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T细胞凋亡导致HIV-1 vpr基因转基因小鼠外周T细胞耗竭。

T cell apoptosis causes peripheral T cell depletion in mice transgenic for the HIV-1 vpr gene.

作者信息

Yasuda J, Miyao T, Kamata M, Aida Y, Iwakura Y

机构信息

Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.

出版信息

Virology. 2001 Jul 5;285(2):181-92. doi: 10.1006/viro.2001.0964.

Abstract

Vpr, an accessory protein of HIV, is known to affect viral replication as well as cell growth, differentiation, and apoptosis in vitro. To investigate its pathogenicity in vivo, we have produced mice transgenic for the HIV-1 vpr gene with the CD4 enhancer/promoter. Interestingly, apoptotic death of T lymphocytes was enhanced in those mice, causing marked reduction of T cells in lymphatic organs and peripheral blood. Involvement of Bcl-x, Bax, and Caspase-1, but not of the Fas-Fas ligand system, was suggested in the apoptotic processes. These observations suggest that Vpr is involved in the pathogenesis of T cell depletion in HIV-infected people.

摘要

Vpr是HIV的一种辅助蛋白,已知它在体外会影响病毒复制以及细胞生长、分化和凋亡。为了研究其在体内的致病性,我们利用CD4增强子/启动子制备了携带HIV-1 vpr基因的转基因小鼠。有趣的是,这些小鼠中T淋巴细胞的凋亡死亡增强,导致淋巴器官和外周血中的T细胞显著减少。凋亡过程提示Bcl-x、Bax和Caspase-1参与其中,但Fas-Fas配体系统未参与。这些观察结果表明,Vpr参与了HIV感染人群中T细胞耗竭的发病机制。

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