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Viral cross talk: Intracellular inactivation of the hepatitis B virus during an unrelated viral infection of the liver

Academic Article
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Overview

authors

  • Guidotti, Luca
  • Borrow, P.
  • Hobbs, M. V.
  • Matzke, B.
  • Gresser, I.
  • Oldstone, Michael
  • Chisari, Francis

publication date

  • May 1996

journal

  • Proceedings of the National Academy of Sciences of the United States of America  Journal

abstract

  • Hepatitis B virus (HBV) infection is thought to be controlled by virus-specific cytotoxic T lymphocytes (CTL). We have recently shown that HBV-specific CTL can abolish HBV replication noncytopathically in the liver of transgenic mice by secreting tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) after antigen recognition. We now demonstrate that hepatocellular HBV replication is also abolished noncytopathically during lymphocytic choriomeningitis virus (LCMV) infection, and we show that this process is mediated by TNF-alpha and IFN-alpha/beta produced by LCMV-infected hepatic macrophages. These results confirm the ability of these inflammatory cytokines to abolish HBV replication; they elucidate the mechanism likely to be responsible for clearance of HBV in chronically infected patients who become superinfected by other hepatotropic viruses; they suggest that pharmacological activation of intrahepatic macrophages may have therapeutic value in chronic HBV infection; and they raise the possibility that conceptually similar events may be operative in other viral infections as well.

subject areas

  • Animals
  • Female
  • Gene Expression
  • Genes, Viral
  • Hepatitis B virus
  • Interferon-alpha
  • Interferon-beta
  • Liver
  • Lymphocytic Choriomeningitis
  • Lymphocytic choriomeningitis virus
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • T-Lymphocytes, Cytotoxic
  • Tumor Necrosis Factor-alpha
  • Virus Replication
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Identity

International Standard Serial Number (ISSN)

  • 0027-8424

Digital Object Identifier (DOI)

  • 10.1073/pnas.93.10.4589

PubMed ID

  • 8643448
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Additional Document Info

start page

  • 4589

end page

  • 4594

volume

  • 93

issue

  • 10

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