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HBV pathogenesis in animal models: recent advances on the role of platelets

Academic Article
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Overview

authors

  • Iannacone, M.
  • Sitia, G.
  • Ruggeri, Zaverio
  • Guidotti, Luca

publication date

  • April 2007

journal

  • Journal of Hepatology  Journal

abstract

  • Hepatitis B virus (HBV) causes acute and chronic necroinflammatory liver diseases and hepatocellular carcinoma (HCC). HBV replicates noncytopathically in the hepatocyte, and most of the liver injury associated with this infection reflects the immune response. While the innate immune response may not contribute significantly to the pathogenesis of liver disease or viral clearance, the adaptive immune response, particularly the cytotoxic T lymphocyte (CTL) response, contributes to both. Recent observations also reveal that antigen-nonspecific inflammatory cells enhance CTL-induced liver pathology and, more surprisingly, that platelets facilitate the intrahepatic accumulation of CTLs, suggesting that the host response to HBV infection is a highly complex but coordinated process. The notion that platelets contribute to liver disease and viral clearance by promoting the recruitment of virus-specific CTLs into the liver is a new concept in viral pathogenesis, which may prove useful to implement treatments of chronic HBV infection in man.

subject areas

  • Animals
  • Blood Platelets
  • Disease Models, Animal
  • Hepatitis B
  • Hepatitis B virus
  • Immunity, Innate
  • T-Lymphocytes, Cytotoxic
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Research

keywords

  • chemokines
  • cytokines
  • cytotoxic T cells
  • hepatitis B virus
  • platelets
  • viral hepatitis
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Identity

PubMed Central ID

  • PMC1892635

International Standard Serial Number (ISSN)

  • 0168-8278

Digital Object Identifier (DOI)

  • 10.1016/j.jhep.2007.01.007

PubMed ID

  • 17316876
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Additional Document Info

start page

  • 719

end page

  • 726

volume

  • 46

issue

  • 4

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