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Pre-S2 Deletions of Hepatitis B Virus and Hepatocellular Carcinoma in Children

机译:小儿乙型肝炎病毒和肝细胞癌的S2前缺失

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The cause of early oncogenesis in hepatitis B virus (HBV)-related childhood hepatocellular carcinoma (HCC) remains unclear. This study investigated whether pre-S deletion of HBV is related to childhood HCC. By using nested polymerase chain reaction, we compared the pre-S sequence of HBV from sera of children with HCC against control children with similar chronic HBV infection. The HBV in sera of children with HCC had a significantly higher rate of pre-S deletion than that of children with chronic HBV infection (p = 0.008). All except one of the pre-S deletions from the HCC group involved the pre-S2 region, whereas no pre-S2 deletion was found in the chronic HBV group (p = 0.003). There was a trend whereby genotype-C sera had a higher rate of pre-S2 deletion than genotype-B sera (p = 0.11). A multivariate logistic regression model revealed that pre-S deletion was an independent risk factor for HCC in children (odds ratio: 36.69, p = 0.015). In conclusion, pre-S2 deletion does not need to take decades to occur; its presence in nearly half of children with HCC, in contrast to its absence in children with chronic HBV infection, suggests a link between pre-S2 deletion and HCC development in children.Abbreviations: HBeAg, hepatitis B virus e antigen; HbsAg, hepatitis B virus surface antigen; HBV, hepatitis B virus; HCC, hepatocellular carcinoma; PHSA, polymerized human serum albumin
机译:尚不清楚乙型肝炎病毒(HBV)相关的儿童期肝细胞癌(HCC)早期致癌的原因。这项研究调查了乙型肝炎病毒前S缺失是否与儿童HCC有关。通过使用巢式聚合酶链反应,我们比较了HCC儿童血清中HBV的pre-S序列与慢性HBV感染相似的对照儿童之间的比较。与慢性HBV感染儿童相比,HCC儿童血清中HBV的S前缺失率明显更高(p = 0.008)。 HCC组中除pre-S缺失之一外的所有基因都涉及pre-S2区域,而在慢性HBV组中未发现pre-S2缺失(p = 0.003)。有一种趋势,即基因型C血清比基因型B血清具有更高的S2前缺失率(p = 0.11)。多元logistic回归模型显示,S前缺失是儿童HCC的独立危险因素(比值比:36.69,p = 0.015)。总而言之,S2之前的删除不需要花费数十年的时间。乙型肝炎病毒,乙型肝炎病毒e抗原,乙型肝炎病毒e抗原,乙型肝炎病毒e抗原,乙型肝炎病毒e抗原,乙型肝炎病毒e抗原,乙型肝炎病毒e抗原,乙型肝炎病毒e抗原,乙型肝炎病毒e抗原和乙型肝炎病毒e抗原均与乙肝病毒/乙肝病毒e抗原相关。 HbsAg,乙肝病毒表面抗原; HBV,乙肝病毒; HCC,肝细胞癌; PHSA,聚合的人血清白蛋白

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