Abstract:
Plasmodium, the causative agent, invades red blood cells on the basis of receptor- ligand interaction. Glycophorin B (GYP B), a transmembrane protein, is among identified red blood cell receptor that binds to P. falciparum Erythrocyte Binding Ligand-1(EBL-1). A mutation in GYP B gene impairs EBL-1 affinity, hence reducing malaria infection in the process. A community in the Democratic Republic of Congo (Efe pygmies) has eliminated glycophorin B gene from their gene pool through gene deletion, allowing them to be partially protected from malaria. Malaria is endemic in both Kisumu and Mombasa, which would cause human hosts to eliminate receptor genes that make them susceptible to infection. Prevalence of GYP B null genotypes and EBL-1 was to be established in Kisumu and Mombasa Districts. Parasite and human DNA was extracted from infected blood samples from children (5 years and older) and adults attending district hospitals in Kisumu and Mombasa, using standard phenol chloroform method. The GYP B and EBL-1 genotypes were detected through amplification using gene specific primers coupled to sequencing of the fragments. Five and 20 percent of the twenty samples each from Kisumu and Mombasa respectively were negative of the amplification (GYP B null genotype), whereas all the samples amplified for EBL-1. Sequenced glycophorin B fragments were aligned to the GYP B sequence in the NCBI database using routines in MEGA 5 genetic analysis software. There was presence of deletion in the GYP B gene, while the parasites have maintained their ligands. This study provides a direction into studying the highly polymorphic GYP B gene which could also be playing part in the recently observed decline in malaria in Kenya and Africa in general. These findings also putatively indicate the susceptibility of people living in Kisumu and Mombasa based on the maintained genes responsible for the malaria parasite receptors on the red blood cells. Hence they may influence public health approaches to malaria control in the regions.
