The Molecular Mechanisms of Erythrocyte Invasion of Plasmodium spp. as a Model Organism of Apicomplexan Protozoa

Abstract

Apicomplexan protozoa are a phylum of parazites that includes medically and agriculturally important pathogens. They are named for their cell apex which contains a number of organelles (rhoptri, micronemes, conoid, apical polar ring, dense granules and apicoplast), important for their invasion and development within host cells. Among important apicomplexan parasites that affect human health directly or indirectly are Plasmodium spp., Toxoplasma gondii, Cryptosporodium, Eimeria, Babesia, and Theileria. Apicomplexan parasites move and actively enter host cells by substrate-dependent gliding motility. In these parasites, gliding motility and host cell invasion are driven by an actomyosin-based system (Glydeosome). A gliding motor machinery is embeded between the plasma membrane and inner membrane complex (IMC), a unique double membrane layer. A unique actomyosin motor powers both host cell invasion and locomotion of apicomplexan invasive stage. The cytoplasmic motor, a transmembrane bridge, and surface ligants essential for cell invasion are conserved among the main apicomplexan pathogens. In this review, erythrocytet invasion of Plasmodial merozit, which is a model organism of apicomplexan parasites, has been reviewed in detail.