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• W2040894217 startingPage "4589" @default.
• W2040894217 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." @default.
• W2040894217 created "2016-06-24" @default.
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• W2040894217 date "1996-05-14" @default.
• W2040894217 modified "2023-10-15" @default.
• W2040894217 title "Viral cross talk: intracellular inactivation of the hepatitis B virus during an unrelated viral infection of the liver." @default.
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• W2040894217 doi "https://doi.org/10.1073/pnas.93.10.4589" @default.
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