BACKGROUND AND OBJECTIVES: The Rh phenotypes hrB- and VS+ are both rare in Whites but more common in Blacks. The high-incidence antigen hrB is present on most red cells that are e+. The presence of VS on red cells is associated with an aberrant expression of e, often called eS. MATERIALS AND METHODS: Using conventional serologic methods, including a monoclonal anti-hrB-like antibody, we studied 65 e+ samples that were apparently hrB-. RESULTS: Of the 65, we found that 59 (91%) were VS+. Recent findings have indicated that in VS+ persons a change from leucine to valine occurs at amino acid 245 of the RHCE-encoded polypeptide. While this residue is predicted to lie within the red cell membrane bilayer, the change presumably affects alanine 226 (that is present when e is expressed) in such a way that eS is seen. CONCLUSIONS: Our findings suggest that the change from e to eS may result in nonexpression or marked depression of expression of hrB that is, perhaps, an epitope of e. While the molecular basis of the hrB-phenotype is not known, it is unlikely that the leucine-to-valine change at residue 245, resulting in the aberrant from of e, explains all hrB-samples. First, hrB-VS+ and hrB- VS- samples must differ. Second, some hrB- VS+ samples are C+, some are C-. Presumably diverse molecular bases are involved in hrB-phenotypes.
BACKGROUND AND OBJECTIVES: The Rh phenotypes hrB- and VS+ are both rare in Whites but more common in Blacks. The high-incidence antigen hrB is present on most red cells that are e+. The presence of VS on red cells is associated with an aberrant expression of e, often called eS. MATERIALS AND METHODS: Using conventional serologic methods, including a monoclonal anti-hrB-like antibody, we studied 65 e+ samples that were apparently hrB-. RESULTS: Of the 65, we found that 59 (91%) were VS+. Recent findings have indicated that in VS+ persons a change from leucine to valine occurs at amino acid 245 of the RHCE-encoded polypeptide. While this residue is predicted to lie within the red cell membrane bilayer, the change presumably affects alanine 226 (that is present when e is expressed) in such a way that eS is seen. CONCLUSIONS: Our findings suggest that the change from e to eS may result in nonexpression or marked depression of expression of hrB that is, perhaps, an epitope of e. While the molecular basis of the hrB-phenotype is not known, it is unlikely that the leucine-to-valine change at residue 245, resulting in the aberrant from of e, explains all hrB-samples. First, hrB-VS+ and hrB- VS- samples must differ. Second, some hrB- VS+ samples are C+, some are C-. Presumably diverse molecular bases are involved in hrB-phenotypes.
Authors: Natasha M Savage; Wadicar F Nugent; Lawrence D Devoe; Roni J Bollag; Lloyd O Cook Journal: Blood Transfus Date: 2010-12-27 Impact factor: 3.443