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.
|Number of pages||6|
|Journal||Proceedings of the National Academy of Sciences of the United States of America|
|Publication status||Published - 1996|
ASJC Scopus subject areas