Relationship of the sickle cell trait with the development of acquired immunity to falciparum malaria in Cameroonian children
Description
Children with the sickle-cell trait are known to be partially protected against Plasmodium falciparum malaria, presumably by mechanisms which are manifested at the level of the erythrocytes. The hypothesis tested in this study is that the protection afforded by the sickle-cell trait does not operate entirely at the erythrocyte level, but that the modulation of the immune response is also involved. The goal of the present study was to determine the differences in the antimalarial immune profiles of sickle-cell trait carriers and children with normal hemoglobin, aged 2 to 5 years, using parasitologic, humoral and cellular immunity parameters The study was carried out in Obala (Cameroon), a malaria endemic area, from September 1989 to January 1990. Children (58 sickle-cell trait carriers (HbAS) and 194 with normal hemoglobin (HbAA)) were randomly selected from the local Catholic School. Blood samples were collected from each child for the electrophoresis of hemoglobin, the determination of parasite density, the study of serum reactivity to malaria antigens by indirect immunofluorescent antibody assay (IFA) and the determination of serum levels of soluble interleukin-2 receptors (sIL-2R). A questionnaire was administered to the study sample to evaluate the influence of chloroquine use on the evolution of malaria parasitemia Plasmodium falciparum infection occurred more frequently in 124/194 (64%) of children with normal hemoglobin, compared with 21/58 (36%) of sickle-cell trait carriers (p $$ 0.05). Serum levels of sIL-2R were similar in sickle-cell trait carriers and in children with normal hemoglobin, parasitemic and non parasitemic children. Parasitized sickle-cell trait carriers had higher serum levels of sIL-2R than parasitized children with normal hemoglobin Cell mediated immune response as measured by the serum levels of soluble interleukin-2 (sIL-2R), explains at least some of the differences observed between malaria-infected sickle-cell carriers and children with normal hemoglobin, supporting the hypothesis that not all of the protection afforded to HbAS individuals is entirely mediated at the level of the erythrocyte