Sterneck M, Kalinina T, Otto S, Günther S, Fischer L, Burdelski M, Greten H, Broelsch C E, Will H
Department of Medicine, Surgery, and Pediatrics, University Hospital Eppendorf, Hamburg, Germany.
J Infect Dis. 1998 May;177(5):1378-81. doi: 10.1086/515269.
Transmission of hepatitis B virus (HBV) from anti-hepatitis B e (anti-HBe)-positive carrier mothers to their infants may result in neonatal fulminant hepatitis B (FHB). We investigated whether HBV variants with a particular DNA sequence and functional phenotype, responsible for FHB, are selected during transmission. Full-length HBV genomes from a mother-infant pair were completely sequenced and transfected into human hepatoma cells. The dominant neonatal and maternal HBV populations were nearly identical (homology 99.8%) and showed a precore stop codon mutation, T-1762 and A-1764 substitutions in the core promoter region, and pre-S2 start codon mutations. Cells transfected with variants from mother and child, compared with wild-type virus, synthesized and released a similar number or fewer HBV DNA-containing particles. In conclusion, no particular HBV strain emerged during neonatal FHB. In this case, a de novo infection with variants showing a defect in HBe antigen and pre-S2 protein synthesis but not a high replication competence probably contributed to the fulminant disease course.
乙型肝炎病毒（HBV）从乙肝e抗体（抗-HBe）阳性携带者母亲传播给其婴儿可能导致新生儿暴发性乙型肝炎（FHB）。我们研究了在传播过程中是否会选择具有特定DNA序列和功能表型、导致FHB的HBV变异体。对一对母婴的全长HBV基因组进行了完全测序，并转染到人肝癌细胞中。主要的新生儿和母亲HBV群体几乎相同（同源性99.8%），并显示出前核心终止密码子突变、核心启动子区域的T-1762和A-1764替换以及前S2起始密码子突变。与野生型病毒相比，用母婴变异体转染的细胞合成并释放了数量相似或更少的含HBV DNA颗粒。总之，在新生儿FHB期间未出现特定的HBV毒株。在这种情况下，感染具有HBe抗原和前S2蛋白合成缺陷但复制能力不高的变异体可能导致了暴发性病程。
