DNA repair in HIV-1 infection: a case for inhibitors of cellular co-factors?

• 影响指数: 1.341
• 发表时间: Oct 2006
• 来源期刊: Curr HIV Res
• DOI: 10.2174/157016206778560027
• PMID: 17073616
• 文章类型: Journal Article
• 中科院分区: Q4
• 方向: 医学
• 作者列表: Daniel R

Mesh: Animals; Anti-HIV Agents / pharmacology; Ataxia Telangiectasia Mutated Proteins; Cell Cycle Proteins / antagonists & inhibitors metabolism; Cell Line; DNA Breaks, Double-Stranded / drug effects; DNA Repair / drug effects; DNA, Viral / drug effects metabolism; DNA-Activated Protein Kinase / antagonists & inhibitors metabolism; DNA-Binding Proteins / antagonists & inhibitors metabolism; Drug Design; HIV Infections / drug therapy virology; HIV-1 / drug effects genetics pathogenicity physiology; Humans; Mice; Mice, SCID; Nuclear Proteins / antagonists & inhibitors metabolism; Protein Kinases / drug effects metabolism; Protein Serine-Threonine Kinases / antagonists & inhibitors metabolism; Tumor Suppressor Proteins / antagonists & inhibitors metabolism; Virus Integration

Abstract

At each step of its life-cycle, human immunodeficiency virus type 1 (HIV-1) interacts with cellular proteins. In some cases, such as the cellular cytidine deaminase APOBEC3G, cellular proteins repress HIV-1 replication. In other cases, cellular proteins serve as essential co-factors, and inhibition of their function blocks HIV-1 replication. This review explores the opportunities for anti-HIV-1 therapy that stem from the recent discoveries that cellular proteins, which are involved in double-strand break DNA repair, are also required for completion of integration of HIV-1 DNA into host cell DNA.