The lifetime risk of HBV carriers to develop cirrhosis, liver failure, or HCC may be as high as 15% to 40%.[1-3] The identification of risk factors for the development of advanced liver disease, including cirrhosis and HCC, in HBV carriers is important for implementing effective Rucaparib treatment. Recently, several qualitative and quantitative hepatitis B viral factors affecting the prognosis of HBV carriers have been identified.[3, 4] Among these viral factors, baseline serum HBV-DNA level is the main driving force for cirrhosis and HCC development in adult HBV

carriers.[5, 6] Recently, quantitative HBsAg (qHBsAg) has been increasingly recognized to be a promising biomarker to predict both favorable and adverse outcomes of HBV carriers. Based on the weight of each risk factor associated with HBV-related HCC and through a stratification process, it is possible to identify HBV carriers who are at an increased risk of disease progression and HCC development (Table 1). In this article, hepatitis B viral factors

leading to disease progression Fulvestrant and the risk stratification for HBV-related HCC will be reviewed and discussed. Low serum level of HBV-DNA Low serum level of HBsAg HBV genotype C/D BCP A1762T/G1764A mutation Pre-S deletion High serum level of HBV-DNA High serum level of HBsAg According to the divergence in the entire HBV genomic sequences, at least 10 HBV genotypes (A to J) have been defined.[7-9] Several studies suggested that HBV genotype can influence the long-term outcomes of HBV infection. For

example, HBV genotype C and D patients, compared with genotype A and B patients, have late or absent HBeAg seroconversion after multiple hepatitis flares that accelerate the progression of chronic hepatitis.[10-12] Most case–control medchemexpress studies and community-based prospective cohort study indicated that patients with genotype C HBV infection have a higher risk of cirrhosis and HCC than those with genotype B infection.[13-17] In addition, several reports have also shown that HBV genotype B was associated with HCC development in young non-cirrhotic patients. Whereas genotype C was associated with HCC development in old cirrhotic patients.[13, 18, 19] Due to the spontaneous error of viral reverse transcription, HBV mutant strains occur during the natural course of infection as well as with antiviral therapy. Mutations in precore, core promoter, and deletion mutation in pre-S/S genes have been reported to be associated with the progression of liver disease, including cirrhosis and HCC. Previous studies revealed that dual mutations in basal core promoter (BCP) A1762T/G1764A were strongly associated with the risk of HCC development.