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Host Cell Remodelling and Sequestration of Malaria Transmission Stages

Subject Area Parasitology and Biology of Tropical Infectious Disease Pathogens
Term Funded in 2009
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 118292138
 
Plasmodium falciparum causes the most severe form of human malaria with over two million deaths per year. The morbidity and mortality of the disease can be attributed exclusively to the asexual stages residing and replicating within red blood cells. Virulence of these asexual stages is linked to the unique capability of P. falciparum to induce cytoadherence of infected red blood cells to the microvascular endothelium, thereby avoiding clearance during spleen passage. While the molecular basis and the selective pressures underlying cytoadherence in asexual parasites have been studied intensively in recent years, little is known about sequestration of young transmission stages, i.e. gametocytes. Understanding the survival strategies of sexual stage parasites during their comparatively long development within the human red blood cells is a prerequisite for novel approaches to block the transmission of this devastating pathogen to its mosquito vector. This project will be supervised by Matthias Marti and aims to gain a better understanding of the molecular basis that defines the host/pathogen-interactions implicated in transmission of P. falciparum. Molecular and cellular insights into this phase of the Plasmodium lifecycle are critical to the two major tasks in malaria research, development of vaccine strategies and new drugs. Using a potent set of state-of-the-art techniques, I will address fundamental issues in malaria transmission, including discovery and validation of novel gametocyte surface antigens as potential cytoadherence determinants. I will also determine sequestration profiles of sexual stage parasites ex vivo.
DFG Programme Research Fellowships
International Connection USA
 
 

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