Abstract
Infection with the protozoan parasite Plasmodium falciparum causes the most severe form of human malaria with over two million deaths per year. The clinical symptoms of malaria infection result from the rapid exponential expansion of parasites during the asexual erythrocytic phase of the P. falciparum life cycle. Invasion of erythrocytes by merozoites is a tightly controlled process that involves specific receptor-ligand interactions between host and parasite molecules. Virulence of P. falciparum parasites has been associated with increased multiplication rates and an ability to invade a greater range of host erythrocytes.1 Here we focus on our understanding of the molecular mechanisms underlying host cell selection and invasion of the host erythrocyte using parasite adhesive proteins. We will consider the parasite strategy of deploying multiple and variant adhesive ligands for successful invasion. An understanding of the molecular mechanism by which these proteins mediate invasion will facilitate their use in the rational design of vaccine and drug strategies.
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Duraisingh, M.T., DeSimone, T., Jennings, C., Refour, P., Wu, C. (2008). Erythrocyte Invasion by Plasmodium falciparum: Multiple Ligand-Receptor Interactions and Phenotypic Switching. In: Burleigh, B.A., Soldati-Favre, D. (eds) Molecular Mechanisms of Parasite Invasion. Subcellular Biochemistry, vol 47. Springer, New York, NY. https://doi.org/10.1007/978-0-387-78267-6_3
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DOI: https://doi.org/10.1007/978-0-387-78267-6_3
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