Systematic -omics analysis of HBV-associated liver diseases.

Hepatitis B virus (HBV) infection causes acute and chronic liver diseases and increases the risk of developing hepatocellular carcinoma (HCC). However, the pathogenesis of HBV infection and carcinogenesis of HBV-associated HCC are still elusive. In this review, systematic -omics studies made in the scales of genomics, transcriptomics and proteomics were discussed. The susceptibility to HBV infection and the course of disease progress are greatly different among individuals. Using population- or/and family-based approaches, relevant genes have been mapped or identified to be associated with host immune responses to HBV antigens and susceptibility to HCC. Comprehensive transcriptomic analyses have shown that the HBV-induced hepatocarcinogenesis may involve the whole course from signal transduction, transcription, translation to protein degradation, which differs in some measure from HCV-induced hepatocarcinogenesis, and that exogenous transcription factor HBX and endogenous NF-kappaB are likely two key points of the course. By the means of proteomics, dozens of important dysregulated proteins (including isoforms or fragments) were identified from carcinogenesis mechanism analysis and biomarker validation. Of them, the alteration of heat shock proteins and impairment of methylation cycle were found to be associated with clinical HBV-associated HCC. As a whole, the systematic -omics analysis of HBV-associated liver diseases has offered multi-scale pathological information in the process from HBV infection to HCC onset.