ABSTRACT
Malaria is an ancient disease that continues to cause enormous human morbidity and mortality mainly due to the invasion of the erythrocyte by the merozoite stage of the Parasite (Plasmodium falciparum), as the parasite spend much of it life intracellularly. Therefore the aim of this paper was to review the state of knowledge on the mechanism of erythrocytic invasion by the merozoite of Plasmodium falciparum. The invasion process is a coordinated series of protein/protein interactions, protease cleavage events, intracellular signals, organelle release and engagement of an actin-myosin motor. The invasion is achieved through either, sialic acid dependent which uses EBA-140,EBA-175,EBA-181 and PfRH1 or sialic acid in-dependent pathways which uses PfRH2 and PfRH4. Successful invasion process is completed in the following steps; Meroziote activation, Merozoite binding, Reorientation and deformation, Junction formation and Parasite entry. Merozoite acitivation involve egresses of the merozite from the erythrocyte where exoneme secretes the first protein called subtisilin-like protease-1 (PfSUB-1) in to the parasitophorous vacuole which ensure primary proteolysis of Serine-Repeat antingen (SERA) which in turn act on Parasitophorous Vacoule and Red Blood Cell to initiate host cell rupture. Dipeptidyl peptidase 3 (DPAP3) also contribute to the egress by regulating the maturation of PfSUB-1. The initial interaction between the merozoite and the erythrocyte is due to random and weak collision and presumptively involves in the first instance a reversible interaction between proteins on the merozoite surface and the host erythrocyte. In this ligands bind to specific receptors on the merozoite, where Erythrocyte Binding Anitigen-175 (EBA-175) bind to Glycophorin A, EBA-140 binds to Glycophorin C, Erythrocyte Binding-like-1 protein (EBL-1) binds to Glycophorin B and PfRh4 binds to Complement Receptor-1 (CR-1) and PfRh5 binds to Basigin (CD147) on the erythrocyte. This is followed by permanent positioning of the apical organelles of the merozoite on to the red blood cell (re-orientation) and release of adhesive proteins (adhesins), Protease and membrane altering agent specifically Subtisilin-2 (PfSUB-2), Apical Membrane Antigen-1 (AMA1).Junction formation is an intimate circumferential contact with the host cell called tight junction and it is formed under the influence of Apical Membrane Antigen 1 (AMA1) and Rhoptery neck (RON). Finally the merozoite penetrates in to the erythrocyte bilayer with the help of Actin- Myosin motor, Thrombospondin-Related Anonymous Protein family (TRAP) and aldolase
Key words: Key Words: Plasmodium falciparum, Merozoite, Activation, Invasion, Invasins, Adhesins.
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