative Physiology Department, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Front Biosci. 2008 May 1;13:3913-8. doi: 10.2741/2979.
The encephalopathy caused by HIV, known clinically as HIV-associated dementia (HAD) and pathologically as HIV encephalitis (HIVE), results from intense infiltration of mononuclear cells, productive replication of the virus in monocyte-derived macrophages/microglia, abortive replication in astrocytes and activation of macrophages/microglia and astrocytes leading to neuronal degeneration in the brains of infected persons. Recent findings have suggested that development of HAD is based more on the activation process than on direct evidence of virus replication in the brain. Since HAD is based on the encephalitic process, major studies have been directed to the mechanisms regulating the inflammatory process. Monocyte chemoattractant protein 1, MCP-1, is a chemokine that is implicated in this process and also in the development of activation in the brain. In this review, we have attempted to identify mechanisms that induce expression of MCP-1 in the brain and the role that it plays in recruitment of mononuclear cells from blood to brain and in the activation processes of inflammatory and neural cells that lead to development of degenerative changes in the neuronal population.
由人类免疫缺陷病毒（HIV）引起的脑病，临床上称为HIV相关痴呆（HAD），病理上称为HIV脑炎（HIVE），是由单核细胞的强烈浸润、病毒在单核细胞衍生的巨噬细胞/小胶质细胞中的有效复制、在星形胶质细胞中的流产性复制以及巨噬细胞/小胶质细胞和星形胶质细胞的激活导致感染者大脑中的神经元变性所致。最近的研究结果表明，HAD的发展更多地基于激活过程，而不是大脑中病毒复制的直接证据。由于HAD基于脑炎过程，主要研究方向是调节炎症过程的机制。单核细胞趋化蛋白1（MCP-1）是一种趋化因子，参与这一过程以及大脑中的激活发展。在这篇综述中，我们试图确定诱导大脑中MCP-1表达的机制，以及它在将单核细胞从血液招募到大脑以及在导致神经元群体发生退行性变化的炎症和神经细胞激活过程中所起的作用。
