Occult hepatitis B in blood donors in Indonesia: altered antigenicity of the hepatitis B virus surface protein

被引:24
|
作者
Thedja, Meta D. [1 ]
Roni, Martono [1 ]
Harahap, Alida R. [1 ,2 ]
Siregar, Nurjati C. [1 ,2 ]
Ie, Susan I. [1 ]
Muljono, David H. [1 ]
机构
[1] Eijkman Inst Mol Biol, Jakarta, Indonesia
[2] Univ Indonesia, Fac Med, Jakarta, Indonesia
关键词
Hepatitis B; Hepatitis B virus; HBV; Occult hepatitis B; OBI; Antigenic index; Antigenic property; Blood donor; ANTI-HBC; IMMUNE GLOBULIN; TRANSFUSION; INFECTION; MUTANTS; GENE; MUTATIONS; VARIANTS; EFFICACY; MOTHERS;
D O I
10.1007/s12072-010-9203-5
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Occult hepatitis B virus infection (OBI) poses a challenge to the safety of blood donation. The prevalence of OBI is not well documented in Indonesia, although this information in such an endemic country is needed. This study was aimed to evaluate the prevalence of occult hepatitis B in blood donors from two cities of Indonesia, and to study the genetic variation and its effect on the predicted antigenicity of HBsAg. Serum samples of 309 regular blood donors negative for HBsAg were tested for anti-HBs and anti-HBc. Hepatitis B virus (HBV) DNA isolated from anti-HBc-positive samples were analyzed by polymerase chain reaction, cloned and sequenced. Antigenic properties of identified HBsAg mutants were predicted by calculation of the antigenic index. Of the 309 HBsAg-negative samples, anti-HBc was positive in 134 (43.4%) and HBV DNA was detected in 25 (8.1%). Seven of the viremic samples had nucleotide substitutions (A521G, A551T, C582T, and A562G) in the S gene, causing amino acid mutations (T123A, M133L, and T143M) in the 'a' determinant of HBsAg that resulted in changes in the predicted antigenicity. OBI was detected in blood donors' samples in Indonesia. Anti-HBc was shown to be a better screening parameter than HBsAg, however, it might result in the loss of donors particularly in endemic countries. HBsAg detection failure in this study might be due to mutations altering the protein antigenicity and/or the low-level carriage of HBV.
引用
收藏
页码:608 / 614
页数:7
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