Plasmodium falciparum: a comparative analysis of the genetic diversity in malaria-mesoendemic areas of Brazil and Madagascar

Abstract

For a better definition of the polymorphic features of Plasmodium falciparum parasite populations, the polymerase chain reaction (PCR) typing technique was used to investigate the genetic diversity and complexity of parasites harbored by acute P. falciparum carriers from three yet unexplored malaria-mesoendemic areas with different transmission levels: two localities in northwestern Brazil (Ariquemes and Porto Velho) and a village in Madagascar (Ankazobe). A total of 89 DNA samples were analyzed by amplification of polymorphic domains from genes encoding merozoite surface antigens 1 and 2 (MSP-1, MSP-2) and thrombospondin-related anonymous protein (TRAP) and by hybridization with allelic-family-specific probes or random-fragment-length polymorphism (RFLP). In all three localities, extensive polymorphism was observed for each marker, but the MSP-2 central repeat was the most diverse one. Similar levels of genetic diversity, allelic frequency, and infection complexity were observed in the two Brazilian localities, although the isolates had been sampled at 2-year intervals, suggesting the stability of the infecting parasite populations presenting in these regions of the Brazilian Amazon. Unexpectedly, although the entomologic inoculation rate was at least 3 times lower in Ankazobe than in the Brazilian areas. Malagasi samples appeared more complex than the Brazilian ones. The implications of these data with regard to parasite population-dynamics studies are discussed.

Genetic polymorphism of merozoite surface protein-1 and merozoite surface protein-2 in Plasmodium falciparum isolates from Brazzaville, Republic of Congo

“…Repeated studies are required to characterize and confirm the real genetic diversity of parasite populations in this area. Limited polymorphism in RO33 family is similar to findings in Senegal [24], Brazil [25] and in Iran [26]. Three and 4 RO33 alleles were found in Gabon [23] and Uganda [27] respectively.…”

Chapter 1 Strain Theory of Malaria

“…Longitudinal studies in humans suggest that competition and immunity mainly affect parasite density, not the time to clearance (Sama et al, 2006); apparent loss of particular genotypes is common, as densities drop below detection limits. Molecular genotyping has confirmed the expectations that 'mixed infections must be the rule ... in localities with even moderate transmission rate' (Babiker et al, 2000;Hackett, 1941;Peyerl-Hoffmann et al, 2001;Sallenave-Sales et al, 2000), that superinfection occurs more commonly in areas of higher transmission (Arnot, 1998), that novel genotypes infecting otherwise immune children give rise to symptomatic infections (Contamin et al, 1996), and that introductions of new phenotypes can cause epidemics of clinical malaria (Arez et al, 1999;Laserson et al, 1999). There is less evidence from these studies of small-scale variations in genotype frequencies that might lead to exposure to new strains after travelling 'relatively short distances in Africa' (Bray et al, 1962), but such variations have been observed in remote South American villages (Machado et al, 2004), suggesting that human population movements can create mosaics of local parasite diversity at various spatial scales.…”

A Molecular Epidemiological Study of var Gene Diversity to Characterize the Reservoir of Plasmodium falciparum in Humans in Africa

“…Age-specific multiplicity of infection (MOI) estimates were derived from the following sources: Bakoumba [20]; Pikine [64] scoring multiple infections as double infections; Kilifi [65] simple average of the two sites; Amele [48] using all three markers; Porto Velho [66] using all three markers and counting multiple infections as double infections. These estimates of MOI reflect the age-range from which the samples were taken and are used to project the total circulating genomes in each population.…”