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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.

Original publication

DOI

10.1073/pnas.93.10.4589

Type

Journal article

Journal

Proc Natl Acad Sci U S A

Publication Date

14/05/1996

Volume

93

Pages

4589 - 4594

Keywords

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