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Hepatitis C virus variants circumventing cytotoxic T lymphocyte activity as a mechanism of chronicity

S L Tsai1, Y M Chen, M H Chen

  • 1Liver Research Unit, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taipei, Taiwan.

Gastroenterology
|September 30, 1998
PubMed

Insights

Hepatitis C virus (HCV) variants with altered peptide ligands emerged in patients who developed chronic infection, antagonizing cytotoxic T lymphocyte (CTL) activity. This suggests a limited T-cell receptor repertoire contributes to HCV chronicity.

Area of Science:

  • Immunology
  • Virology
  • Hepatology

Background:

  • High rates of chronic hepatitis C virus (HCV) infection are not fully explained by a multispecific cytotoxic T lymphocyte (CTL) response.
  • Investigating the role of viral variants in CTL activity is crucial for understanding HCV chronicity.

Purpose of the Study:

  • To examine the impact of HCV variants on CTL activity in patients with acute HCV infection.
  • To elucidate the mechanisms underlying the development of chronic HCV infection.

Main Methods:

  • Generation of CTL clones specific to a decapeptide epitope from HCV hypervariable region 1 in HLA-A2-positive patients.
  • In vitro stimulation with synthetic peptides and examination of sequential epitope changes and CTL recognition.

Main Results:

  • HCV variants with altered peptide ligands that antagonize CTL activity emerged in patients who developed chronic infection.
  • No variants were observed in patients who recovered from acute HCV.
  • CTL clones from chronic patients utilized specific T-cell receptor (TCR) genes (AV6 and BV17).

Conclusions:

  • A narrow T-cell repertoire responding to a single viral peptide/HLA ligand may be involved in HCV chronicity.
  • Emergence of HCV variants with altered peptide ligands acting as TCR antagonists, coupled with a limited TCR repertoire, may drive HCV chronicity.
Abstract

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