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Titlebook: Chronically Evolving Viral Hepatitis; C. Bac,G. Taliani,W. H. Gerlich Conference proceedings 1992 Springer-Verlag/Wien 1992 Antigen.HIV.In

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978-3-211-82350-7Springer-Verlag/Wien 1992
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https://doi.org/10.1007/978-3-642-00771-2In an effort to elucidate the mechanism of liver damage resulting from Hepatitis A virus (HAV) infection, we have studied infected skin fibroblasts and autologous lymphocytes from HAV patients. We report here that HLA-restricted virus-specific T cells play an essential role in HAV-related hepatocellular injury.
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https://doi.org/10.1007/978-3-642-00771-2Saimiri monkeys were inoculated three times with hepatitis A virus and observed in a follow-up study for sixteen months. The monkeys developed recurrent hepatitis involving liver damage and cycles of HAV antigen shedding in stools. The relapses were presumably due to immune response effects.
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,Chromium – Molybdenum – Zirconium,We have studied the . gene as a possible target of HBV X protein in liver carcinogenesis. Our results indicate that .-activation by X protein occurs via PKC/AP1 signal transduction, suggesting a possible two-step mechanism in HBV related liver carcinogenesis.
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Immune pathogenesis of hepatitis AIn an effort to elucidate the mechanism of liver damage resulting from Hepatitis A virus (HAV) infection, we have studied infected skin fibroblasts and autologous lymphocytes from HAV patients. We report here that HLA-restricted virus-specific T cells play an essential role in HAV-related hepatocellular injury.
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Relapsing hepatitis A in Saimiri monkeys experimentally reinfected with a wild type hepatitis A viruSaimiri monkeys were inoculated three times with hepatitis A virus and observed in a follow-up study for sixteen months. The monkeys developed recurrent hepatitis involving liver damage and cycles of HAV antigen shedding in stools. The relapses were presumably due to immune response effects.
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