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

L. G. Guidotti, P. Borrow, M. V. Hobbs, B. Matzke, I. Gresser, M. B A Oldstone, F. V. Chisari

Research output: Contribution to journalArticle

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 α (TNF-α) and interferon γ (IFN-γ) 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-α and IFN-α/β 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.

Original languageEnglish
Pages (from-to)4589-4594
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume93
Issue number10
DOIs
Publication statusPublished - 1996

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ASJC Scopus subject areas

  • Genetics
  • General

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