Pathology of livers infected with “silent” hepatitis B virus mutant

Authors

  • Toshikazu Uchida M.D.,

    Corresponding author
    1. Department of Pathology, Nihon University School of Medicine, Tokyo and Department of Medicine, Hokkaido Kin-ikyo Chuo Hospital, Sapporo, Japan
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  • Seiichi Shimojima,

    1. Department of Pathology, Nihon University School of Medicine, Tokyo and Department of Medicine, Hokkaido Kin-ikyo Chuo Hospital, Sapporo, Japan
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  • Kenichiro Gotoh,

    1. Department of Pathology, Nihon University School of Medicine, Tokyo and Department of Medicine, Hokkaido Kin-ikyo Chuo Hospital, Sapporo, Japan
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  • Toshio Shikata,

    1. Department of Pathology, Nihon University School of Medicine, Tokyo and Department of Medicine, Hokkaido Kin-ikyo Chuo Hospital, Sapporo, Japan
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  • Satoaki Mima

    1. Department of Pathology, Nihon University School of Medicine, Tokyo and Department of Medicine, Hokkaido Kin-ikyo Chuo Hospital, Sapporo, Japan
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Department of Pathology, Nihon University School of Medicine, 30–1 Oyaguchi-Kamimachi, Itabashi-ku, Tokyo 173, Japan

Abstract

We have discovered that non-A, non-B, non-C, non-D, non-E (so-called type F) acute and chronic hepatitis is caused by a hepatitis B virus (HBV) variant with mutations in the X open reading frame. This silent HBV mutant does not induce immunoserological markers. In the present investigation we attempted to elucidate the putative mechanism of hepatocellular necrosis and expression patterns of hepatitis B surface antigen (HBsAg) and core antigen (HBcAg) in biopsied liver tissue. The subjects consisted of 14 patients with acute hepatitis, 11 with chronic hepatitis and eight with liver cirrhosis, all of whom had been previously diagnosed as having so-called hepatitis F. Nine of the 14, 10 of the 11 and all eight, respectively, of the above patients exhibited significant positive immunostaining for HBsAg within their hepatocellular cytoplasm, diffusely or focally. HBcAg stained in a few hepatocellular nuclei in 24.2% of the patients. Histological features were characterized by necroinflammation, indicating immune-mediated hepatocellular necrosis. Despite the serological-marker negativity, the results of immunostaining for HBsAg and HBcAg support replication and expression of HBV DNA, though weak.

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