Polymorphisms of RhD&lt;sup&gt;Va&lt;/sup&gt; and a New RhD&lt;sup&gt;Va&lt;/sup&gt;&amp;ndash;Like Variant Found in Japanese Individuals

Hyodo, Hideo; Ishikawa, Yoshihide; Kashiwase, Koichi; Ogawa, Atsuko; Watanabe, Yoshihisa; Tsuneyama, Hatsue; Toyoda, Chizu; Uchikawa, Makoto; Akaza, Tatsuya; Fujii, Tomoyuki; Kozuma, Shiro; Taketani, Yuji; Juji, Takeo

doi:10.1159/000031162

Cited by 7 publications

(8 citation statements)

References 14 publications

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“…Despite DAU-1 having a much higher antigen density than DAU-2, more anti-D antibodies agglutinated DAU-2 than DAU-1 red blood cells. The profile of DAU-4 was almost identical to that reported for DHK, 32 alias DYO, 33 which shared the E233K substitution. DAU-0 had a normal D-positive epitope pattern.…”

Section: Phenotypes Of Dau Allelessupporting

confidence: 72%

The DAU allele cluster of the RHDgene

Wagner

Ladewig

Angert

et al. 2002

Blood

135

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Section: Phenotypes Of Dau Allelessupporting

confidence: 72%

The DAU allele cluster of the RHDgene

Wagner

Ladewig

Angert

et al. 2002

Blood

135

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“…The encoded phenotypes are not identical; they differ in D antigen strength and expression of the DVI-associated antigen BARC (Mouro et al, 1994;Avent et al, 1997;Wagner et al, 1998;Esteban et al, 2006). Likewise, there are seven types of RHD*DV, all encoding Glu233Gln, but all except RHD*DV type 4 have additional mutations in exon 5 (Rouillac et al, 1995;Omi et al, 1999;Hyodo et al, 2000;M€ uller et al, 2001).…”

Section: Rhd Rhcementioning

confidence: 99%

Variants of RhD – current testing and clinical consequences

2013

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Anti-D (-RH1) of the Rh blood group system is clinically important as it causes haemolytic transfusion reactions and haemolytic disease of the fetus and newborn. Although most people are either D+ or DÀ, there is a plethora of D variants, often categorized as either weak D or partial D. These two types are inadequately defined and the dichotomy is potentially misleading. DVI is the D variant most commonly associated with anti-D production and UK guidelines recommend that patients are tested with anti-D reagents that do not react with DVI. Weak D types 1, 2, and 3 are seldom, if ever, associated with alloanti-D production, so a policy recommendation would be to treat patients with those D variants as D+, to preserve DÀ stocks, whereas patients with all other D variants would be treated as DÀ. All donors with D variant red cells, including DVI, should be treated as D+. The frequency of the D+ phenotype is about 85% in Caucasians, around 95% in sub-Saharan Africa, and greater than 99Á5% in eastern Asia (Daniels, 2013). Although most people are either D+ or DÀ, a grey area exists in the form of a plethora of D variants: the so-called weak D, partial D, and DEL phenotypes. These ill-defined terms are often a cause of consternation beyond their clinical relevance. Over its history of well over a century, blood group serology has been fraught with problems arising from nomenclature, and the terminology applied to D variants has led to confusion.In this review I will attempt to clarify the situation, recommend a testing and transfusion strategy that minimizes the risk of alloimmunization without undue waste of DÀ blood stocks, and describe the clinical issues relating to these aberrant forms of D.

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“…The lack of expression of some of the epitopes at the surface of red blood cells defines the D category, or partial D phenotype. Based on the reactivity with anti-D sera from immunized partial D carriers or differential monoclonal anti-D antibodies, partial D phenotypes have been classified into six distinct categories-D II to D VII (Tippett et al 1996 (Rouillac et al 1995;Omi et al 1999;Hyodo et al 2000). D category VI is subdivided into type I, type II, and, recently, type III (Wagner et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Whole exon 5 and intron 5 replaced by RHCE in DVa(Hus)

2004

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The D Va (Hus) was previously investigated through cDNA analysis, which revealed an RHD-CE(5)-D hybrid allele. However, the 5' and 3' breakpoints remain unknown. In this article, gene recombinations between the RHD and RHCE alleles were investigated by a combination approach of a sequence-specific primer PCR (PCR-SSP) and an RHD full-length coding region sequencing method on two Chinese subjects with weak D phenotypes. The hybrid Rhesus box of each individual was also investigated through an established PCR-based method. As a result, two partial D phenotypes, D Va (Hus) and D VI type III, were identified, each carrying one hybrid RHD-CE-D allele. The two samples were also serotyped with Rh phenotypes of DccEe and DCcee, respectively. Other sequencing analyses of the D Va (Hus) sample showed that the sequence of intron 4 is identical with RHD, whereas the whole sequence of exon 5 and intron 5 is identical with RHCE except for seven polymorphisms in the intron 5. We may concluded that in the case of this Chinese D Va (Hus), the whole exon 5 and complete intron 5 of a total segment of 1801 nucleotides were replaced by RHCE suggesting that the breakpoints of the replaced region are the 5' end of the exon 5 and the 3' end of the intron 5.

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Polymorphisms of RhD<sup>Va</sup> and a New RhD<sup>Va</sup>–Like Variant Found in Japanese Individuals

Cited by 7 publications

References 14 publications

The DAU allele cluster of the RHDgene

The DAU allele cluster of the RHDgene

Variants of RhD – current testing and clinical consequences

Whole exon 5 and intron 5 replaced by RHCE in DVa(Hus)

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