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

Research output: Contribution to journalArticle

65 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)719-726
Number of pages8
JournalJournal of Hepatology
Volume46
Issue number4
DOIs
Publication statusPublished - Apr 2007

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Hepatitis B virus
Blood Platelets
Animal Models
Liver Diseases
Cytotoxic T-Lymphocytes
Virus Diseases
Liver
Chronic Hepatitis B
Adaptive Immunity
Innate Immunity
Hepatocytes
Hepatocellular Carcinoma
Pathology
Viruses
Antigens
Wounds and Injuries
Infection
Therapeutics

Keywords

  • Chemokines
  • Cytokines
  • Cytotoxic T cells
  • Hepatitis B virus
  • Platelets
  • Viral hepatitis

ASJC Scopus subject areas

  • Gastroenterology

Cite this

HBV pathogenesis in animal models : Recent advances on the role of platelets. / Iannacone, Matteo; Sitia, Giovanni; Ruggeri, Zaverio M.; Guidotti, Luca G.

In: Journal of Hepatology, Vol. 46, No. 4, 04.2007, p. 719-726.

Research output: Contribution to journalArticle

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