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Hepatitis B Virus Replication, Liver Disease, and Hepatocellular Carcinoma
Book chapter

Hepatitis B Virus Replication, Liver Disease, and Hepatocellular Carcinoma

William S Mason, Alison A Evans and W. Thomas London
Human Tumor Viruses
11 May 1998
DOI: https://doi.org/10.1128/9781555818289.ch8

Abstract

antiviral therapy cell proliferation chronic infection hepadnavirus proteins hepatitis B virus replication hepatocellular carcinoma liver disease
One factor that has been of great importance to the study of hepatitis B virus (HBV) replication, and which will become of increasing importance in characterizing the biology of infection, is the existence of hepadnaviruses in other species. The two families of viruses infecting mammals and birds are subdivided into Orthohepadnaviridae and Avihepadnaviridae, respectively. To appreciate the hepadnavirus replication scheme, it is important, first, to appreciate that hepadnaviruses have one of the smallest of all animal virus genomes. The viral envelope proteins are produced in greater abundance than required for virion production. Traditionally, the envelope gene and the corresponding regions of the envelope proteins are divided into preSl, preS2, and S domains. The hepadnaviruses all replicate via reverse transcription. However, despite some similarities to retrovirus replication, an important difference is that hepadnavirus replication does not involve formation of an integrated provirus. The potentially important but poorly understood issue in the biology of infections is the effect of hepatocyte proliferation on virus replication and on the evolution of liver disease. Constant stimulation of progenitor cell proliferation may be important in the disease process leading to hepatocellular carcinoma (HCC), tumors possibly arising from incompletely differentiated progenitor cells. The International Agency for Research on Cancer evaluated the evidence and concluded that “chronic infection with HBV is carcinogenic to humans” and classified HBV as a group 1 carcinogen. Therapy with a nucleoside analog inhibitor of virus replication appears likely, from preliminary results, to have the same limitation as interferon (IFN).

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