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Related Experiment Videos

Molecular basis of weak D phenotypes

F F Wagner1, C Gassner, T H Müller

  • 1Abteilung Transfusionsmedizin, Universitätsklinikum Ulm and DRK-Blutspendedienst Baden-Württemberg, Institut Ulm, Ulm, Germany.

Blood
|December 24, 1998
PubMed
Summary

Most weak D phenotypes, previously thought to have normal RhD proteins, actually carry altered RhD proteins. This discovery aids in classifying weak D types and informs transfusion policies for individuals prone to developing anti-D.

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Area of Science:

  • Genetics
  • Immunology
  • Hematology

Background:

  • Weak D phenotype, a variant of Rhesus D (RhD) antigen expression, affects 0.2%–1% of white individuals.
  • Previously, the molecular basis for weak D was unknown, with red blood cells presumed to have complete D antigens.

Purpose of the Study:

  • To investigate the molecular cause of the weak D red blood cell phenotype.
  • To identify genetic variations in the RHD gene responsible for weak D expression.

Main Methods:

  • Sequencing of all 10 RHD exons in weak D samples.
  • Utilizing polymerase chain reaction-restriction fragment length polymorphism and sequence-specific priming for genotyping.

Main Results:

  • Identified 16 distinct molecular weak D types and two partial D alleles among investigated samples.

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  • Found that all 161 weak D samples analyzed possessed altered RHD exon sequences, not normal ones.
  • Amino acid substitutions in weak D types were localized to specific protein regions.

    • Conclusions:

    • Weak D phenotypes are associated with altered RhD proteins, challenging previous assumptions.
    • Developed methods for specific detection and classification of weak D types.
    • Genotyping weak D can guide transfusion policies, particularly for those at risk of anti-D development.