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Erythrocyte Invasion by Plasmodium falciparum: Multiple Ligand-Receptor Interactions and Phenotypic Switching

  • Manoj T. Duraisingh
  • Tiffany DeSimone
  • Cameron Jennings
  • Philippe Refour
  • Chenwei Wu
Part of the Subcellular Biochemistry book series (SCBI, volume 47)

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.

Keywords

Plasmodium Falciparum Parasite Line Plasmodium Knowlesi Invasion Pathway Tight Junction Formation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Landes Bioscience and Springer Science+Business Media 2008

Authors and Affiliations

  • Manoj T. Duraisingh
    • 1
  • Tiffany DeSimone
    • 1
  • Cameron Jennings
    • 1
  • Philippe Refour
    • 1
  • Chenwei Wu
    • 1
  1. 1.Department of Immunology and Infectious DiseasesHarvard School of Public HealthBostonUSA

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