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Four novel silenced RHCE.
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Among the weak D phenotypes in Tunisia, no novel RHD allele was found and almost 90% were caused by alleles of the weak D Type 4 cluster, of which 88% represented the weak D Type 4.0 allele. Based on established RH haplotypes for variant RHD and RHCE alleles and the lack of adverse clinical reports, we recommend D+ transfusions for patients with weak D Type 4.0 in Tunisia.
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study 94.9% of the partial D samples revealed altered RHCE variant alleles and 5.7% of the samples with altered RHD allele predicted partial c, partial e and the lack of the high prevalence hr(B) and hr(S) antigens.
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sequence comparisons revealed high sequence similarity between Patr_RHbeta and Hosa_RHCE, while the chimpanzee Rh gene closest to Hosa_RHD was not Patr_RHalpha but rather Patr_RHgamma
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The purpose of this study was to determine the diversity and frequency of RHD-CE genotypes, predicting partial antigens in patients with sickle cell disease and in African Brazilian donors in order to find, through the use of RH genotyping, more closely matched donors for sickle cell disease patients who are alloimmunised to Rh antigens.
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The RHCE gene intron 4 of Han Chinese, Tibetans, and Mongols differs from the RHD gene intron 4 in the presence of a 652-bp fragment.
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Six new RHCE alleles were identified, namely, RHCE*cE84A, RHCE*ce202G, RHCE*ce307T, RHCE*Ce377G, RHCE*ce697G,712G,733G,744C, and RHCE*Ce733G in individuals of diverse racial origin.
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RHCE*cE94G encodes variable expression of c (RH4).
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Rh antibodies in SCD patients with RH variants can be clinically significant and, therefore, matching patients based on RH variants should be considered.
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Through molecular genotyping we also identified polymorphisms in RhCE, Kell, Duffy, Colton, Lutheran and Scianna loci in donors and patients.
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An uneven distribution of RH variant alleles between Dogon and Fulani, in Mali. A high incidence of predicted partial-C phenotype encoded by RHCE*Ce-D(4)-ce was found in Fulani.
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These data showed the presence of the (C)ce(s) haplotype at a low frequency (0.625%) compared to that among Africans in whom it is common. Nevertheless, the presence of RHD-CE-D(s) in Tunisians, even at a lower frequency
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One allele was found to be the known allele RHCE*Ol.20.01(RHCE*ce733G) and the second was novel: RHCE*Ol.06.02(RHCE*ce254G,733G).
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RHD*weak partial 4.0 is associated with an altered RHCE*ce(48C, 105T, 733G, 744C, 1025T) allele in the Tunisian population.
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RHCE*ceMO was present in one in 50 African-American persons with an allele frequency of 0.01, is often linked to RHD*DAU0, and is potentially of clinical significance for transfusion.
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In addition to hybrid alleles and nucleotide deletion, intronic mutations may be associated with the nonexpression of RhCE antigens.
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A QMPSF-based method is reliable to individually quantify the exons of both RH genes, including hybrid D-CE genes in compound heterozygous samples.
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Frequencies of aberrant RHD and RHCE alleles were similar, irrespective of location and ethnicity.
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A novel RHCE*cE allele, RHCE*cE734C, was found in two probands whose red blood cells had weakened c expression and typed E- with conventional anti-E reagents.
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RHD*DIVa and RHCE*ceTI almost always, but not invariably, travel together. This haplotype is found in people of African ancestry and the red blood cells can demonstrate aberrant reactivity with anti-C. RHCE*ceTI encodes partial c and e antigens.
