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Export of intracellular HBsAg in chronic hepatitis B virus infection is related to viral replication

Authors

  • Dr. Johnson Y. N. Lau,

    Corresponding author
    1. Institute of Liver Studies, King's College School of Medicine and Dentistry and King's College Hospital, London SE5 9PJ, United Kingdom
    • Institute of Liver Studies, King's College Hospital, Denmark Hill, London SE5 9RS, UK
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    • J.Y.N. Lau is a Croucher Foundation Fellow.

  • Vincent G. Bain,

    1. Institute of Liver Studies, King's College School of Medicine and Dentistry and King's College Hospital, London SE5 9PJ, United Kingdom
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  • Susan E. Davies,

    1. Institute of Liver Studies, King's College School of Medicine and Dentistry and King's College Hospital, London SE5 9PJ, United Kingdom
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  • Graeme J. M. Alexander,

    1. Institute of Liver Studies, King's College School of Medicine and Dentistry and King's College Hospital, London SE5 9PJ, United Kingdom
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  • Roger Williams

    1. Institute of Liver Studies, King's College School of Medicine and Dentistry and King's College Hospital, London SE5 9PJ, United Kingdom
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  • This work was presented in part at the British Society of Gastroenterology Autumn Meeting 1990 in Southampton.

Abstract

Serum and liver HBsAg bear an inverse relation to each other during the evolution of chronic hepatitis B virus infection and the quantity of HBsAg in tissue rises gradually with time. In this study, intracellular and extracellular levels of HBsAg were measured by radioimmunoassay in primary culture of hepatocytes from 30 patients with chronic hepatitis B virus infection to determine a possible relationship with hepatitis B virus replication.

Serum levels of HBsAg correlated with markers of active viral replication (serum hepatitis B virus DNA, p < 0.005, and tissue HBcAg, p < 0.02) but inversely with tissue HBsAg (p < 0.05). In similar fashion, in vitro export of HBsAg was also related to the presence of active viral replication markers (serum hepatitis B virus DNA, p < 0.02, and tissue HBcAg, p < 0.05) and negatively with tissue HBsAg (p < 0.001). Export of HBeAg also correlated positively with markers of active viral replication (serum hepatitis B virus DNA, p < 0.05 and tissue HBcAg, p < 0.05). Further experiments indicated that intrahepatic pre-S1 and pre-S2 correlated closely with intrahepatic HBsAg, indicating that a failure to export HBsAg was unlikely to be attributable to deficient intracellular expression of pre-S1 or pre-S2.

These data indicate that in vitro primary hepatocyte culture of hepatitis B virus—infected cells provides an accurate reflection of in vivo export of HBsAg and that this is closely related to the presence of active viral replication.

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