Interaction of Hepatitis B virus with cellular processes in liver carcinogenesis

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.