Abstract
Approximately 30-40% of patients infected with the human immunodeficiency virus (HIV) in the U.S. are also infected with the hepatitis C virus (HCV). Studies have shown that HIV can worsen hepatitis C, while the impact of hepatitis C on HIV disease is less clear. In this study, we described that HCV NS3/4A protein can activate HIV-1 transcription from its long terminal repeat (LTR) region, while the serine protease-inactive mutant of NS3/4A fails to do so. The activation effect of NS3/4A to HIV-1 transcription can be explained by its ability to enhance DNA binding activities of the transcription factor AP-1. These results have provided insights into the mechanism involved in the co-infection of HCV and HIV.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Carrier Proteins / genetics
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Carrier Proteins / metabolism*
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Cell Line
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Gene Expression Regulation, Viral*
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Genes, Reporter
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HIV Infections / virology
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HIV Long Terminal Repeat*
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HIV-1 / genetics*
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Hepacivirus / genetics
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Hepacivirus / metabolism*
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Hepatitis C / complications
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Hepatitis C / virology*
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Humans
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Intracellular Signaling Peptides and Proteins
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Mutation
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Serine Endopeptidases / genetics
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Serine Endopeptidases / metabolism
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Transcription Factor AP-1 / genetics
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Transcription Factor AP-1 / metabolism
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Transcription, Genetic*
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Viral Nonstructural Proteins / genetics
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Viral Nonstructural Proteins / metabolism*
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Viral Proteins / genetics
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Viral Proteins / metabolism*
Substances
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Carrier Proteins
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Intracellular Signaling Peptides and Proteins
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NS3 protein, hepatitis C virus
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NS4A cofactor peptide, Hepatitis C virus
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Transcription Factor AP-1
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Viral Nonstructural Proteins
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Viral Proteins
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Serine Endopeptidases