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lüll Impact of hepatitis B virus (HBV) x gene mutations on hepatocellular carcinoma development in chronic HBV infection Lee JH; Han KH; Lee JM; Park JH; Kim HSClin Vaccine Immunol 2011[Jun]; 18 (6): 914-21The hepatitis B virus (HBV) PreS mutations C1653T, T1753V, and A1762T/G1764A were reported as a strong risk factor of hepatocellular carcinoma (HCC) in a meta-analysis. HBV core promoter overlaps partially with HBx coding sequence, so the nucleotide 1762 and 1764 mutations induce HBV X protein (HBx) 130 and 131 substitutions. We sought to elucidate the impact of HBx mutations on HCC development. Chronically HBV-infected patients were enrolled in this study: 42 chronic hepatitis B (CHB) patients, 23 liver cirrhosis (LC) patients, and 31 HCC patients. Direct sequencing showed HBx131, HBx130, HBx5, HBx94, and HBx38 amino acid mutations were common in HCC patients. Of various mutations, HBx130+HBx131 (double) mutations and HBx5+HBx130+HBx131 (triple) mutations were significantly high in HCC patients. Double and triple mutations increased the risk for HCC by 3.75-fold (95% confidence interval [CI] = 1.101 to 12.768, P = 0.033) and 5.34-fold (95% CI = 1.65 to 17.309, P = 0.005), respectively, when HCC patients were compared to CHB patients. Functionally, there were significantly higher levels of NF-kappaB activity in cells with the HBx5 mutant and with the double mutants than that of wild-type cells and the triple-mutant cells. The triple mutation did not increase NF-kappaB activity. Other regulatory pathways seem to exist for NF-kappaB activation. In conclusion, a specific HBx mutation may contribute to HCC development by activating NF-kappaB activity. The HBx5 mutation in genotype C2 HBV appears to be a risk factor for the development of HCC and may be used to predict the clinical outcomes of patients with chronic HBV infection.|*Mutation, Missense[MESH]|Adult[MESH]|Amino Acid Substitution/genetics[MESH]|Carcinoma, Hepatocellular/*virology[MESH]|Female[MESH]|Hepatitis B virus/*genetics/isolation & purification[MESH]|Hepatitis B, Chronic/*complications/*virology[MESH]|Humans[MESH]|Male[MESH]|Middle Aged[MESH]|NF-kappa B/biosynthesis[MESH]|Trans-Activators/*genetics[MESH]|Viral Regulatory and Accessory Proteins[MESH]|Virulence Factors/*genetics[MESH] |