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Suppression of interferon-related promoter activation by hepatitis C virus proteins expressed in cultured cells

Akira Hiramatsu1, Bin Gotoh, Yutaka Fujii

  • 1Department of Virology, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima 734-8551, Japan.

Hiroshima Journal of Medical Sciences
|September 26, 2006
PubMed

Insights

Hepatitis C virus (HCV) proteins core, E1, NS4A, and NS4B can block the host's interferon antiviral response. This suggests multiple viral proteins contribute to interferon antagonism, with E1 and NS4B playing potentially novel roles.

Area of Science:

  • Virology
  • Immunology
  • Hepatitis C Research

Background:

  • Interferon is crucial for host antiviral defense.
  • Hepatitis C virus (HCV) proteins E2, NS3/4A, and NS5A are known to interfere with interferon's antiviral activity.
  • The specific roles of individual HCV proteins in counteracting interferon remain unclear.

Purpose of the Study:

  • To investigate the effects of individual HCV-K proteins on interferon signal transduction.
  • To identify which HCV proteins antagonize the host's interferon response.
  • To explore potential novel roles of HCV E1 and NS4B proteins in interferon antagonism.

Main Methods:

  • Isolation of an HCV strain (HCV-K) from an acute hepatitis patient.
  • Nucleotide sequencing of the entire genomic DNA of HCV-K, identifying it as genotype 1b.
  • Expression of individual HCV-K proteins in mammalian cells.
  • Assessment of the impact of expressed proteins on interferon signal transduction pathways, including ISRE and GAS reporter activation.

Main Results:

  • The core, E1, NS4A, and NS4B proteins of HCV-K were found to suppress the activation of interferon stimulation responsive element (ISRE) and gamma activation sequence (GAS) reporters.
  • These findings indicate that multiple HCV proteins possess the ability to inhibit interferon-induced antiviral effects.
  • The study highlights a potential novel role for E1 and NS4B proteins in HCV's strategy to antagonize interferon.

Conclusions:

  • Multiple hepatitis C virus proteins, including core, E1, NS4A, and NS4B, actively suppress the host's interferon-mediated antiviral defenses.
  • The findings suggest a complex interplay where various viral components contribute to overcoming interferon's action.
  • This research points to a potentially novel function for HCV E1 and NS4B proteins in evading the host immune response through interferon antagonism.

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