Role of cellular iron and oxygen in the regulation of HIV-1 infection

被引：35

作者：

Nekhai, Sergei ^{[1
]}

Kumari, Namita ^{[1
]}

Dhawan, Subhash ^{[2
]}

机构：

[1] Howard Univ, Dept Med, Ctr Sickle Cell Dis, Washington, DC 20059 USA

[2] US FDA, Div Emerging & Transfus Transmitted Dis, Ctr Biol Evaluat & Res, Bethesda, MD 20014 USA

来源：

FUTURE VIROLOGY | 2013年 / 8卷 / 03期

关键词：

CDK2; CDK9; HIV-1; hypoxia; iron chelators; protein phosphatase-1; Tat; HUMAN-IMMUNODEFICIENCY-VIRUS; DEPENDENT KINASE INHIBITORS; P-TEFB; GENE-EXPRESSION; TRANSCRIPTION-ELONGATION; INTRACELLULAR IRON; 7SK SNRNP; BLOOD-CELLS; PROTEIN; TAT;

D O I：

10.2217/FVL.13.6

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Despite efficient antiretroviral therapy, eradication of HIV-1 infection is challenging and requires novel biological insights and therapeutic strategies. Among other physiological and environmental factors, intracellular iron greatly affects HIV-1 replication. Higher iron stores were shown to be associated with faster progression of HIV-1 infection and to inversely correlate with the survival of HIV-1 infected patients. Iron is required for several steps in the HIV-1 life cycle, including reverse transcription, HIV-1 gene expression and capsid assembly. Here, the authors present a comprehensive review of the molecular mechanisms involved in iron- and oxygen-mediated regulation of HIV-1 replication. We also propose key intracellular pathways that may be involved in regulating HIV-1 replication via protein kinase complexes, CDK9/cyclin T1 and CDK2/cyclin E, protein phosphatase-1 and other host factors.

引用

页码：301 / 311

页数：11

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