HCV NS3/4A protein activates HIV-1 transcription from its long terminal repeat.

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.