期刊
MICROBES AND INFECTION
卷 8, 期 5, 页码 1347-1357出版社
ELSEVIER
DOI: 10.1016/j.micinf.2005.11.014
关键词
apoptosis; CCL2; glutamate; NeuroAIDS; inflammation
资金
- NIAID NIH HHS [AI-051519] Funding Source: Medline
- NIGMS NIH HHS [5 T32 GM007288] Funding Source: Medline
- NIMH NIH HHS [MH0702297, MH52974, K01 MH076679] Funding Source: Medline
- NINDS NIH HHS [NS11920, NS07098] Funding Source: Medline
HIV tat is the transactivator of HIV-1, supporting efficient viral replication by stabilizing the transcription of viral genes. Tat can be released from HIV-infected cells and alter several functions in uninfected cells. In the brain, tat induces neuronal dysfunction/toxicity, even though neurons cannot be directly infected with HIV, resulting in CNS pathology, such as the dementia and encephalitis associated with NeuroAIDS. This review discusses the most recent data addressing tat-induced neurotoxicity and integrates these new findings in the context of NeuroAIDS. (c) 2006 Elsevier SAS. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据