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Immune tolerance split between hepatitis B virus precore and core proteins

Academic Article
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Overview

authors

  • Chen, M.
  • Sallberg, M.
  • Hughes, J.
  • Jones, J.
  • Guidotti, Luca
  • Chisari, Francis
  • Billaud, J. N.
  • Milich, D. R.

publication date

  • March 2005

journal

  • Journal of Virology  Journal

abstract

  • The function of the hepatitis B virus (HBV) precore or HBeAg is largely unknown because it is not required for viral assembly, infection, or replication. However, the HBeAg does appear to play a role in viral persistence. It has been suggested that the HBeAg may promote HBV chronicity by functioning as an immunoregulatory protein. As a model of chronic HBeAg exposure and to examine the tolerogenic potential of the HBV precore and core (HBcAg) proteins, HBc/HBeAg-transgenic (Tg) mice crossed with T cell receptor (TCR)-Tg mice expressing receptors for the HBc/HBeAgs (i.e., TCR-antigen double-Tg pairs) were produced. This study revealed three phenotypes of HBe/HBcAg-specific T-cell tolerance: (i) profound T-cell tolerance most likely mediated by clonal deletion, (ii) T-cell clonal ignorance, and (iii) nondeletional T-cell tolerance mediated by clonal anergy and dependent on the structure, location, and concentration of the tolerogen. The secreted HBeAg is significantly more efficient than the intracellular HBcAg at eliciting T-cell tolerance. The split T-cell tolerance between the HBeAg and the HBcAg and the clonal heterogeneity of HBc/HBeAg-specific T-cell tolerance may have significant implications for natural HBV infection and especially for precore-negative chronic hepatitis.

subject areas

  • Animals
  • Animals, Newborn
  • Female
  • Hepatitis B Antibodies
  • Hepatitis B Core Antigens
  • Hepatitis B e Antigens
  • Hepatitis B virus
  • Immune Tolerance
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Phenotype
  • Pregnancy
  • Receptors, Antigen, T-Cell
  • Recombinant Proteins
  • T-Lymphocytes
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Identity

International Standard Serial Number (ISSN)

  • 0022-538X

Digital Object Identifier (DOI)

  • 10.1128/jvi.79.5.3016-3027.2005

PubMed ID

  • 15709022
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Additional Document Info

start page

  • 3016

end page

  • 3027

volume

  • 79

issue

  • 5

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