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. 2018 Aug 30;4(8):e00760.
doi: 10.1016/j.heliyon.2018.e00760. eCollection 2018 Aug.

Role of genetic factors and ethnicity on the multiplicity of Plasmodium falciparum infection in children with asymptomatic malaria in Yaoundé, Cameroon

Dongang Nana Rodrigue Roman  1   2   3 , Ngono Ngane Rosalie Anne  1 , Vineeta Singh  3 , Koanga Mogtomo Martin Luther  1 , Ngonde Essome Marie Chantal  2   4 , Mouelle Sone Albert  5
Affiliations

Role of genetic factors and ethnicity on the multiplicity of Plasmodium falciparum infection in children with asymptomatic malaria in Yaoundé, Cameroon

Dongang Nana Rodrigue Roman et al. Heliyon. .

Abstract

In this cross-sectional study, we investigated host genetic factors and ethnic variation in circulating Plasmodium falciparum merozoite surface protein 2 (msp-2) clones among children with asymptomatic malaria. Isolates from seventy two asymptomatic malaria children were used for genotyping block 3 of msp-2 gene by nested polymerase chain reaction (PCR). Sickle cell trait and glucose-6-phosphate dehydrogenase (G6PD) deficiency were analysed by restriction fragment length polymorphism of DNA products from PCR targeting codons 6 and 68 of the beta-globin (HBB) and G6PD genes respectively. ABO blood group was typed by agglutination method. A total of forty two msp-2 genotypes (20 for 3D7 and 22 for FC27) were detected for an average (standard error of mean) multiplicity of infection (MOI) of 2.45 (0.16). The MOI was statistically the same among the five identified ethnic groups (P = 0.83). The overall prevalence of sickle cell trait and G6PD deficiency were 12.50 % and 22.22 % respectively. MOI was similar between children with Hb AA and Hb AS genotypes (P = 0.42). MOI was significantly high among children with a mutant G6PD genotype (P = 0.017). MOI was significantly higher in blood group O than group A (P = 0.03). Our findings show that although ethnicity and sickle cell trait have no association with MOI, the association was observed with G6PD genotype and ABO group. The results suggest the need for extension and expansion of the current study in order to investigate the mechanisms involved.

Keywords: Clinical genetics; Epidemiology; Infectious disease; Pediatrics.

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Figures

Fig. 1
Fig. 1
Gel picture showing PCR amplicons and RFLP fragments. (A): represents PCR products, lines 1 – 11 are samples for sickle cell (a) and G6PD studies (b); line M represents 100 bp ladder molecular size marker. (B): presents restrictions fragments after digestion with enzyme. Lines 1, 2, 3, 4, 5 and 6 shows bands before digestion and lines 1’, 2’, 3’ 4’ 5’ and 6’ after digestion for the same isolates. Line M represents 50 bp ladder molecular size marker. G6PD: Glucose-6-phosphate dehydrogenase.
Fig. 2
Fig. 2
Multiplicity of infection (MOI) according to erythrocyte polymorphism in asymptomatic malaria children (*: significant difference at 0.05 level). Hb AS: Children with sickle cell trait, Hb AA: Children with normal haemoglobin; G6PD Deficient: children with the genotype resulting in a deficiency in the enzymatic activity of glucose-6-phosphate dehydrogenase (G6PD), G6PD Normal: children with the genotype conferring a normal enzymatic activity of G6PD; MOI: Multiplicity of infection.
Fig. 3
Fig. 3
Allele frequencies and erythrocyte polymorphism (*: statistical significant with Fisher's exact test) Hb AS: Children with sickle cell trait, Hb AA: Children with normal haemoglobin; G6PD Deficient: children with the genotype resulting in a deficiency in the enzymatic activity of Glucose-6-phosphate dehydrogenase (G6PD), G6PD Normal: children with the genotype conferring a normal enzymatic activity of G6PD; MOI: Multiplicity of infection.
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