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Three Molecular Structures Cause Rhesus D Category VI Phenotypes
With Distinct Immunohematologic Features
Franz F. Wagner,
Christoph Gassner,
Thomas H. Müller,
Diether Schönitzer,
Friedrich Schunter, and
Willy A. Flegel
From Abteilung Transfusionsmedizin, Universität Ulm and
DRK-Blutspendezentrale Ulm, Ulm, Germany; Zentralinstitut für
Bluttransfusion und Immunologische Abteilung Innsbruck, Innsbruck,
Austria; and Institut Oldenburg, DRK-Blutspendedienst
Niedersachsen-Oldenburg, Oldenburg, Germany.
Rhesus D category VI (DVI) is the clinically most
important partial D. DVI red blood cells were
assumed to possess very low RhD antigen density and to be caused by two
RHD-CE-D hybrid alleles. Because there was no population-based
work-up, we screened three populations in central Europe for
DVI. Twenty-six DVI samples were detected and
examined by exon-specific RHD polymerase chain reaction with
sequence-specific primers (PCR-SSP). A new genotype,
hereby designated D category VI type III, was characterized as
a RHD-Ce(3-6)-D hybrid allele by sequencing of the cDNA, parts of intron 1, and by PCR-restriction fragment length polymorphism (PCR-RFLP) of intron 2. Rhesus introns 5 and 6 were sequenced and the 3 breakpoints of all known
DVI types shown to be distinct. We differentiated
the 5 breakpoints of DVI type I and
DVI type II by a newly devised RHD-PCR.
Thus, the DVI phenotype originated in at least three
independent molecular events. Each DVI type showed
distinct immunohematologic features in flow cytometry. The number of
RhD proteins accessible on the red blood cells' surface of
DVI type III was normal (about 12,000 antigens/cell; DVI type I, 500;
DVI type II, 2,400) based on the
determination of an RhD epitope density profile. DVI
type II and DVI type III occurred as CDe
haplotypes, and DVI type I as a cDE haplotype.
The distribution of the DVI types varied
significantly in three German-speaking populations. Genotyping
strategies should take account of allelic variations in partial
RhD. The reconsideration of previous serologic and clinical data for
partial D in view of the underlying molecular structures may be
worthwhile.
Blood, Vol. 91 No. 6 (March 15), 1998:
pp. 2157-2168
© 1998 by The American Society of Hematology.
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