Hepatitis B Virus Infection, the Immune Response and Hepatocellular Carcinoma

Milich, David R.; Jones, Joyce; Hughes, Janice; Maruyama, Toshiaki

doi:10.1002/9780470514672.ch8

Cited by 4 publications

(1 citation statement)

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“…HBV induces HCC through two main paths: liver inflammation caused by viral hepatitis, and the pathogen-host interplay mediated by the HBV proteins (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21). Viral hepatitis induces the release of proinflammatory cytokines as a result of immune responses; this causes the generation of reactive oxygen species (ROS) and hepatotoxicity (22)(23)(24)(25). Viral HBx protein and surface protein interact with host factors in DNA repair, cell cycle checkpoints, and signal transduction, and consequently lead to cell proliferation and transformation (26)(27)(28)(29)(30)(31)(32)(33).…”

Section: Introductionmentioning

confidence: 99%

Genomic instability caused by hepatitis B virus: into the hepatoma inferno

Hsieh

Hsu

et al. 2011

Front Biosci

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Chronic hepatitis B virus (HBV) infection is an important cause of hepatocellular carcinoma (HCC) worldwide, especially in Asia. HBV induces HCC through multiple oncogenic pathways. Hepatitis-induced hepatocyte inflammation and regeneration stimulates cell proliferation. The interplay between the viral and host factors activates oncogenic signaling pathways and triggers cell transformation. In this review, we summarize previous studies, which reported that HBV induces host genomic instability and that HBV-induced genomic instability is a significant factor that accelerates carcinogenesis. The various types of genomic changes in HBV-induced HCC--chromosomal instability, telomere attrition, and gene-level mutations--are reviewed. In addition, the two viral factors, HBx and the pre-S2 mutant large surface antigen, are discussed for their roles in promoting genomic instability as their main features as viral oncoproteins.

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