POSTTRANSFUSION FULMINANT HEPATITIS-B ASSOCIATED WITH PRECORE-DEFECTIVE HBV MUTANTS

被引：80

作者：

KOJIMA, M

SHIMIZU, M

TSUCHIMOCHI, T

KOYASU, M

TANAKA, S

IIZUKA, H

TANAKA, T

OKAMOTO, H

TSUDA, F

MIYAKAWA, Y

MAYUMI, M

机构：

[1] JICHI MED SCH,DIV IMMUNOL,MINAMI KAWACHI,TOCHIGI 32904,JAPAN

[2] KOSIMA INT CLIN,GIFU,JAPAN

[3] GIFU PREFECTURAL HOSP,DEPT INTERNAL MED,GIFU,JAPAN

[4] SAITAMA CANC CTR,DEPT LAB MED,INA,SAITAMA 362,JAPAN

[5] TOKYO METROPOLITAN KOMAGOME HOSP,DEPT HEPATOL,TOKYO,JAPAN

[6] JAPANESE RED CROSS,CTR BLOOD,SAITAMA,JAPAN

[7] KITASATO INST,IMMUNOL SECT,TOKYO 108,JAPAN

[8] MITA INST,TOKYO,JAPAN

来源：

VOX SANGUINIS | 1991年 / 60卷 / 01期

关键词：

D O I：

10.1111/j.1423-0410.1991.tb00868.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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.

引用

页码：34 / 39

页数：6

共 33 条

[1] TYPE B-HEPATITIS - INFECTIVITY OF BLOOD POSITIVE FOR E ANTIGEN AND DNA-POLYMERASE AFTER ACCIDENTAL NEEDLESTICK EXPOSURE [J].