Lee Y I, Hur G M, Suh D J, Kim S H
Biomedicine Research Group, Korea Research Institute of Bioscience and Biotechnology, KIST, Taejon, Korea.
J Gen Virol. 1996 Jun;77 ( Pt 6):1129-38. doi: 10.1099/0022-1317-77-6-1129.
We have analysed serum samples taken from hepatitis B virus (HBV) e antigen (HBeAg)-positive and HBeAg-negative chronic active hepatitis (CAH) patients by PCR using primers spanning the pre-core/core (C) and pre-S1/S2 ORFs. Nucleotide sequence analysis showed that among 18 HBV-infected CAH patients, 11 had virus with a G to A mutation (nucleotide 1896; leading to the formation of a stop codon) and one patient also had virus with an additional G to A mutation three nucleotides downstream (nucleotide 1899). HBV from three patients that were HBeAg-negative showed a 1 bp deletion at nucleotide 1937, causing pre-termination of the C gene. Mutation frequencies in the sequences identified as coding for cytotoxic T lymphocyte epitopes, B cell epitopes, CD4+ helper T cell epitopes and arginine-rich regions of the HBV C peptide were investigated. Mutations were more frequently identified in these regions, suggesting that the mutations might have been selected as a result of immune responses.
我们使用跨越前核心/核心（C）和前S1/S2开放阅读框的引物，通过聚合酶链反应（PCR）分析了从乙肝病毒（HBV）e抗原（HBeAg）阳性和HBeAg阴性的慢性活动性肝炎（CAH）患者采集的血清样本。核苷酸序列分析显示，在18例HBV感染的CAH患者中，11例病毒存在G到A的突变（核苷酸1896；导致形成终止密码子），1例患者的病毒在下游三个核苷酸处（核苷酸1899）还存在额外的G到A突变。3例HBeAg阴性患者的HBV在核苷酸1937处有1个碱基缺失，导致C基因提前终止。我们研究了鉴定为编码细胞毒性T淋巴细胞表位、B细胞表位、CD4 +辅助性T细胞表位以及HBV C肽富含精氨酸区域的序列中的突变频率。这些区域中更频繁地发现了突变，这表明这些突变可能是免疫反应的结果而被选择出来的。
