title: Longitudinal study of Plasmodium falciparum infection and immune responses in infants with or without the sickle cell trait.
abstract: BACKGROUND
  Individuals may be homozygous (SS) or heterozygous (AS) sickle cell gene carriers or have normal adult haemoglobin (AA). Haemoglobin S could have a protective role against malaria but evidence is sparse and the operating mechanisms are poorly known.
  
  
  METHODS
  We followed two cohorts of children. The first was enrolled at birth (156 newborn babies) and the second at 24-36 months old (84 children). Both cohorts were followed for 30 months; monthly for parasitological data and half yearly for immunological data.
  
  
  RESULTS
  In the first cohort, 22%, and in the second 13% of children were AS. Whatever their age parasite prevalence rates were similar in AA and AS individuals. Mean parasite densities increased less rapidly with age in AS than in AA children, and were significantly lower in AS than in AA children >48 months old. The AA children tended to be more often admitted to hospital than AS children (22% versus 11%, NS). Both anti-Plasmodium falciparum and anti-Pfl55/RESA antibody rates increased more rapidly in AA than in AS children. Conversely, the prevalence rate of cellular responders to the Pfl55/RESA antigen was similar in AA and AS children during the first 2 years of life, then it was higher in AS than in AA children.
  
  
  CONCLUSIONS
  Sickle cell trait related antimalarial protection varies with age. The role of the modifications of the specific immune response to P. falciparum in explaining the protection of AS children against malaria is discussed.
authors.affiliation: Institut National de la Santé et de la Recherche Medicale, Unite 13 Institut de Medecine et d'Epidemiologie Africaine, Paris, France.
authors.forename: J Y
authors.initials: JY
authors.lastname: Le Hesran
authors.forename: I
authors.initials: I
authors.lastname: Personne
authors.forename: P
authors.initials: P
authors.lastname: Personne
authors.forename: N
authors.initials: N
authors.lastname: Fievet
authors.forename: B
authors.initials: B
authors.lastname: Dubois
authors.forename: M
authors.initials: M
authors.lastname: Beyemé
authors.forename: C
authors.initials: C
authors.lastname: Boudin
authors.forename: M
authors.initials: M
authors.lastname: Cot
authors.forename: P
authors.initials: P
authors.lastname: Deloron
mesh_terms: D000818:Animals; D000913:Antibodies, Protozoan / Q000032:analysis; D002163:Cameroon / Q000453:epidemiology; D002675:Child, Preschool; D004912:Erythrocytes / Q000276:immunology / Q000378:metabolism / Q000469:parasitology*; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D006441:Hemoglobin A / Q000235:genetics; D006451:Hemoglobin, Sickle / Q000235:genetics; D006801:Humans; D007111:Immunity, Cellular; D007223:Infant; D007231:Infant, Newborn; D016778:Malaria, Falciparum / Q000150:complications / Q000453:epidemiology / Q000276:immunology* / Q000469:parasitology; D008297:Male; D010963:Plasmodium falciparum / Q000276:immunology* / Q000302:isolation & purification; D015995:Prevalence; D015800:Protozoan Proteins / Q000276:immunology; D012189:Retrospective Studies; D012805:Sickle Cell Trait / Q000097:blood / Q000150:complications / Q000276:immunology*
chemical_list: D000913:Antibodies, Protozoan; D006451:Hemoglobin, Sickle; D015800:Protozoan Proteins; C050256:ring-infected erythrocyte surface antigen (RESA), Plasmodium falciparum; C028672:hemoglobin AA; C028671:hemoglobin AS; D006441:Hemoglobin A