Microglia in human disease, with an emphasis on acquired immune deficiency syndrome.
Microglia in human disease, with an emphasis on acquired immune deficiency syndrome.
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发表时间：
1991-02
期刊：
影响因子：
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通讯作者：
Dennis W. Dickson;L. Mattiace;K. Kure;Kenneth D. Hutchins;W. D. Lyman;Celia F. Brosnan
中科院分区：
文献类型：
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作者：
Dennis W. Dickson;L. Mattiace;K. Kure;Kenneth D. Hutchins;W. D. Lyman;Celia F. Brosnan
总之，有压倒性的证据表明，中枢神经系统内活跃的 HIV-1 感染的主要部位是小胶质细胞。中枢神经系统感染可能与单核细胞（小胶质细胞周转）对中枢神经系统的正常再增殖有关，单核细胞将潜伏感染带入中枢神经系统。病毒感染的激活可能取决于小胶质细胞分化、可溶性因子（细胞因子）和/或共存感染。小胶质细胞的感染可能会扰乱小胶质细胞与其他胶质细胞之间以及小胶质细胞与神经元之间存在的正常止血平衡，这些过程最近才在分子水平上进行探索。 HIV 感染小胶质细胞可能对突触完整性的影响尚不清楚。细胞因子似乎是小胶质细胞感染对其他中枢神经系统细胞、髓磷脂和内皮细胞的一些不利影响的主要候选介质。
In conclusion, there is overwhelming evidence that within the CNS the primary sites of active HIV-1 infection are microglia. CNS infection may be related to the normal repopulation of the CNS by monocytes (microglial turnover) that carry latent infection into the CNS. Activation of viral infection may depend upon microglial differentiation, soluble factors (cytokines), and/or coexistent infections. Infection of microglia may disturb the normal hemostatic balance that exists between microglia and other glia, and between microglia and neurons, processes that are only recently being explored at the molecular level. The impact that HIV infection of microglia may have on synaptic integrity is unknown. Cytokines appear to be prime candidates as mediators of some of the adverse effects of microglial infection on other CNS cells, myelin and endothelial cells.