Analysis of RHD genes in Taiwanese RhD-negative donors by the multiplex PCR method
| Autor: | Wang L, Chiou Hl, Hu Sn, Yao-Ling Lee |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Microbiology (medical)
Genotype Oncogene Proteins Fusion Sequence analysis Recombinant Fusion Proteins Clinical Biochemistry Taiwan Polymerase Chain Reaction Serology Exon Antigen Hemolytic disease of the newborn (ABO) Multiplex polymerase chain reaction medicine Immunology and Allergy Humans DNA Primers Rh-Hr Blood-Group System biology Biochemistry (medical) Public Health Environmental and Occupational Health Infant Newborn Hematology Exons Sequence Analysis DNA Original Articles medicine.disease Molecular biology Medical Laboratory Technology Phenotype Blood Grouping and Crossmatching biology.protein Antibody |
| Zdroj: | Journal of clinical laboratory analysis. 17(3) |
| ISSN: | 0887-8013 |
| Popis: | The determination of the RhD phenotype is important in transfusion medicine. However, due to the complexity of D antigen expression, the routine serological method cannot differentiate all RhD variants. In addition, the induction of the anti‐D antibody is still the major cause of severe hemolytic disease of the newborn (HDN). Therefore, it is important to understand RHD gene profiles. To analyze the RHD gene profiles of Taiwanese RhD‐negative donors, the multiplex PCR method was applied to amplify RHD specific exons 3, 4, 5, 7, and 9. Based on the PCR results, the 156 RhD‐negative donors were divided into 12 groups according to the different expression patterns of the RHD gene. These 12 groups were further divided into three categories: type I=Rh D(el) (21.8%); type II = partial D, containing some exons (9.0%); and type III = true RhD‐negative (69.2%). The results indicated that 21.8% of RhD‐negative donors in Taiwan were RhD(el), and 9% carried a part of the RHD gene. Six defined RhD variants were found in this study: four R(O) (Har), one D(Va), and two D(IVb). However, no true RhD‐negative or RhD(el) donor with the CcdEe phenotype was found in this analysis. J. Clin. Lab. Anal. 17:80–84, 2003. © 2003 Wiley‐Liss, Inc. |
| Databáze: | OpenAIRE |
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