Project description:The malaria parasite, Plasmodium falciparum, exploits multiple ligand-receptor interactions, called invasion pathways, to invade the host erythrocyte. Strains of P.falciparum vary in their dependency on sialated red cell receptors for invasion. We show that switching from sialic acid-dependent to –independent invasion is reversible and depends on parasite ligand utilisation. Expression of P.falciparum reticulocyte-binding like homologue 4 (PfRh4) correlates with sialic acid-independent invasion and PfRh4 is essential for switching invasion pathways. Differential activation of PfRh4 represents a novel mechanism of invasion pathway control and provides P.falciparum with exquisite adaptability in the face of erythrocyte receptor polymorphisms and host immune responses. Keywords: Plasmodium falciparum, erythrocyte invasion, invasion pathways, EBA175, Rh4
Project description:Transcriptomic Analysis of Cultured Sporozoites of P. falciparum RNA-seq reads from each of three developmental stages (2 replicates per sample) were mapped to the reference Plasmodium falciparum genome, and gene expression levels were calculated for each sample.