| Full text | |
| Author(s): Show less - |
Carvalho, Bruna O.
[1, 2]
;
Lopes, Stefanie C. P.
[1]
;
Nogueira, Paulo A.
[2]
;
Orlandi, Patricia P.
[2]
;
Bargieri, Daniel Y.
[3, 4]
;
Blanco, Yara C.
[1]
;
Mamoni, Ronei
[1]
;
Leite, Juliana A.
[1]
;
Rodrigues, Mauricio M.
[3, 4]
;
Soares, Irene S.
[5]
;
Oliveira, Tatiane R.
[5]
;
Wunderlich, Gerhard
[6]
;
Lacerda, Marcus V. G.
[7]
;
del Portillo, Hernando A.
[8, 9]
;
Araujo, Maria O. G.
[10]
;
Russell, Bruce
[11]
;
Suwanarusk, Rossarin
[11]
;
Snounou, Georges
[11, 12, 13, 14]
;
Renia, Laurent
[11]
;
Costa, Fabio T. M.
[1]
Total Authors: 20
|
| Affiliation: Show less - | [1] Univ Estadual Campinas, Inst Biol, Dept Genet Evolucao & Bioagentes, BR-13083970 Campinas, SP - Brazil
[2] Fiocruz MS, Inst Leonidas & Maria Deane, Rio De Janeiro - Brazil
[3] Univ Fed Sao Paulo, Dept Microbiol Imunol & Parasitol, Sao Paulo - Brazil
[4] Univ Fed Sao Paulo, Ctr Interdisciplinar Terapia Genica, Sao Paulo - Brazil
[5] Univ Sao Paulo, Fac Ciencias Farmaceut, Dept Anal Clin & Toxicol, Sao Paulo - Brazil
[6] Univ Sao Paulo, Dept Parasitol, Inst Ciencias Biol, Sao Paulo - Brazil
[7] Univ Estado Amazonas, Manaus, Amazonas - Brazil
[8] Inst Catalana Recerca & Estudis Avancats, Barcelona - Spain
[9] Barcelona Ctr Int Hlth Res, Barcelona - Spain
[10] Univ Brasilia, Brasilia, DF - Brazil
[11] Natl Univ Singapore, Singapore Immunol Network, Agcy Sci Technol & Res, Singapore 117548 - Singapore
[12] Natl Univ Singapore, Dept Microbiol, Singapore 117548 - Singapore
[13] INSERM, Unite Mixte Rech S945, Paris - France
[14] Univ Paris 06, Fac Med Pitie Salpetriere, Paris - France
Total Affiliations: 14
|
| Document type: | Journal article |
| Source: | Journal of Infectious Diseases; v. 202, n. 4, p. 638-647, AUG 15 2010. |
| Web of Science Citations: | 165 |
| 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. (AU) | |
| FAPESP's process: | 04/00638-6 - Analysis of the immune response against surface antigens of human erythrocytes infected by Plasmodium spp.: emphasis on the improvement of vaccines and development of monoclonal antibodies |
| Grantee: | Fabio Trindade Maranhão Costa |
| Support Opportunities: | Research Grants - Young Investigators Grants |