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.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Animals
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Anti-HIV Agents / pharmacology*
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Ataxia Telangiectasia Mutated Proteins
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Cell Cycle Proteins / antagonists & inhibitors
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Cell Cycle Proteins / metabolism
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Cell Line
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DNA Breaks, Double-Stranded / drug effects*
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DNA Repair / drug effects*
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DNA, Viral / drug effects
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DNA, Viral / metabolism*
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DNA-Activated Protein Kinase / antagonists & inhibitors
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DNA-Activated Protein Kinase / metabolism
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DNA-Binding Proteins / antagonists & inhibitors
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DNA-Binding Proteins / metabolism
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Drug Design
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HIV Infections / drug therapy
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HIV Infections / virology*
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HIV-1 / drug effects*
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HIV-1 / genetics
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HIV-1 / pathogenicity
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HIV-1 / physiology
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Humans
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Mice
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Mice, SCID
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Nuclear Proteins / antagonists & inhibitors
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Nuclear Proteins / metabolism
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Protein Kinases / drug effects*
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Protein Kinases / metabolism
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Protein Serine-Threonine Kinases / antagonists & inhibitors
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Protein Serine-Threonine Kinases / metabolism
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Tumor Suppressor Proteins / antagonists & inhibitors
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Tumor Suppressor Proteins / metabolism
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Virus Integration*
Substances
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Anti-HIV Agents
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Cell Cycle Proteins
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DNA, Viral
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DNA-Binding Proteins
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Nuclear Proteins
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Tumor Suppressor Proteins
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Protein Kinases
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ATM protein, human
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ATR protein, human
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Ataxia Telangiectasia Mutated Proteins
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Atm protein, mouse
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DNA-Activated Protein Kinase
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Protein Serine-Threonine Kinases