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. Author manuscript; available in PMC: 2013 May 15.
Published in final edited form as: Int J Parasitol. 2012 Apr 19;42(6):575–582. doi: 10.1016/j.ijpara.2012.03.006

Fig. 1.

Fig. 1

Host-parasite interactions that facilitate erythrocyte invasion and erythrocyte remodeling. (A) The erythrocytic stage of the Plasmodium life cycle depends on host proteins at a number of stages: schizont maturation, merozoite egress, merozoite attachment, merozoite invasion, and intracellular growth and parasite protein trafficking to the surface of the infected erythrocyte. Throughout this process, host Calpain-1 has been determined to be critical for parasite escape from the parasitophorous vacuole and erythrocyte egress, binding to erythrocyte blood group receptors has been shown to be required for invasion, signaling via G-protein coupled receptors (GPCRs) and host kinases have been shown to be necessary for intracellular establishment, and normal hemoglobin has been shown to be required for proper actin network formation and parasite adhesive protein export to the surface of the erythrocyte. (B) The host-parasite interface is shown in detail with respect to the invading merozoite. Parasite invasion ligands (Parasite Determinants) and human erythrocyte receptors (Host Determinants) which have been identified to date are shown. Host receptor modifications (glycosylation and terminal sialic acid residues) are shown. GPA, glycophorin A; GPB, glycophorin B; GPC, glycophorin C; CR1, complement receptor 1; BSG, Basigin; EBA, erythrocyte binding antigen; Rh, reticulocyte binding protein homolog.