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

Xiaoyun Wu1, Musarat Ishaq, Jiajie Hu

  • 1State Key Laboratory of Virology and the Modern Virology Research Center, College of Life Sciences, Wuhan University, Wuhan 430072, PR China.

Virus Research
|April 25, 2008
PubMed

Insights

Hepatitis C virus (HCV) protein NS3/4A activates human immunodeficiency virus (HIV-1) transcription. This activation occurs by enhancing the DNA binding of the transcription factor AP-1, offering insights into HIV-HCV co-infection mechanisms.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Co-infection with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) is common, affecting 30-40% of US HIV patients.
  • While HIV exacerbates HCV, the impact of HCV on HIV disease progression remains less understood.

Purpose of the Study:

  • To investigate the molecular mechanisms by which HCV influences HIV-1 transcription.

Main Methods:

  • The study examined the effect of the HCV NS3/4A protein on HIV-1 transcription from its long terminal repeat (LTR) region.
  • A serine protease-inactive mutant of NS3/4A was used to determine the role of protease activity.
  • The impact of NS3/4A on the DNA binding activity of the transcription factor AP-1 was assessed.

Main Results:

  • The active HCV NS3/4A protein significantly activated HIV-1 transcription.
  • A mutant NS3/4A lacking serine protease activity failed to activate HIV-1 transcription.
  • NS3/4A enhanced the DNA binding activity of AP-1, suggesting a mechanism for HIV-1 activation.

Conclusions:

  • The HCV NS3/4A serine protease plays a critical role in activating HIV-1 transcription.
  • Enhanced AP-1 DNA binding is a key mechanism through which HCV NS3/4A influences HIV-1.
  • These findings provide crucial insights into the pathogenesis of HIV-HCV co-infection.

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