Search bioRxiv⌕ Search

Biology subjects

Nsango, S. E.

Publications and source records attributed to Nsango, S. E..

3 recordsLinked to original sources

Genetic diversity of Plasmodium falciparum and Plasmodium malariae and its association with infectivity of Anopheles coluzzii in the Mfou Health District, Central Region of Cameroon

Background Malaria remains a major public health challenge in Cameroon, with sustained transmission particularly in forest-savannah transition zones. Although Plasmodium falciparum is the predominant malaria parasite, non-falciparum species such as P. malariae also contribute to the human infectious reservoir and to onward transmission. Parasite genetic diversity and multiplicity of infection (MOI) are recognized determinants of malaria transmission and may influence the prevalence and intensity of infection in mosquito vectors. However, whether parasite genetic diversity and MOI differentially influence the infectivity of P. falciparum and P. malariae to local Anopheles coluzzii populations remains poorly characterized. This knowledge gap is particularly relevant in the Mfou Health District, where malaria transmission persists and both P. falciparum and non-falciparum infections occur. Methods A cross-sectional survey was conducted between September 2022 and November 2023 in twelve primary schools in the Mfou Health District. Finger-prick blood samples were collected from children aged 3-17 years and examined by microscopy to identify Plasmodium infections and gametocyte carriers. Gametocyte-positive participants were enrolled in direct membrane feeding assays (DMFA) using locally reared Anopheles coluzzii. Blood samples were tested under two conditions: whole blood (WB) and replacement with naive AB serum. Mosquito infection outcomes were assessed at the oocyst (day 7) and sporozoite stages (day 14). Parasite species were confirmed by quantitative PCR (qPCR), and genetic diversity was assessed using seven microsatellite loci, together with msp1 and msp2 markers for P. falciparum and pmmsp1 for P. malariae. MOI and expected heterozygosity (He) were calculated, and their associations with mosquito infection prevalence and intensity were evaluated using generalized linear models. Results Among 2,807 children screened, 2,111 (75.2%) were infected with Plasmodium, and 388 (18.4%) carried gametocytes. A total of 169 children aged 4-13 years were selected for membrane feeding assays using Anopheles coluzzii, of whom 68% successfully infected mosquitoes. Among 10,872 dissected mosquitoes, 20.2% were infected at the oocyst stage, with both infection prevalence and intensity being higher in mosquitoes fed on AB serum-reconstituted blood than with whole blood. Sporozoite-stage infections were detected in 5.8% of mosquitoes, predominantly under AB serum conditions. Mosquito infection prevalence and intensity increased with gametocyte density, although submicroscopic gametocyte carriers were also infectious. P. falciparum exhibited high genetic diversity (MOI 2.4 {+/-} 0.8; He 0.72 {+/-} 0.07), while P. malariae showed limited diversity (MOI 0.11-0.21; He {approx} 0). Mixed-species and polyclonal infections were associated with enhanced infection outcomes. Moreover, the msp2 FC27 allelic family in P. falciparum and the 800-bp pmmsp1 allele in P. malariae were associated with oocyst development. Overall, parasite genetic diversity, multiplicity of infection, and species composition were positively associated with mosquito infectivity, with only minor seasonal variation observed. Conclusion Malaria transmission in Mfou is sustained by genetically diverse and multiclonal P. falciparum infections, with P. malariae also contributing to the human infectious reservoir. The association of parasite genetic diversity, MOI, and allele-specific factors with mosquito infectivity underscores the importance of addressing asymptomatic and multiclonal infections in malaria control strategies.

genetics↗

Genotypic evidence of vector-mediated selection on Plasmodium falciparum in infected field-collected Anopheles mosquitoes

Malaria-causing Plasmodium parasites are transmitted between vertebrate hosts via diverse species of Anopheles mosquitoes. The P47 protein in Plasmodium falciparum has been shown to affect transmission in various anopheline species by mediating evasion of mosquito innate immunity in an allele-specific manner. The Pfs47 gene that encodes P47 exhibits high genetic divergence across continents, as well as high genetic diversity within many parasite populations, but the impact of polymorphisms on transmission success in different sympatric vectors has not been previously studied in a field context. Here we report parasite genotyping data from naturally infected, field-collected mosquitoes at sites harboring at least two prevalent sympatric vector species, targeting Pfs47 in addition to the CSP, AMA1, SERA2, and TRAP parasite antigens. Collections took place at Ndangueng, Cameroon and Benguia, Gabon between November 2019 and July 2021, yielding infected Anopheles gambiae at both sites in addition to Anopheles moucheti in Cameroon and Anopheles funestus in Gabon. We found no significant difference in the mean number of parasite strains in infected sympatric mosquito species from each site. However, Pfs47 exhibited a significant difference in the prevalence of an amino acid polymorphism (I248L) between An. moucheti and An. gambiae in Cameroon. Polymorphisms at two additional positions (N272Y/I and P369H) displayed significant linkage disequilibrium with I248L, and there were significant differences in the distribution of Pfs47 haplotypes between sympatric mosquito species at both sites. These findings demonstrate divergent selection on P. falciparum mediated by sympatric vector species, suggesting that parasite genotype significantly impacts local vectorial capacity by modulating species-specific vector competence.

evolutionary biology↗

Sickle cell status skews malaria parasite genotype at infection

Sickle cell hemoglobin (HbS) confers protection against symptomatic malaria caused by Plasmodium falciparum. HbS carriers with symptomatic malaria harbour parasites enriched for sickle-associated alleles (Pfsa+), which appear to partially overcome HbS-mediated protection, but their role in asymptomatic infections is unclear. Here, we conducted a cross-sectional survey of 2,246 healthy school children in a region of high malaria transmission region in Cameroon. Analysing parasite Pfsa and human HbS genotypes for 1,701 asymptomatic P. falciparum infections confirmed that heterozygous HbS (HbAS) and homozygous non-HbS (HbAA) genotypes have similar rates of asymptomatic infection. However, the HbS genotype is strongly associated with parasites carrying Pfsa+ alleles at Pfsa1 and Pfsa3 loci, indicating a selective advantage for these alleles in HbS carriers. Our findings reveal that the protective effect of HbS is complex, where HbS has a protective effect prior to symptoms against Pfsa- parasites and Pfsa+ alleles may contribute to lower rates of symptomatic disease in HbS carriers. HbS protection against malarial disease should consider both resistance and tolerance and ongoing co-evolution with parasites.

genetics↗