Interaction of Hepatitis B Virus with Cellular Processes in Liver Carcinogenesis

Abstract

Hepatitis B infection is strongly linked epidemiologically to hepatocellular carcinoma development. This article reviews the molecular mechanisms by which hepatitis B encoded proteins such as hepatitis B x and hepatitis B surface transactivators may interact with gene transcription, tumor suppression, apoptosis, and signalling pathways of the liver cell with the possible consequence of tumor induction. Data on the interaction between hepatitis B proteins and cellular processes are often conflicting indicating a non-specific simultaneous interaction with antagonistic cellular processes that result in the formation of escape mutants that are not subject to these selective pressures.

KEYWORDS: :

• animal
• carcinoma
• hepatocellular/virology
• cells
• genes
• hepatitis B/virology
• hepatitis B surface antigens/*metabolism
• hepatitis B Virus/genetics/*metabolism/ultrastructure
• human
• support
• non-U.S. Gov't. trans-activation (genetics)
• trans-activators/metabolism.