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目的探索肝细胞癌(HCC)相关乙肝病毒(HBV)变异在母婴传播和婴儿慢性感染中的变化规律,为肝细胞癌的防控提供理论依据。方法将413名HBV表面抗原(HBsAg)阳性产妇及其新生儿纳入本研究。应用定量PCR检测产妇外周血和新生儿脐带血HBV DNA,应用巢式PCR和克隆测序方法测定前S区和核心启动子区的HCC相关HBV变异。新生儿出生后均经标准HBV免疫,7个月后对104名婴儿HBV感染情况进行随访,对外周血HBV DNA阳性婴儿测定HCC相关HBV变异发生情况。结果在413名新生儿中,41名(9.9%)HBV DNA水平≥103 copies/mL。随访到的104名婴儿中,4名(占3.8%)HBV DNA≥103 copies/mL。与未发生HBV跨胎盘传播的产妇相比,发生HBV跨胎盘传播者外周血HBV核心启动子变异没有增加,但在C2基因亚型的前S区中,T2898G/C、C3000T、C3116T、T31C和T52C变异增加HBV跨胎盘传播的风险(P<0.05)。HBV基因组中前S区和核心启动子区的HCC相关变异的频率在产妇外周血和新生儿脐带血中无明显差别,但是在母婴传播的7个月龄HBV DNA阳性婴儿中,检测出极少数量。结论 HBV C2基因亚型的前S区某些变异可能影响HBV跨胎盘传播,但是具有HCC相关HBV变异的准种没有造成婴儿慢性感染的优势,促进HBV致癌的变异体是在漫长的慢性感染过程中逐渐被选择出来的。
Objective To explore the variation of hepatitis B virus (HBV) associated with hepatocellular carcinoma (HCC) in the transmission of mother-to-infant and chronic infection in infants and to provide a theoretical basis for the prevention and control of hepatocellular carcinoma. Methods 413 HBsAg positive mothers and their newborns were included in this study. Quantitative PCR was used to detect HBV DNA in maternal peripheral blood and neonatal umbilical cord blood. Nested PCR and cloning sequencing were used to detect HCC-associated HBV mutations in pre-S and core promoter regions. After birth, all newborns were immunized with standard HBV. After 7 months, 104 infants with HBV infection were followed up, and HCC-related HBV mutations were detected in peripheral blood HBV DNA positive infants. Results Of the 413 newborns, 41 (9.9%) had HBV DNA levels ≥103 copies / mL. Of the 104 infants who followed, 4 (3.8%) had HBV DNA ≥ 103 copies / mL. Compared with those without HBV transplacental transmission, there was no increase in the HBV core promoter in peripheral blood of patients with HBV transplacental transmission, but in the pre-S region of C2 subtype, T2898G / C, C3000T, C3116T, T31C and T52C mutation increases the risk of HBV trans-placental transmission (P <0.05). The frequency of HCC-associated mutations in the pre-S and core promoter regions of the HBV genome was not significantly different between maternal peripheral blood and neonatal umbilical cord blood but was detected in maternal-to-infant 7-month-old HBV DNA positive mothers A small number. Conclusion Some mutations in the pre-S region of HBV C2 subtypes may affect HBV trans-placental transmission. However, the quasispecies with HCC-associated HBV mutation do not have the advantage of chronic infection in infants. The variants that promote HBV carcinogenesis are the result of long chronic infection Gradually be chosen.