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10th Malaria Meeting

Working party Malaria / Section Antiparasitic Chemotherapy of the Paul-Ehrlich-Society (PEG e.V.) in cooperation with the German Society for Tropical Medicine and International Health (DTG e.V.) and the German Society for Parasitology (DGP e.V.)

09.11. - 10.11.2012, Marburg an der Lahn

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Unravelling the role of erythrocyte deformability in Plasmodium falciparum transmission

Meeting Abstract

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  • S. Sanyal - Weill Cornell Medical College of Cornell University, New York, USA
  • M. Tiburcio - Istituto Superiore di Sanità, Rome, Italy
  • G. Deplaine - INSERM-UPMC, Paris, France
  • S. Perrot - Institut Pasteur, Paris, France
  • G. Milon - Institut Pasteur, Paris, France
  • O. Mercereau-Puijalon - Institut Pasteur, Paris, France
  • P. Buffet - INSERM-UPMC, Paris, France
  • P. David - Institut Pasteur, Paris, France
  • T. Templeton - Weill Cornell Medical College of Cornell University, New York, USA
  • P. Alano - Istituto Superiore di Sanità, Rome, Italy
  • C. Lavazec - Institut Pasteur, Paris, France

10th Malaria Meeting. Marburg, 09.-10.11.2012. Düsseldorf: German Medical Science GMS Publishing House; 2013. Doc12mal05

doi: 10.3205/12mal05, urn:nbn:de:0183-12mal050

Published: January 8, 2013

© 2013 Sanyal et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

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Achievement of malaria elimination requires development of novel strategies interfering with parasite transmission, including targeting the parasite sexual stages (gametocytes). The formation of Plasmodium falciparum gametocytes in the human host takes several days during which immature Gametocyte-Infected Erythrocytes (GIE) sequester in host tissues. Only mature stage GIEs circulate in the peripheral blood, available to uptake by the Anopheles vector. Mechanisms underlying GIE sequestration and release in circulation are virtually unknown. We show here that mature GIE are more deformable than immature stages using ektacytometry and microsphiltration methods, and that a switch in cellular deformability in the transition from immature to mature gametocytes is accompanied by the de-association of parasite-derived STEVOR proteins from the infected erythrocyte membrane. We hypothesize that mechanical retention contributes to sequestration of immature GIE and that regained deformability of mature gametocytes is associated with their release in the bloodstream and ability to circulate. These processes are proposed to play a key role in P. falciparum gametocyte development in the host and to represent novel and unconventional targets for interfering with parasite transmission.