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Description
Sulin Zhang1 Yao Zhang3 Leann Tilley4 Ju Li2 Subra Suresh5

1, The Pennsylvania State University, University Park, Pennsylvania, United States
3, Northwestern University, Evanston, Illinois, United States
4, The University of Melbourne, Melbourne, Victoria, Australia
2, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States
5, Nanyang Technological University, Singapore, , Singapore

A normal human red blood cell (RBC) is characterized by two distinct features: high deformability and discocyte shape, which underlie its biological functions, demonstrated by the repeated transit of RBCs (diameter ~8 mm) through narrow capillaries and and 1-2 mm interendothelial slits in the spleen. These two distinct features of RBCs can be comprised genetically or in a variety of pathological conditions, leading to severe RBC diseases. Here we present a coarse-grained RBC membrane model integrating an one-agent-thick lipid bilayer model and a string-of-bead spectrin network model to simulate the change of deformability of the infected RBCs by the malaria parasites (plasmodium falciparum). In particular, we show how malaria parasites harness several materials principles simultaneously to render the RBC losing its deformability during asexual stage (disease-causing stage) and how the parasites alter the entropy of the spetrin network to enable the RBC regain the deformability during the sexual stage (disease-transmission stage). Our simulation results suggest potential targets for the development of new antimalarial therapies

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