Research
Plasmodium falciparum parasites causing cerebral malaria share variant surface antigens, but are they specific?
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* Corresponding author: Agnès Aubouy agnes.aubouy@ird.fr
1 Institut de Recherche pour le Développement (IRD) UMR216, Mother and Child faced with tropical infections Unit, Paris, 75006, France
2 Université Paris Descartes, Faculté de Pharmacie, Paris, 75270, France
3 UMR216 IRD, Cotonou, Benin
4 Paediatric Department, Centre National Hospitalo-Universitaire (CNHU), Cotonou, Benin
5 Unité de recherche en biologie et épidémiologie parasitaires, Institut de Recherche Biomédicale des Armées - Antenne de Marseille & Unité de recherche en maladies infectieuses et tropicales émergentes, UMR6236, Marseille, France
6 Département des Sciences Biologiques, Faculté de Médecine et des Sciences Pharmaceutiques, Université de Douala, BP2701, Douala, Cameroun
Malaria Journal 2010, 9:220 doi:10.1186/1475-2875-9-220
Published: 27 July 2010Abstract
Background
Variant surface antigens (VSA) expressed on the surface of Plasmodium falciparum-infected red blood cells constitute a key for parasite sequestration and immune evasion. In distinct malaria pathologies, such as placental malaria, specific antibody response against VSA provides protection. This study investigated the antibody response specifically directed against VSA expressed by parasites isolated from individuals presenting a given type of clinical presentation.
Methods
Plasma and isolates were obtained from four groups of Beninese subjects: healthy adults, patients presenting uncomplicated malaria (UM), cerebral malaria (CM), or pregnancy-associated malaria (PAM). The reactivity of plasma samples from each clinical group was measured by flow cytometry against parasites isolated from individuals from each clinical group.
Results
Antibody responses against VSAUM were predominant in CM, UM and HA plasmas. When analysed according to age in all plasma groups, anti-VSACM and -VSAUM antibody levels were similar until six years of age. In older groups (6-18 and >19 years of age), VSAUM antibody levels were higher than VSACM antibody levels (P = .01, P = .0008, respectively). Mean MFI values, measured in all plasmas groups except the PAM plasmas, remained low for anti-VSAPAM antibodies and did not vary with age. One month after infection the level of anti-VSA antibodies able to recognize heterologous VSACM variants was increased in CM patients. In UM patients, antibody levels directed against heterologous VSAUM were similar, both during the infection and one month later.
Conclusions
In conclusion, this study suggests the existence of serologically distinct VSACM and VSAUM. CM isolates were shown to share common epitopes. Specific antibody response to VSAUM was predominant, suggesting a relative low diversity of VSAUM in the study area.