On the Cytoadhesion of Plasmodium vivax-Infected Erythrocytes

On the Cytoadhesion of Plasmodium vivax-Infected Erythrocytes

Author Carvalho, Bruna O. Google Scholar
Lopes, Stefanie C. P. Google Scholar
Nogueira, Paulo A. Google Scholar
Orlandi, Patricia P. Google Scholar
Bargieri, Daniel Youssef Autor UNIFESP Google Scholar
Blanco, Yara C. Google Scholar
Mamoni, Ronei Google Scholar
Leite, Juliana A. Google Scholar
Rodrigues, Mauricio Martins Autor UNIFESP Google Scholar
Soares, Irene S. Google Scholar
Oliveira, Tatiane R. Google Scholar
Wunderlich, Gerhard Google Scholar
Lacerda, Marcus V. G. Google Scholar
del Portillo, Hernando A. Google Scholar
Araujo, Maria O. G. Google Scholar
Russell, Bruce Google Scholar
Suwanarusk, Rossarin Google Scholar
Snounou, Georges Google Scholar
Renia, Laurent Google Scholar
Costa, Fabio Trindade Maranhão Autor UNIFESP Google Scholar
Institution 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
INSERM
Univ Paris 06
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.
Language English
Sponsor Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Doencas Negligenciadas
Coordenacao de Aperfeicoamento de Pessoal de Nivel
Agency for Science, Technology, and Research, Singapore
Institut National de la Sante et de la Recherche Medicale, France
Grant number FAPESP: 04/00638-6
FAPESP: 05/60569-0
FAPESP: 09/52013-3
Doencas Negligenciadas: 576128/2008-2
Date 2010-08-15
Published in Journal of Infectious Diseases. Cary: Oxford Univ Press Inc, v. 202, n. 4, p. 638-647, 2010.
ISSN 0022-1899 (Sherpa/Romeo, impact factor)
Publisher Oxford Univ Press Inc
Extent 638-647
Origin http://dx.doi.org/10.1086/654815
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000279886600017
URI http://repositorio.unifesp.br/handle/11600/32822

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