Kojima M, Shimizu M, Tsuchimochi T, Koyasu M, Tanaka S, Iizuka H, Tanaka T, Okamoto H, Tsuda F, Miyakawa Y
Kojima Internal Clinic, Gifu-Ken, Japan.
Vox Sang. 1991;60(1):34-9. doi: 10.1111/j.1423-0410.1991.tb00868.x.
Fulminant hepatitis B developed in 8 recipients of blood units without detectable hepatitis B surface antigen on routine screening. All 124 hepatitis B virus (HBV) DNA clones propagated from their sera possessed defects in the precore region. A point mutation from guanine to adenine at nucleotide 83, converting codon 28 for tryptophan (TGG) to a stop codon (TAG), was the commonest, and it was found in all 113 clones from 7 cases. The remaining case displayed 1 clone with this point mutation and 10 clones with an insertion of 2 base pairs after nucleotide 26. Antibody to hepatitis B core antigen (anti-HBc) was detected in a high titer in 1 of 10 pilot plasma samples of blood units transfused to this case. HBV DNA clones propagated from it exhibited the same precore-region defects as those from the recipient. On the basis of these results HBV mutants, defective in the precore region, would appear to be responsible for posttransfusion fulminant hepatitis B, and the exclusion of blood units with high-titered anti-HBc would be efficacious in preventing it.
8名接受常规筛查时未检测到乙型肝炎表面抗原的血液单位受血者发生了暴发性乙型肝炎。从他们的血清中增殖的所有124个乙型肝炎病毒（HBV）DNA克隆在前核心区都有缺陷。核苷酸83处从鸟嘌呤到腺嘌呤的点突变，将色氨酸（TGG）的密码子28转换为终止密码子（TAG），是最常见的，并且在来自7例患者的所有113个克隆中都发现了这种突变。其余1例显示1个具有该点突变的克隆和10个在核苷酸26后插入2个碱基对的克隆。在输给该患者的10份血液单位的预试验血浆样本中的1份中检测到高滴度的乙型肝炎核心抗原抗体（抗-HBc）。从其中增殖的HBV DNA克隆表现出与受血者相同的前核心区缺陷。基于这些结果，前核心区有缺陷的HBV突变体似乎是输血后暴发性乙型肝炎的病因，排除抗-HBc高滴度的血液单位在预防该病方面将是有效的。
