Allelic polymorphism of MSP2 gene in severe P. falciparum malaria in an area of low and seasonal transmission

Abstract

The severe malaria (SM) and uncomplicated malaria (UM) infections are expected to have different genetic makeup. In this study, blood samples were obtained from 325 donors with SM and UM and malaria-free donors (including asymptomatic submicroscopic malaria--ASUM), from Eastern Sudan. The SM group included patients with cerebral malaria (CM), severe malarial anemia (SMA), and other complications. The MSP2 locus was exploited for parasite genotyping. We found that the genetic diversity of the parasite population was marked (51 genotypes). The overall multiplicity of infection (MOI) was 1.5, and it was comparable between SM and UM. However, the MOI in ASUM (1.0) and fatal CM (1.14) was comparable and significantly lower than in UM (1.53), SMA (1.52), and nonfatal CM (1.7). The ratio of the IC1 to FC27 allele families was comparable between SM and UM, and the distribution of the allele sizes was correlated (correlation coefficient = 0.59 and 0.718; P < 0.001). It is interesting to note that the FC27 genotype was overrepresented in ASUM (68.2%) and was not recognized in fatal CM, while in mixed-clone infections, the clearance of IC1 after quinine treatment was faster than FC27 clearance. Finally, the composition of the multiclone infections (IC1 and FC27) was suggesting a stronger cross-immunity within rather than between MSP2 gene families.

Genetic diversity of Plasmodium falciparum field isolates in central Sudan inferred by PCR genotyping of Merozoite surface protein 1 and 2

“…The number of alleles detected for MSP1 and MSP2 were 11 and 16, respectively. This data is consistent with that of previous studies in low and unstable malaria transmission regions in eastern Sudan[330] and other areas of seasonal unstable malaria in Sudan (Alyamani L.Y., M.Sc thesis, University of Khartoum, 2002) and in central Africa. [3132]…”

Genetic diversity of Plasmodium falciparum infections in mild and severe malaria of children from Kampala, Uganda

“…The data of A-Elbasit et al (2007), Durand et al (2008) and Rout et al (2009), in which no significant association was found between the occurrence of a specific genotype and the severity of malaria, support our findings. In French Guiana, it was demonstrated that a specific msp1 allele bearing a specific variant gene ( var-D ) was associated with severe malaria (Ariey et al 2001).…”

“…These findings seem to suggest that the use of single genetic markers may underestimate the diversity of infections. The observed results of a higher MOI are consistent with those of smaller studies done in India (Ranjit et al 2004, 2005; Rout et al 2009) but in contrast to reports from Senegal (Robert et al 1996) or Nigeria (Amodu et al 2008), where the severe malaria category had a lower MOI than the mild type; and also studies from Ghana (Nielsen et al 2002), Gabon (Mayengue et al 2007), Sudan (A-Elbasit et al 2007) and Madagascar (Durand et al 2008) where comparable levels of MOI were observed among mild and severe malaria cases. The studies in India included adult patients with severe malaria in whom severe complications developed following initial treatment at rural health centres (Ranjit et al 2004, 2005; Rout et al 2009).…”

“…falciparum , multiplicity of infection (MOI) and severity of clinical episodes is not well understood and the findings have been inconsistent (Table 1). Some studies have demonstrated a higher MOI in severe cases (Ranjit et al 2005; Rout et al 2009) and in others similar numbers of genotypes per infection between the categories have been observed (A-Elbasit et al 2007; Conway et al 1991; Durand et al 2008; Kun et al 1998; Nielsen et al 2002). Besides MOI, it is also not yet clear whether there are gene polymorphisms that cause some P .…”

“…The initial treatment among the study cases from the different sites could have reduced the diversity of the isolates (Amodu et al 2008; Durand et al 2008; Ranjit et al 2004, 2005; Robert et al 1996; Rout et al 2009). Additionally, differences in transmission intensity according to study sites may result in variable results when comparing MOI from different groups (A-Elbasit et al 2007; Amodu et al 2008; Robert et al 1996). Differences in genotyping methods and/or interpretation of data as well as the heterogeneity of the various study populations may also partly explain the variability of results among studies.…”