title: On the cytoadhesion of Plasmodium vivax-infected erythrocytes.
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.
authors.affiliation: Departamento de Genética, Evolução e Bioagentes, Instituto de Biologia, Universidade Estadual de Campinas, Campinas, Brazil.
authors.forename: Bruna O
authors.initials: BO
authors.lastname: Carvalho
authors.forename: Stefanie C P
authors.initials: SC
authors.lastname: Lopes
authors.forename: Paulo A
authors.initials: PA
authors.lastname: Nogueira
authors.forename: Patricia P
authors.initials: PP
authors.lastname: Orlandi
authors.forename: Daniel Y
authors.initials: DY
authors.lastname: Bargieri
authors.forename: Yara C
authors.initials: YC
authors.lastname: Blanco
authors.forename: Ronei
authors.initials: R
authors.lastname: Mamoni
authors.forename: Juliana A
authors.initials: JA
authors.lastname: Leite
authors.forename: Mauricio M
authors.initials: MM
authors.lastname: Rodrigues
authors.forename: Irene S
authors.initials: IS
authors.lastname: Soares
authors.forename: Tatiane R
authors.initials: TR
authors.lastname: Oliveira
authors.forename: Gerhard
authors.initials: G
authors.lastname: Wunderlich
authors.forename: Marcus V G
authors.initials: MV
authors.lastname: Lacerda
authors.forename: Hernando A
authors.initials: HA
authors.lastname: del Portillo
authors.forename: Maria O G
authors.initials: MO
authors.lastname: Araújo
authors.forename: Bruce
authors.initials: B
authors.lastname: Russell
authors.forename: Rossarin
authors.initials: R
authors.lastname: Suwanarusk
authors.forename: Georges
authors.initials: G
authors.lastname: Snounou
authors.forename: Laurent
authors.initials: L
authors.lastname: Rénia
authors.forename: Fabio T M
authors.initials: FT
authors.lastname: Costa
mesh_terms: D000818:Animals; D002448:Cell Adhesion; D042783:Endothelial Cells / Q000473:pathology; D004912:Erythrocytes / Q000469:parasitology* / Q000473:pathology; D005260:Female; D006801:Humans; D016780:Malaria, Vivax / Q000473:pathology*; D010920:Placenta / Q000473:pathology; D010966:Plasmodium vivax / Q000472:pathogenicity*; D011247:Pregnancy; D012453:Saimiri