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Blood, Vol. 93 No. 1 (January 1), 1999:
pp. 385-393
Molecular Basis of Weak D Phenotypes
Franz F. Wagner,
Christoph Gassner,
Thomas H. Müller,
Diether Schönitzer,
Friedrich Schunter, and
Willy A. Flegel
From Abteilung Transfusionsmedizin, Universitätsklinikum Ulm
and DRK-Blutspendedienst Baden-Württemberg, Institut Ulm, Ulm,
Germany; Zentralinstitut für Bluttransfusion und Immunologische
Abteilung Innsbruck, Innsbruck, Austria; and Institut Oldenburg,
DRK-Blutspendedienst Niedersachsen-Oldenburg, Oldenburg, Germany.
A Rhesus D (RhD) red blood cell phenotype with a weak expression of
the D antigen occurs in 0.2% to 1% of whites and is called weak D,
formerly Du. Red blood cells of weak D phenotype have a
much reduced number of presumably complete D antigens that were
repeatedly reported to carry the amino acid sequence of the regular RhD
protein. The molecular cause of weak D was unknown. To evaluate the
molecular cause of weak D, we devised a method to sequence all 10 RHD exons. Among weak D samples, we found a total of 16 different molecular weak D types plus two alleles characteristic of
partial D. The amino acid substitutions of weak D types were located in
intracellular and transmembraneous protein segments and clustered in
four regions of the protein (amino acid positions 2 to 13, around 149, 179 to 225, and 267 to 397). Based on sequencing, polymerase chain reaction-restriction fragment length polymorphism and polymerase chain
reaction using sequence-specific priming, none of 161 weak D samples
investigated showed a normal RHD exon sequence. We concluded, that in contrast to the current published dogma most, if not all, weak
D phenotypes carry altered RhD proteins, suggesting a causal relationship. Our results showed means to specifically detect and to
classify weak D. The genotyping of weak D may guide Rhesus negative
transfusion policy for such molecular weak D types that were prone to
develop anti-D.
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