Growth control of liver cancer cells by targeting viral-host chimeric transcript resulted from hepatitis B virus integration

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Hepatitis B virus (HBV) has been known to be integrated in the host genome in hepatocellular carcinoma. Here, we have clearly demonstrated that HBV integration occurs in chronic hepatitis tissues. These events can cause insertional mutagenesis in integrated genes and influence the transcription of the affected genes. We also found that HBV integration has favorite sites, such as chromosome 3 and common fragile sites, demonstrating that HBV integration is not a random event, but may result in some selection probably by affected genes. These findings suggest that HBV integration causes host genome mutation at early stages of chronic HBV infection preceding hepatocellular carcinoma and may be associated with persisitence and carcinogenesis of affected cells.