Magnitude of activity in chronic hepatitis C is influenced by apoptosis of T cells responsible for hepatitis C virus

J Gastroenterol Hepatol. 1999 Oct;14(10):1018-24. doi: 10.1046/j.1440-1746.1999.01993.x.

Abstract

Background: The mechanisms of hepatitis C virus (HCV) persistence are unknown, but down-regulation of immune response in a host is likely to play a major role in it.

Methods: To investigate whether T cell apoptosis contributes to such down-regulation, we compared peripheral T cell apoptosis in patients with chronic hepatitis C (CHC) with the serum titre of HCV-RNA, serum alanine aminotransferase (sALT) levels and its change, or peripheral T cell proliferation to the recombinant core antigen of HCV, JCC-1.

Results: The percentage of apoptosis in T cells was 0.30 +/- 0.31% (mean +/- SD) in 44 patients with CHC and 0.10 +/- 0.05% in 10 normal volunteers (P < 0.05). In patients with CHC there was no statistical correlation between apoptosis in T cells and sALT levels, titre of HCV-RNA or T cell proliferation to JCC-1 antigen. But, in patients showing relatively more apoptosis in T cells (more than mean + 2SD of apoptosis in T cells from normal volunteers), sALT levels decreased.

Conclusions: Thus, T cell apoptosis in patients with CHC is considered to cause a reduction in sALT, contributing to HCV persistence in patients with CHC.

MeSH terms

  • Alanine Transaminase / blood
  • Apoptosis / immunology*
  • Cell Division / drug effects
  • Cell Division / immunology
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Female
  • Hepacivirus / immunology*
  • Hepatitis C, Chronic / blood
  • Hepatitis C, Chronic / immunology*
  • Hepatitis C, Chronic / metabolism
  • Hepatitis C, Chronic / virology*
  • Humans
  • Lymphocyte Activation / drug effects
  • Lymphocyte Activation / immunology
  • Male
  • Middle Aged
  • RNA, Viral / blood
  • T-Lymphocytes / cytology
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism
  • Viral Core Proteins / immunology
  • Viral Core Proteins / pharmacology
  • Virus Latency / immunology
  • fas Receptor / biosynthesis

Substances

  • RNA, Viral
  • Viral Core Proteins
  • fas Receptor
  • nucleocapsid protein, Hepatitis C virus
  • Alanine Transaminase