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Title: On the Cytoadhesion of Plasmodium vivax-Infected Erythrocytes
Authors: Carvalho, Bruna O.
Lopes, Stefanie C. P.
Nogueira, Paulo A.
Orlandi, Patricia P.
Bargieri, Daniel Youssef [UNIFESP]
Blanco, Yara C.
Mamoni, Ronei
Leite, Juliana A.
Rodrigues, Mauricio Martins [UNIFESP]
Soares, Irene S.
Oliveira, Tatiane R.
Wunderlich, Gerhard
Lacerda, Marcus V. G.
del Portillo, Hernando A.
Araujo, Maria O. G.
Russell, Bruce
Suwanarusk, Rossarin
Snounou, Georges
Renia, Laurent
Costa, Fabio Trindade Maranhão [UNIFESP]
Universidade Estadual de Campinas (UNICAMP)
Fiocruz MS
Univ Estado Amazonas
Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Universidade de Brasília (UnB)
Barcelona Ctr Int Hlth Res
Inst Catalana Recerca & Estudis Avancats
Natl Univ Singapore
Univ Paris 06
Issue Date: 15-Aug-2010
Publisher: Oxford Univ Press Inc
Citation: Journal of Infectious Diseases. Cary: Oxford Univ Press Inc, v. 202, n. 4, p. 638-647, 2010.
Abstract: Background. Plasmodium falciparum and Plasmodium vivax are responsible for most of the global burden of malaria. Although the accentuated pathogenicity of P. falciparum occurs because of sequestration of the mature erythrocytic forms in the microvasculature, this phenomenon has not yet been noted in P. vivax. the increasing number of severe manifestations of P. vivax infections, similar to those observed for severe falciparum malaria, suggests that key pathogenic mechanisms (eg, cytoadherence) might be shared by the 2 parasites.Methods. Mature P. vivax-infected erythrocytes (Pv-iEs) were isolated from blood samples collected from 34 infected patients. Pv-iEs enriched on Percoll gradients were used in cytoadhesion assays with human lung endothelial cells, Saimiri brain endothelial cells, and placental cryosections.Results. Pv-iEs were able to cytoadhere under static and flow conditions to cells expressing endothelial receptors known to mediate the cytoadhesion of P. falciparum. Although Pv-iE cytoadhesion levels were 10-fold lower than those observed for P. falciparum-infected erythrocytes, the strength of the interaction was similar. Cytoadhesion of Pv-iEs was in part mediated by VIR proteins, encoded by P. vivax variant genes (vir), given that specific antisera inhibited the Pv-iE-endothelial cell interaction.Conclusions. These observations prompt a modification of the current paradigms of the pathogenesis of malaria and clear the way to investigate the pathophysiology of P. vivax infections.
ISSN: 0022-1899
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