Clinical and serological events accompanying changes in hepatitis B viral replication: case reports

Authors

  • G. M. Dusheiko,

    Corresponding author
    1. Departments of Medicine and Pathology, University of the Witwatersrand Medical School, South African Institute for Medical Research, and the Johannesburg and Hillbrow Hospitals, Johannesburg, South Africa
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  • S. M. Bowyer,

    1. Departments of Medicine and Pathology, University of the Witwatersrand Medical School, South African Institute for Medical Research, and the Johannesburg and Hillbrow Hospitals, Johannesburg, South Africa
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  • A. Paterson,

    1. Departments of Medicine and Pathology, University of the Witwatersrand Medical School, South African Institute for Medical Research, and the Johannesburg and Hillbrow Hospitals, Johannesburg, South Africa
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  • E. Song,

    1. Departments of Medicine and Pathology, University of the Witwatersrand Medical School, South African Institute for Medical Research, and the Johannesburg and Hillbrow Hospitals, Johannesburg, South Africa
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  • A. Dibisceglie,

    1. Departments of Medicine and Pathology, University of the Witwatersrand Medical School, South African Institute for Medical Research, and the Johannesburg and Hillbrow Hospitals, Johannesburg, South Africa
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  • M. C. Kew

    1. Departments of Medicine and Pathology, University of the Witwatersrand Medical School, South African Institute for Medical Research, and the Johannesburg and Hillbrow Hospitals, Johannesburg, South Africa
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University of the Witwatersrand Medical School Department of Medicine York Road Parktown 2193 Johannesburg South Africa

Abstract

ABSTRACT— We measured serum markers of hepatitis B virus replication in two HBsAg-, HBeAg-positive hepatitis B carriers with chronic active hepatitis and cirrhosis. The first of these patients was HBsAg-, HBeAg-, HBV DNA- and HBV DNA polymerase-positive initially and spontaneously lost HBV DNA polymerase and HBV DNA. During the HBeAg-positive, DNA polymerase-negative “window phase”, an increase in viral replication, characterized by the reappearance of HBV DNA and HBV DNA polymerase occurred, together with an aggravation of the underlying chronic hepatitis. In the second HBsAg-, HBeAg-positive carrier, spontaneous fluctuations in HBV replication were associated with clinical deterioration. Delta agent and hepatitis A virus superinfection were excluded. These observations suggest that spontaneous low-grade fluctuations of HBV replication accompanied by an increase in the biochemical activity of the underlying chronic hepatitis can be observed in certain HBV carriers.

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