The Deformability of Red Blood Cells Parasitized byPlasmodium falciparumandP. vivax
Author(s) -
Rossarin Suwanarusk,
Brian M. Cooke,
Arjen M. Dondorp,
Kamolrat Silamut,
Jetsumon Sattabongkot,
Nicholas J. White,
Rachanee Udomsangpetch
Publication year - 2004
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/380468
Subject(s) - plasmodium falciparum , biology , red blood cell , spleen , erythrocyte deformability , plasmodium vivax , immunology , parasite hosting , andrology , malaria , microbiology and biotechnology , medicine , world wide web , computer science
Red blood cells (RBCs) must deform considerably during their multiple passages through the microvasculature and the sinusoids of the spleen. RBCs infected with Plasmodium falciparum (Pf-IRBCs) become increasingly rigid as they mature but avoid splenic clearance by sequestering in venules and capillaries. In contrast, RBCs infected with P. vivax (Pv-IRBCs) do not sequester. We compared the effects of P. vivax and P. falciparum infection on RBC deformability in a laminar shear flow system. Pf-IRBCs became more rigid as the parasite matured, but equivalent maturation of Pv-IRBCs resulted in a doubling of flexibility. Coincidentally, the IRBC surface area increased from 56.7+/-1.3 microm2 to 74.7+/-0.6 microm2 to 90.9+/-1.1 microm2 in ring-, trophozoite-, and schizont-stage Pv-IRBCs, respectively, whereas Pf-IRBCs did not increase in size. P. vivax increases the deformability of IRBCs and thereby avoids splenic entrapment.
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