title: Associations between red cell polymorphisms and Plasmodium falciparum infection in the middle belt of Ghana.
abstract: BACKGROUND
  Red blood cell (RBC) polymorphisms are common in malaria endemic regions and are known to protect against severe forms of the disease. Therefore, it is important to screen for these polymorphisms in drugs or vaccines efficacy trials. This study was undertaken to evaluate associations between clinical malaria and RBC polymorphisms to assess biological interactions that may be necessary for consideration when designing clinical trials.
  
  
  METHODS
  In a cross-sectional study of 341 febrile children less than five years of age, associations between clinical malaria and common RBC polymorphisms including the sickle cell gene and G6PD deficiency was evaluated between November 2008 and June 2009 in the middle belt of Ghana, Kintampo. G6PD deficiency was determined by quantitative methods whiles haemoglobin variants were determined by haemoglobin titan gel electrophoresis. Blood smears were stained with Giemsa and parasite densities were determined microscopically.
  
  
  RESULTS
  The prevalence of clinical malarial among the enrolled children was 31.9%. The frequency of G6PD deficiency was 19.0% and that for the haemoglobin variants were 74.7%, 14.7%, 9.1%, 0.9% respectively for HbAA, HbAC, HbAS and HbSS. In Multivariate regression analysis, children with the HbAS genotype had 79% lower risk of malaria infection compared to those with the HbAA genotypes (OR = 0.21, 95% CI: 0.06-0.73, p = 0.01). HbAC genotype was not significantly associated with malaria infection relative to the HbAA genotype (OR = 0.70, 95% CI: 0.35-1.42, p = 0.33). G6PD deficient subgroup had a marginally increased risk of malaria infection compared to the G6PD normal subgroup (OR = 1.76, 95% CI: 0.98-3.16, p = 0.06).
  
  
  CONCLUSIONS
  These results confirm previous findings showing a protective effect of sickle cell trait on clinical malaria infection. However, G6PD deficiency was associated with a marginal increase in susceptibility to clinical malaria compared to children without G6PD deficiency.
authors.affiliation: Kintampo Health Research Centre, Kintampo, Brong Ahafo Region, Ghana.
authors.forename: Nicholas
authors.initials: N
authors.lastname: Amoako
authors.affiliation: Kintampo Health Research Centre, Kintampo, Brong Ahafo Region, Ghana.
authors.forename: Kwaku Poku
authors.initials: KP
authors.lastname: Asante
authors.affiliation: Kintampo Health Research Centre, Kintampo, Brong Ahafo Region, Ghana.
authors.forename: George
authors.initials: G
authors.lastname: Adjei
authors.affiliation: Infectious Diseases Research Laboratory, Department of Biochemistry, Cell and Molecular Biology. University of Ghana, Legon, Ghana.
authors.forename: Gordon A
authors.initials: GA
authors.lastname: Awandare
authors.affiliation: Department of Animal Biology and Conservation Science, University of Ghana, Legon, Ghana.
authors.forename: Langbong
authors.initials: L
authors.lastname: Bimi
authors.affiliation: Kintampo Health Research Centre, Kintampo, Brong Ahafo Region, Ghana.
authors.forename: Seth
authors.initials: S
authors.lastname: Owusu-Agyei
mesh_terms: D002675:Child, Preschool; D003430:Cross-Sectional Studies; D005260:Female; D005838:Genotype; D005869:Ghana / Q000453:epidemiology; D005954:Glucosephosphate Dehydrogenase / Q000235:genetics*; D005955:Glucosephosphate Dehydrogenase Deficiency / Q000097:blood / Q000453:epidemiology* / Q000235:genetics; D006455:Hemoglobins, Abnormal / Q000235:genetics*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D016778:Malaria, Falciparum / Q000097:blood / Q000453:epidemiology* / Q000469:parasitology; D008297:Male; D010963:Plasmodium falciparum / Q000502:physiology; D011110:Polymorphism, Genetic; D012307:Risk Factors; D012805:Sickle Cell Trait / Q000097:blood / Q000453:epidemiology* / Q000235:genetics
chemical_list: D006455:Hemoglobins, Abnormal; D005954:Glucosephosphate Dehydrogenase