Hepatitis B Virus PreS Variant and Hepatocellular Carcinoma

authors:

avatar Zahra Goodarzi 1 , avatar Seyed Mohamad Jazayeri 2 , *

Baqiyatallah Research Center for Gastroenterology and Liver Disease (BRCGL), Baqiyatallah University of Medical Sciences, IR-Iran
Department of Virology, Faculty of Public Health, Tehran University of Medical Sciences, jazayerism@sina.tums.ac.ir, IR-Iran
Hepatitis Monthly: Vol.8, issue 2; 129-133
article type: Review Article
received: December 22, 2007
accepted: May 11, 2008

how to cite: Goodarzi Z, Jazayeri S. Hepatitis B Virus PreS Variant and Hepatocellular Carcinoma. Hepat Mon. 2008;8(2): 129-133. 

Abstract

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. HCC is associated with multiple risk factors. Although the association between chronic hepatitis B virus (HBV) infection and HCC is well established, the underlying mechanism of HBV-related hepatocarcinogenesis still remains elusive. Viral proteins such as X protein and the truncated middle S protein have been implicated to be tranactivators. Recently, studies are focused on mutations within the HBV genome that may be associated with HCC. Deletions in the 3' end of preS1 and 5' terminal of preS2 may emerge during the course of chronic HBV infection which may potentially lead to impairment in immune clearance of these variants. The preS mutant proteins are localized in the endoplasmic reticulum (ER) and have been implicated in the induction of ER stress responses. The ER stress response induces a series of signal transduction pathways and oxidative DNA damage. Furthermore, preS2 mutant protein can upregulate cyclin A expression and induce nodular proliferation of hepatocytes. The findings in this review are important to study the correlation between HCC and preS deletion mutants.

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