Impact of mitochondrial regulation of apoptosis on the pathogenesis and treatment of HIV-1-induced immunodeficiency

被引:9
作者
Buenz, EJ
Badley, AD
机构
[1] Mayo Clin & Mayo Fdn, Coll Med, Div Infect Dis, Program Translat Immunovirol & Biodef, Rochester, MN 55905 USA
[2] Mayo Clin & Mayo Fdn, Coll Med, Mol Neurosci Program, Rochester, MN 55905 USA
关键词
HIV; apoptosis; mitochondria;
D O I
10.1016/j.mito.2004.05.017
中图分类号
Q2 [细胞生物学];
学科分类号
071009 [细胞生物学]; 090102 [作物遗传育种];
摘要
HIV-1 infection causes the depletion of CD4 T cells, which results in AIDS. There are numerous potential mechanisms by which this cell death can occur, and a majority of the molecular mechanisms involve the mitochondria. Furthermore, current HIV therapies also have an impact on mitochondrial stability. The alteration in apoptotic homeostasis induced by HIV, HIV proteins, the host response to HIV infection and/or HIV therapies either promote apoptosis or inhibit apoptotic signals depending on the cellular context. Latent HIV reservoirs prevent the eradication of the virus because these cells are resistant to apoptosis: a change potentially induced at the level of the mitochondria. Many of the novel treatment strategies aimed at eradicating the virus involve alterations of mitochondrial regulation of apoptosis. (C) 2004 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
引用
收藏
页码:235 / 254
页数:20
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