Genetic characterization of Plasmodium falciparum allelic variants infecting mothers at delivery and their children during their first plasmodial infections.
BACKGROUND
Infants born to mothers with placental malaria at delivery develop Plasmodium falciparum parasitemia earlier than those born to mothers without placental infection. This phenomenon may be explained by the development of immune tolerance due to exposure to P. falciparum antigens in utero. The hypothesis of this study is that this increased susceptibility might be related to infections by parasites expressing the same blood stage allele's antigens as those to which the infants were exposed in utero.


METHODS
The comparison of P.falciparum msp2 (3D7 and FC27) and glurp gene polymorphisms of infected mothers at delivery to those of their offspring's infections during infancy was realized and the possible associations of the different polymorphisms with clinical outcomes were assessed. A second approach consisted in the use of a Geographic Information System to determine whether the antigen alleles were homogeneously distributed in the area of study. This was necessary to analyze whether the biological observations were due to high exposure to a particular antigen allelic form in the environment or to high infant permissiveness to the same allelic antigen polymorphism as the placental one.


RESULTS
Infants born to mothers with placental malaria at delivery were more susceptible to infections by parasites carrying the same glurp allele as encountered in utero compared to distinct alleles, independently of their geographic distribution.


CONCLUSIONS
The increased permissiveness of infants to plasmodial infections with shared placental-infant glurp alleles sheds light on the role that P. falciparum blood stage antigen polymorphisms may play in the first plasmodial infections in infancy.
Institut de Recherche Pour le Développement, UMR 216 Mère et Enfant Face Aux Infections Tropicales, Paris, France; PRES Sorbonne Paris Cité, Université Paris Descartes, Faculté de Pharmacie, Paris, France. Electronic address: celia.dechavanne@gmail.com.
Célia
C
Dechavanne
Charlotte
C
Pierrat
Emmanuelle
E
Renard
Bruno
B
Costes
Natacha
N
Martin
Rodolphe
R
Ladekpo
Claude
C
Ahouangninou
Violeta Moya
VM
Alvarez
Bich Tram
BT
Huynh
André
A
Garcia
Florence
F
Migot-Nabias
D000483:Alleles; D000953:Antigens, Protozoan / Q000235:genetics*; D016054:DNA, Protozoan / Q000235:genetics; D005260:Female; D014644:Genetic Variation; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D018445:Infectious Disease Transmission, Vertical; D016778:Malaria, Falciparum / Q000469:parasitology / Q000635:transmission*; D008297:Male; D010920:Placenta / Q000469:parasitology*; D010922:Placenta Diseases / Q000469:parasitology; D010963:Plasmodium falciparum / Q000235:genetics* / Q000276:immunology; D020641:Polymorphism, Single Nucleotide; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000469:parasitology; D015800:Protozoan Proteins / Q000235:genetics*; D017422:Sequence Analysis, DNA
D000953:Antigens, Protozoan; D016054:DNA, Protozoan; D015800:Protozoan Proteins; C065974:merozoite surface protein 2, Plasmodium; C072492:glutamate-rich protein, Plasmodium
Antigen polymorphisms; Immune tolerance; Infant; Malaria; Merozoite surface proteins; P. falciparum