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ORIGINAL ARTICLE  
Ahead of print publication
Prevalence of GP. Mur variant phenotype among Malaysian blood donors


1 School of Dental Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia
2 School of Dental Sciences, Universiti Sains Malaysia; Human Genome Centre, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia
3 Department of Hematology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia
4 CAS Key Lab of Bio-Medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, Suzhou, China
5 School of Dental Sciences, Universiti Sains Malaysia; Department of Hematology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia

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Date of Submission31-Aug-2021
Date of Decision27-Sep-2021
Date of Acceptance10-Oct-2021
Date of Web Publication26-Sep-2022
 

   Abstract 

BACKGROUND AND OBJECTIVE: A number of glycophorin variant phenotypes or hybrid glycophorin variants of the MNS blood group system bear multiple immunogenic antigens such as Mia, Mur, and MUT. In the East and Southeast Asian populations, glycoprotein (GP.) Mur is the most common glycophorin variant phenotype expressing those three immunogens. The aim of this study was to detect MNS system glycophorin variant phenotypes (GP. Mur, GP. Hop, GP. Bun, GP. HF, and GP. Hut) among Malaysian blood donors.
MATERIALS AND METHODS: In this cross-sectional study, 144 blood donors were selected under stratified random sampling. The deoxyribonucleic acid was extracted from whole blood samples, followed by a polymerase chain reaction assay. Sanger sequencing was used to identify the specific MNS variants and then validated by a serological crossmatch with known anti-Mur and anti-MUT.
RESULTS: GP. Mur was identified among Malaysian blood donors with a prevalence of 6.94%, and no other variants of the MNS system were found.
CONCLUSION: The present study substantiates that GP. Mur is the main variant of the MNS system glycophorin (B-A-B) hybrid in Malaysian blood donors. GP. Mur-negative red blood cells must therefore be considered in the current transfusion policy in order to prevent alloimmunization and immune-mediated transfusion reactions, particularly in transfusion-dependent patients.

Keywords: GP. Mur, Malaysians, MNS blood group system, MNS hybrid glycophorins, MNS variant phenotype


How to cite this URL:
Hassan SN, Mohamad S, Kannan TP, Hassan R, Wei S, Wan Ab Rahman WS. Prevalence of GP. Mur variant phenotype among Malaysian blood donors. Asian J Transfus Sci [Epub ahead of print] [cited 2022 Dec 4]. Available from: https://www.ajts.org/preprintarticle.asp?id=356855



   Introduction Top


The MNS is one of 43 blood group systems recognized by the International Society of Blood Transfusion. The MNS blood group system is highly polymorphic, which comprises 50 distinct antigens.[1],[2] The antigens of the MNS system are expressed in the red blood cell (RBC) membrane on glycophorin A (GPA), glycophorin B (GPB), or hybrids of both and fully developed at birth.[3] GPA and GPB are encoded by the homologous glycophorin genes GYPA and GYPB, respectively. The GYPA has seven exons, while GYPB has five exons and a pseudoexon 3 or noncoding exon 3 (ψ3). The homologous regions encompass introns flanking exons 1–5 of both glycophorin genes with 95.5% homologous sequence.[4]

Hybrid glycophorins of the MNS system originated from unequal crossing over or gene conversion events between the homologous regions of GYPA and GYPB. Quick, several different alleles of GYP (B-A-B) hybrid give rise to GP. Mur, GP. Hop, GP. Bun, GP. HF, and GP. Kip glycophorin variant phenotypes that express a series of low-incidence antigens in the MNS blood group system.[5],[6] Indeed, some of the low-incidence antigens including Mia (MNS7), Mur (MNS10), and MUT (MNS35) are relatively immunogenic.[7],[8],[9],[10]

In the East and Southeast Asian populations, GP. Mur is the main glycophorin variant phenotype expressing Mia, Mur, and MUT antigens.[10],[11],[12],[13] It was commonly detected in the populations of China (5%–10%),[11],[12] Taiwan (4%–6%),[13],[14] and Thailand (8%–10%).[15],[16] GP. Mur is also found up to 88.4% in indigenous Taiwanese Ami,[17] 6.5% in Vietnamese,[18] 7.6% in Filipinos, and 2.1% in Indonesians.[19] As for the multi-ethnic Malaysian population, the prevalence was discovered to be 3.8%.[20]

Detection of MNS system glycophorin variant phenotypes is known to be limited to phenotyping reagents, which are not commercially available, and certainly genotyping assays, including polymerase chain reaction (PCR)-based deoxyribonucleic acid (DNA) typing, are applicable as reliable and reproducible alternatives.[11],[12],[13],[14],[15],[21],[22],[23],[24],[25],[26],[27] In this study, the target DNA for GP. Mur, GP. Hop, GP. Bun, GP. HF, and GP. Hut variant phenotypes was amplified by PCR assay, and then, the specific variant was confirmed using Sanger sequencing and validated by a serological crossmatch with known anti-Mur and anti-MUT.


   Materials and Methods Top


Study design, sample size determination, and sampling method

This cross-sectional study was conducted from January 2016 to January 2017. The sample size was determined using a single population proportion formula, N = (Zα⁄2)2 p (1 − p)/d2. In this sample size calculation, 95% confidence intervals with Z α/2 value of 1.96, 2.8% proportion (p),[20] 3% margin of error (d), and 20% nonresponse rate were applied (N = [1.96]2 0.028 [1 − 0.028]/0.032 = 116.17 = 120 + 24 = the final sample size was 144). Then, the stratified random sampling method was used to recruit 144 blood donors equally according to ABO blood types (n = 36 for each type) in the Transfusion Medicine Unit (TMU) at Hospital Universiti Sains Malaysia (USM). This study conformed to the ethical guidelines and was approved by the Human Research Ethics Committee of USM (JEPeM-USM/259.3.[13]/March 14, 2014–September 13, 2017).

Deoxyribonucleic acid extraction

The DNA was extracted from whole blood samples using NucleoSpin® Blood L (Macherey-Nagel, Duren, Germany) as described by the manufacturer. A NanoDrop ND-1000 spectrophotometer (NanoDrop Technologies, USA) was used to measure the concentration and purity of the DNA samples.

Control deoxyribonucleic acid

Human genomic DNA controls of known negative and positive GP. Mur genotype and phenotype were obtained from blood donors in the TMU of Hospital USM. The plasmid DNA served as a GP. Mur-positive control was a generous gift from Dr. ShuangShi Wei (Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, China).

Primers

The primers were PCR grade synthesized by the First BASE Laboratories Sdn Bhd (Malaysia) and received in lyophilized (desalted) form. According to Palacajornsuk et al.,[15] F2/Rccgg amplified GP. Mur/GP. Hop/GP. Bun and GP. Hut/GP. HF with a product size of 148 bp and 151 bp, respectively. While, a primer pair of the human growth hormone (HGH) gene for an internal PCR efficiency control was with a product size of 434 bp.[15],[28] F2 (5´-ccc ttt ctc aac ttc tct tat atg cag ATAA-3´) is located in intron 2 and extends four nucleotides into exon 3. Rccgg (5´-gag caa cta ttt aaa act aag aac ata cCG G-3´) is located in exon 3 and extends 28 nucleotides into intron 3. FHGH5580 (5´-TGC CTT CCC AAC CAT TCC CTT A-3´) is located in exon 2; RHGH5967 (5´-cca ctc acG GAT TTC TGT TGT GTT TC-3´) is located in exon 3 and extends eight nucleotides into intron 3 of the HGH gene.

Polymerase chain reaction assay

DNA samples and controls were amplified by F2/Rccgg primer set with FHGH5580/RHGH5967 primer set under PCR conditions as described by Palacajornsuk et al.,[15] PCR was performed in the Veriti™ thermal cycler (Applied Biosystems, USA) with a final reaction volume of 20.0 μl, containing 2.0 μl of 100 ng DNA template, 2.0 μl of CoralLoad PCR buffer (Qiagen, USA), 2.0 μl of deoxyribonucleotide triphosphate (Fermentas, USA), 1.2 μl of magnesium chloride (Qiagen, USA), 4.6 μl of nuclease-free water (Qiagen, USA), 1.0 μl of 10 μM primer mix (F2/Rccgg), 1.0 μl of 10 μM primer mix (FHGH5580/RHGH5967), 6.0 μl of Q-solution (Qiagen, USA), and 0.20 μl of HotStarTaq Plus DNA Polymerase (Qiagen, USA). The PCR products were electrophoresed on 2% agarose gel with 100 bp DNA Ladder (Thermo Fisher Scientific, USA) in ×1 TBE buffer (Promega, USA) at 100 volts for 60 min. The gel was stained with Diamond Nucleic Acid Dye (Promega, USA) for 3 h and was visualized using AlphaImager gel documentation system (Alpha Innotech, USA).

Identification of glycophorin variant subtype by sequencing

The unpurified PCR products were sent to First BASE Laboratories Sdn Bhd (Malaysia) for purification and DNA Sanger sequencing services. The primers used for sequencing were the same as for PCR. The nucleotide sequences of the samples were blasted against GenBank (https://blast.ncbi.nlm.nih.gov/Blast.cgi) and analyzed using BioEdit software version 7.0.5 (http://www.mbio.ncsu.edu/BioEdit/bioedit.html). The nucleotide sequences of the samples were aligned and compared with reference sequences from the National Center for Biotechnology Information database: GYPA (NG_007470.3), GYPB (NG_007483.2), GYPE (NG_009173.1), GYP*Mur (AF090739), GYP*Hop (KR815995), GYP*Bun (1) (M60710.1), GYP*Bun (2) (KR363627.1), GYP*HF (M81079.1), and GYP*Kip (KF501485). GYP*Bun (2) differed from that of GYP*Bun (1) by the distal breakpoint in intron 3 and the length of GYPA replacement.[11],[29]

Validation for Mur and MUT antigens by serological crossmatch

The anti-Mur serum was provided by Dr. ShuangShi Wei from Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, China. It was identified using multiple panel cells and was positive for GP. Mur, GP. Hop, and GP. Bun, and Mur was the most common antigen.[12] While the anti-MUT plasma was detected in a patient who was admitted to Hospital USM. It was characterized using antibody screening and identification panel cells such as ID-DiaCell I-II-III Asia (Mia+) (Bio-Rad, USA), ID-DiaPanel (IAT and NaCl test) (Bio-Rad, USA), ID-DiaPanel-P (papainized, enzyme test) (Bio-Rad, USA), and Phenocell 0.8% C (Seqirus, Australia) that includes Mur or MUT expressing cells. The RBC suspension (0.8%) was prepared by adding 4 μl of packed RBCs into 500 μl of ID-Diluent 2 (Bio-Rad, USA). Briefly, 50 μl of 0.8% RBC suspension was added with 25 μl of serum/plasma with known anti-Mur/anti-MUT antibody compatible to their ABO and Rhesus (Rh) D blood types. The anti-IgG + Cd3 gel card (Bio-Rad, USA) was incubated at 37°C for 15 min and then centrifuged at 85 × g for 10 min. The gel card was directly examined macroscopically and graded as a weak positive (+1), +2, +3, +4, and negative (0).


   Results Top


Demographic profile

Frequency analysis in this study showed that the majority of blood donors were Malays (85.4%) aged between 18 and 30 years (66.7%) [Table 1]. All randomly selected blood donors for each ABO blood type were Rh D positive.
Table 1: Demographic profile of blood donors (n=144)

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Electrophoretic analysis

Ten out of 144 samples showed the presence of the target band, represented by [Figure 1]. Note that the bands for product sizes 148 bp (GP. Mur/GP. Hop/GP. Bun) and 151 bp (GP. HF/GP. Hut) could not be distinguished on the basis of gel electrophoresis.
Figure 1: Representative electrophoretic analysis of PCR products; GP. Mur-positive samples (148 bp) are boxed in white, and the bands (434 bp) are internal PCR control (HGH gene). Lanes 1 to 26; Lane P1: Human GP. Mur-positive control (148 bp), Lane C1: Human GP. Mur-negative control, Lane Pls: GP. Mur-positive control plasmid DNA (148 bp), Lane N: Non-template negative control, Lanes M: 100 bp deoxyribonucleic acid ladder, and Lanes 1 to 8, 9 to 20: Deoxyribonucleic acid samples

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Sequencing analysis

All ten samples confirmed GYP*Mur (AF090739) and no other glycophorin variant was identified in the targeted region [Figure 2]a. In addition, the difference in nucleotides between GYP*Mur and GYPB observed in those samples was a single peak, subtracted and demonstrated by sequencing chromatogram in [Figure 2]b.
Figure 2: Representative sequencing analysis of GYP*Mur-positive samples (a) Contig consensus nucleotide sequence from forward and reverse sequencing of GYP*Mur-positive sample alignment to GYPA (NG_007470.3), GYPB (NG_007483.2), GYPE (NG_009173.1), GYP*Mur (AF090739), GYP*Hop (KR815995), GYP*Bun (1) (M60710.1), GYP*Bun (2) (KR363627.1), GYP*HF (M81079.1), and GYP*Kip (KF501485) in the region of partial intron 2, exon 3/ψ3, and partial intron 3 on chromosome 4. Forward primer sequence (F2) and reverse complement sequence of Rccgg are shown in gray color. The 3´ splice site adjacent to exon 3/ψ3 and 5´ splice site adjacent to exon 3/ψ3 are boxed in pink. The polymorphic positions are marked as c. 140, c. 165, c. 203, c. 212, c. 223, c. 226, c. 230, IVS3 + 1, and IVS3 + 25. A single-nucleotide polymorphism (SNP) between GYP*Mur and GYP*Bun is located at c. 203 (G vs. C).[29] In the targeted region, GYP*Mur and GYP*Hop differed at c. 203; GYP*Mur and a novel GYP*Bun allele (2) differed at c. 203 and IVS3 + 25; GYP*Mur and GYP*HF differed by a number of nucleotides, including at c. 165; and GYP*Mur and GYP*Kip differed at c. 203 and c. 212. In addition, the polymorphism that distinguishes GYP*Kip from other GYP (B-A-B) hybrid variants (GYP*Mur, GYP*Hop, GYP*Bun, and GYP*HF) is located at c. 212. According to Lopez et al.,[30] GYP*Kip has the TCC codon encoding serine (p.Ser51), while other GYP (B-A-B) hybrid variants have the TAC codon encoding tyrosine (p.Tyr51), marked with a red line and arrow. (b) Sequencing chromatogram of GYP*Mur-positive sample in the region of partial exon 3/ψ3 and intron 3. Seven nucleotide positions where GYP*Mur differs from GYPB are indicated by the yellow arrows; five are in the exon 3/ψ3 (c. 203, c. 212, c. 223, c. 226, and c. 230), one is at the 5´ splice site of intron 3 (IVS3 + 1), and one is in the intron 3 near the 5´ splice site (IVS3 + 25)

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Serological analysis

The results of the PCR and serological assays were matched; all GYP*Mur-positive samples were agglutinated (agglutination strength of 3+/4+) with known anti-Mur and anti-MUT [Supplementary Figure 1]. The positive agglutination confirmed the Mur-and MUT-positive phenotype.




   Discussion Top


In this study, GP. Mur was identified in 10 out of 144 blood samples, representing a prevalence of 6.94% (5.55% in Malays and 1.39% in Malaysian Thais) in the Malaysian blood donor population. Malaysia constitutes a diverse ethnicity comprising Malays who are the majority, Chinese, and Indians, as well as many other ethnic minorities, including Malaysian Thais. The absence of detection in Chinese and Indian blood donors could be attributed to the small number of those ethnicities in the study region. Previously, GP. Mur was found to be 2.8% in Malays (n = 249), 4.9% in Chinese (n = 306), and 3.0% in Indians (n = 100).[20]

The molecular bases of five GYP (B-A-B) hybrid variant alleles, GYP*Mur, GYP*Hop, GYP*Bun, GYP*HF, and GYP*Kip, have been well characterized. The alleles derived from GYPB, but also had a small segment of GYPA, and each allele differed by the length of GYPA sequence insert and the location of the breakpoints, which resulted in a series of exonic and intronic SNPs.[27],[29],[30],[31] With regard to GYP*Mur, the replacement of the short segment of GYPB ψ3 and intron 3 (has an inactivated 5´ splice site) by the homologous segment of GYPA exon 3 and intron 3 (has an active 5´ splice site) has reverted the first nucleotide at the 5´ splice site of intron 3 (T > G). This allows the exon 3/ψ3 to be spliced and expressed in GYP*Mur rather than unspliced and unexpressed in GYPB.[29],[32] In addition, the proximal (B-A) breakpoint located between nucleotides 827 and 852 [between c. 177 and c. 202 in [Figure 2]a] and the distal (A-B) breakpoint located downstream in intron 3 from IVS3 + 24.[29]

Besides that, a detailed description of the GYP*Mur zygosity is beyond the scope of this study. However, several studies have defined the zygosity of GYP*Mur by molecular methods, such as Sanger sequencing,[12],[21] high-resolution melting (HRM),[1],[21] and multiplex ligation-dependent probe amplification (MLPA).[11] The sequence chromatograms for the homozygous GYP*Mur (+/+) showed a single peak, while the heterozygous GYP*Mur (+/–) showed double peaks of comparable intensities at the seven nucleotide positions where GYP*Mur differed from GYPB.[12],[21] The results of the HRM curve analysis showed a single peak for GYP*Mur (+/+) and double peaks for GYP*Mur (+/–).[1],[21] In the same fashion, MLPA analysis for the GYP*Mur (+/+) exhibited two copies of GYP*Mur-specific signal peak and the absence of the signal peak for the wild-type 5´ splice site of the GYPB intron 3, while the GYP*Mur (+/–) exhibited one copy of GYP*Mur-specific signal peak and one copy of the signal peak for the wild-type 5´ splice site of the GYPB intron 3.[11] In a word, the GYP*Mur (+/+) expresses only GYP*Mur, while the GYP*Mur (+/–) expresses both GYP*Mur and GYPB.

In terms of clinical significance, antibodies (anti-Mur, anti-Mia, and anti-MUT) to GP. Mur are typically associated with hemolytic transfusion reaction and hemolytic disease of the fetus and newborn,[7],[8],[9],[10],[33] and these antibodies are commonly found in East and Southeast Asian populations.[10],[34],[35],[36],[37] In Malaysia, a retrospective study showed that the antibodies to MNS variants (Mia, MUT, and Mur antigens) increased from 0.94% (2004–2008 years) to 5.82% (2009–2010 years).[38] In another study, anti-MUT and anti-Mur were detected in alloimmunized patients with a prevalence of 5.0% and 0.7%, respectively.[39] In addition, a recent study found that anti-MUT (0.32%) and anti-Mur (0.22%) were among the most common antibodies in nontransfused and transfused patients.[34] It was also shown that the cumulative alloimmunization incidence for MUT and Mur increased in proportion to the blood unit received.

As far as the transfusion reactions are concerned, the current major crossmatch practice in pretransfusion testing still poses a risk of receiving GP. Mur-positive RBCs. Indeed, although ABO/Rh (D) compatible RBC units are deemed safe for transfusion, the risk of alloimmunization to GP. Mur is indisputable. In Taiwan, the transfusion reaction rate decreased with the administration of GP. Mur-negative RBCs to patients with anti-Mia.[40] Henceforth, screening for GP. Mur in blood donors is essential to prevent alloimmunization and immune-mediated transfusion reactions. In transfusion-dependent patients, the transfusion policy for GP. Mur-negative RBCs to patients with anti-Mia, anti-MUT, and anti-Mur should be considered.


   Conclusion Top


GP. Mur is the main variant of the MNS system glycophorin (B-A-B) hybrid in Malaysian blood donors.

Acknowledgments

We would like to thank Ms. Selamah Ghazali (Department of Hematology) and Transfusion Medicine Unit, Hospital USM, for allowing us to utilize the laboratory facilities and for supplying the blood samples with the blood phenotype profile. Wan Suriana Wan Ab Rahman designed the research plan. Siti Nazihahasma Hassan performed the experiments and analysis of the data and drafted the manuscript. Wan Suriana Wan Ab Rahman, Thirumulu Ponnuraj Kannan, Suharni Mohamad, Rosline Hassan, and Shuangshi Wei verified the results and approved the manuscript. All the authors read and approved the manuscript. Siti Nazihahasma Hassan acknowledges the fellowship provided by Universiti Sains Malaysia and My Brain15 by the Ministry of Higher Education Malaysia.

Financial support and sponsorship

This study was funded by Universiti Sains Malaysia Short Term Grant (304/PPSG/61312118).

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Lopez GH, Wilson B, Liew YW, Kupatawintu P, Emthip M, Hyland CA, et al. An alloantibody in a homozygous GYP*Mur individual defines JENU (MNS49), a new high-frequency antigen on glycophorin B. Transfusion 2017;57:716-7.  Back to cited text no. 1
    
2.
Ito S, Kaito S, Miyazaki T, Kikuchi G, Isa K, Tsuneyama H, et al. A new antigen SUMI carried on glycophorin A encoded by the GYPA*M with c. 91A>C (p.Thr31Pro) belongs to the MNS blood group system. Transfusion 2020;60:1287-93.  Back to cited text no. 2
    
3.
Reid ME. MNS blood group system: A review. Immunohematology 2009;25:95-101.  Back to cited text no. 3
    
4.
Kudo S, Fukuda M. Structural organization of glycophorin A and B genes: Glycophorin B gene evolved by homologous recombination at Alu repeat sequences. Proc Natl Acad Sci U S A 1989;86:4619-23.  Back to cited text no. 4
    
5.
Lomas-Francis C. Miltenberger phenotypes are glycophorin variants: A review. ISBT Sci Ser 2011;6:296-301.  Back to cited text no. 5
    
6.
Blumenfeld OO, Huang CH. Molecular genetics of the glycophorin gene family, the antigens for MNSs blood groups: Multiple gene rearrangements and modulation of splice site usage result in extensive diversification. Hum Mutat 1995;6:199-209.  Back to cited text no. 6
    
7.
Cheng G, Hui CH, Lam CK, Hal SY, Wong L, Mak KH, et al. Haemolytic transfusion reactions due to Mi-antibodies; need to include MiltenbergerIII positive cells in pre-transfusion antibody screening in Hong Kong. Clin Lab Haematol 1995;17:183-4.  Back to cited text no. 7
    
8.
Wu KH, Chang JG, Lin M, Shih MC, Lin H, Lee CC, et al. Hydrops foetalis caused by anti-Mur in first pregnancy – A case report. Transfus Med 2002;12:325-7.  Back to cited text no. 8
    
9.
Bakhtary S, Gikas A, Glader B, Andrews J. Anti-Mur as the most likely cause of mild hemolytic disease of the newborn. Transfusion 2016;56:1182-4.  Back to cited text no. 9
    
10.
Heathcote DJ, Carroll TE, Flower RL. Sixty years of antibodies to MNS system hybrid glycophorins: What have we learned? Transfus Med Rev 2011;25:111-24.  Back to cited text no. 10
    
11.
Wei L, Shan ZG, Flower RL, Wang Z, Wen JZ, Luo GP, et al. The distribution of MNS hybrid glycophorins with Mur antigen expression in Chinese donors including identification of a novel GYP.Bun allele. Vox Sang 2016;111:308-14.  Back to cited text no. 11
    
12.
Wei SS, Sun AN, Ding SH, Meng QL, Wang HM, Duan SB, et al. Mur (MNS 10) screening with a novel loop-mediated isothermal amplification assay in Zhongshan, China. Transfus Med 2016;26:215-9.  Back to cited text no. 12
    
13.
Chen TD, Chen DP, Wang WT, Sun CF. MNSs blood group glycophorin variants in Taiwan: A genotype-serotype correlation study of 'Mi (a)' and St (a) with report of two new alleles for St (a). PLoS One 2014;9:e98166.  Back to cited text no. 13
    
14.
Shih MC, Yang LH, Wang NM, Chang JG. Genomic typing of human red cell miltenberger glycophorins in a Taiwanese population. Transfusion 2000;40:54-61.  Back to cited text no. 14
    
15.
Palacajornsuk P, Nathalang O, Tantimavanich S, Bejrachandra S, Reid ME. Detection of MNS hybrid molecules in the Thai population using PCR-SSP technique. Transfus Med 2007;17:169-74.  Back to cited text no. 15
    
16.
Chandanyingyong D, Pejrachandra S. Studies on the Miltenberger complex frequency in Thailand and family studies. Vox Sang 1975;28:152-5.  Back to cited text no. 16
    
17.
Broadberry RE, Lin M. The distribution of the MiIII (Gp.Mur) phenotype among the population of Taiwan. Transfus Med 1996;6:145-8.  Back to cited text no. 17
    
18.
Huynh NT, Ford DS, Duyen TT, Huong MT. Jk and Mi.III phenotype frequencies in North Vietnam. Immunohematology 2003;19:57-8.  Back to cited text no. 18
    
19.
Hsu K, Lin YC, Chao HP, Lee TY, Lin M, Chan YS. Assessing the frequencies of GP.Mur (Mi.III) in several Southeast Asian populations by PCR typing. Transfus Apher Sci 2013;49:370-1.  Back to cited text no. 19
    
20.
Prathiba R, Lopez CG, Usin FM. The prevalence of GP Mur and anti-”Mia” in a tertiary hospital in Peninsula Malaysia. Malays J Pathol 2002;24:95-8.  Back to cited text no. 20
    
21.
Hsu K, Lin YC, Chang YC, Chan YS, Chao HP, Lee TY, et al. A direct blood polymerase chain reaction approach for the determination of GP.Mur (Mi.III) and other Hil+Miltenberger glycophorin variants. Transfusion 2013;53:962-71.  Back to cited text no. 21
    
22.
Wei L, Lopez GH, Zhang Y, Wen J, Wang Z, Fu Y, et al. Genotyping analysis of MNS blood group GP (B-A-B) hybrid glycophorins in the Chinese Southern Han population using a high-resolution melting assay. Transfusion 2018;58:1763-71.  Back to cited text no. 22
    
23.
Haer-Wigman L, Ji Y, Lodén M, de Haas M, van der Schoot CE, Veldhuisen B. Comprehensive genotyping for 18 blood group systems using a multiplex ligation-dependent probe amplification assay shows a high degree of accuracy. Transfusion 2013;53 11 Suppl 2:2899-909.  Back to cited text no. 23
    
24.
Vongsakulyanon A, Kitpoka P, Kunakorn M, Srikhirin T. Miltenberger blood group typing by real-time polymerase chain reaction (qPCR) melting curve analysis in Thai population. Transfus Med 2015;25:393-8.  Back to cited text no. 24
    
25.
Schoeman EM, Lopez GH, McGowan EC, Millard GM, O'Brien H, Roulis EV, et al. Evaluation of targeted exome sequencing for 28 protein-based blood group systems, including the homologous gene systems, for blood group genotyping. Transfusion 2017;57:1078-88.  Back to cited text no. 25
    
26.
Meyer S, Vollmert C, Trost N, Sigurdardottir S, Portmann C, Gottschalk J, et al. MNSs genotyping by MALDI-TOF MS shows high concordance with serology, allows gene copy number testing and reveals new St (a) alleles. Br J Haematol 2016;174:624-36.  Back to cited text no. 26
    
27.
Wei L, Lopez GH, Ji Y, Condon JA, Irwin DL, Luo G, et al. Genotyping for glycophorin GYP (B-A-B) hybrid genes using a single nucleotide polymorphism-based algorithm by matrix-assisted laser desorption/ionisation, time-of-flight mass spectrometry. Mol Biotechnol 2016;58:665-71.  Back to cited text no. 27
    
28.
Storry JR, Poole J, Condon J, Reid ME. Identification of a novel hybrid glycophorin gene encoding GP.Hop. Transfusion 2000;40:560-5.  Back to cited text no. 28
    
29.
Huang CH, Blumenfeld OO. Molecular genetics of human erythrocyte MiIII and MiVI glycophorins. Use of a pseudoexon in construction of two delta-alpha-delta hybrid genes resulting in antigenic diversification. J Biol Chem 1991;266:7248-55.  Back to cited text no. 29
    
30.
Lopez GH, Wei L, Ji Y, Condon JA, Luo G, Hyland CA, et al. GYP*Kip, a novel GYP (B-A-B) hybrid allele, encoding the MNS48 (KIPP) antigen. Transfusion 2016;56:539-41.  Back to cited text no. 30
    
31.
Huang CH, Kikuchi M, McCreary J, Blumenfeld OO. Gene conversion confined to a direct repeat of the acceptor splice site generates allelic diversity at human glycophorin (GYP) locus. J Biol Chem 1992;267:3336-42.  Back to cited text no. 31
    
32.
Hsu K, Yao CC, Lin YC, Chang CL, Lee TY. Dissecting alternative splicing in the formation of Miltenberger glycophorin subtype III (GYP.Mur). Vox Sang 2015;108:403-9.  Back to cited text no. 32
    
33.
Lin CK, Mak KH, Szeto SC, Poon KH, Yuen CM, Chan NK, et al. First case of haemolytic disease of the newborn due to anti-Mur in Hong Kong. Clin Lab Haematol 1996;18:19-22.  Back to cited text no. 33
    
34.
Nadarajan VS. The prevalence, immunogenicity, and evanescence of alloantibodies to MUT and Mur antigens of GP.Mur red blood cells in a Southeast Asian patient cohort. Transfusion 2018;58:1189-98.  Back to cited text no. 34
    
35.
Srijinda S, Bosuwan S, Nuanin C, Suwanasophon C. Anti-Mi and Anti-E: The most common clinically significant red cell alloantibodies in patients at Phramongkutklao hospital. เวช สาร แพทย์ ทหาร บก Royal Thai Army Med J 2017;70:65-71.  Back to cited text no. 35
    
36.
Chen C, Tan J, Wang L, Han B, Sun W, Zhao L, et al. Unexpected red blood cell antibody distributions in Chinese people by a systematic literature review. Transfusion 2016;56:975-9.  Back to cited text no. 36
    
37.
Promwong C, Siammai S, Hassarin S, Buakaew J, Yeela T, Soisangwan P, et al. Frequencies and specificities of red cell alloantibodies in the Southern Thai population. Asian J Transfus Sci 2013;7:16-20.  Back to cited text no. 37
[PUBMED]  [Full text]  
38.
Nadarajan VS, Laing AA, Saad SM, Usin M. Prevalence and specificity of red-blood-cell antibodies in a multiethnic South and East Asian patient population and influence of using novel MUT+Mur+kodecytes on its detection. Vox Sang 2012;102:65-71.  Back to cited text no. 38
    
39.
Yousuf R, Abdul Aziz S, Yusof N, Leong CF. Incidence of red cell alloantibody among the transfusion recipients of Universiti Kebangsaan Malaysia Medical Centre. Indian J Hematol Blood Transfus 2013;29:65-70.  Back to cited text no. 39
    
40.
Yang CA, Lin JA, Chang CW, Wu KH, Yeh SP, Ho CM, et al. Selection of GP. Mur antigen-negative RBC for blood recipients with anti-'Mia ' records decreases transfusion reaction rates in Taiwan. Transfus Med 2016;26:349-54.  Back to cited text no. 40
    

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Correspondence Address:
Wan Suriana Wan Ab Rahman,
School of Dental Sciences, Universiti Sains Malaysia, Kubang Kerian 16150, Kelantan
Malaysia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajts.ajts_125_21



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2006 - Asian Journal of Transfusion Science | Published by Wolters Kluwer - Medknow
Online since 10th November, 2006