Chronic Hepatitis B virus (HBV) infection remains the number one risk factor for hepatocellular carcinoma (HCC), accounting for more than 600000 deaths per year. Despite highly effective antiviral treatment options, chronic hepatitis B (CHB), subsequent end stage liver disease and HCC development remain a major challenge worldwide. In CHB, liver damage is mainly caused by the influx of immune cells and destruction of infected hepatocytes causing necroinflammation. Treatment with nucleos(t)id analogs can effectively suppress HBV replication in patients with CHB and thus decrease the risk for HCC development. Nevertheless, the risk of HCC in treated patients showing sufficient suppression of HBV DNA replication is significantly higher than in patients with inactive CHB, regardless of the presence of baseline liver cirrhosis, suggesting direct, long lasting, predisposing effects of HBV. Direct oncogenic effects of HBV include integration in the host genome leading to deletions, cis- / trans-activation, translocations, the production of fusion transcripts, and generalized genomic instability, as well as pleiotropic effects of viral transcripts (HBsAg and HBx). Analysis of these viral factors in active surveillance may allow early identification of high-risk patients, and their integration into a molecular classification of HCC subtypes might help in the development of novel therapeutic approaches.
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Chronic Hepatitis B virus (HBV) infection remains the number one risk factor for hepatocellular carcinoma (HCC), accounting for more than 600000 deaths per year. Despite highly effective antiviral treatment options, chronic hepatitis B (CHB), subsequent end stage liver disease and HCC development remain a major challenge worldwide. In CHB, liver damage is mainly caused by the influx of immune cells and destruction of infected hepatocytes causing necroinflammation. Treatment with nucleos(t)id ana...
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