Diversity of Plasmodium falciparum clones infecting children living in a holoendemic area in north-eastern Tanzania

Within-Host Competition in Genetically Diverse Malaria Infections: Parasite Virulence and Competitive Success

“…In nature, malarial infections are often genetically diverse, with human hosts typically harboring more than one genotype of the same species (reviewed by Arnot 1999;Read and Taylor 2001). These mixed infections can be extremely common, constituting over 80% of infections in high-transmission areas (e.g., Day et al 1992;Druilhe et al 1998;Babiker et al 1999;Konaté et al 1999;Magesa et al 2002;Jafari et al 2004). Experimental evidence from rodent models demonstrates that genetically distinct malaria clones compete within hosts (e.g., Snounou et al 1989;Read et al 2002;de Roode et al 2003de Roode et al , 2004ade Roode et al ,b, 2005a, and a variety of nonexperimental observations imply that competition also occurs in human malaria infections (e.g., Daubersies et al 1996;Mercereau-Puijalon 1996;Arnot 1999;Smith et al 1999;Bruce et al 2000).…”

“…These clones are a sample of P. chabaudi parasites circulating in the wild, so that this study mimics a scenario where parasite genotypes with divergent genetic and antigenic properties coinfect the same host. The majority of human malaria infections are of this sort (e.g., Day et al 1992;Druilhe et al 1998;Babiker et al 1999;Konaté et al 1999;Magesa et al 2002;Jafari et al 2004) and arise when individual hosts are infected with unrelated parasites from multiple mosquito bites or from single bites of multiply infected mosquitoes. Malaria parasites differ widely in their antigenic properties, and immune responses are at least partly strain specific (e.g., Jarra and Brown 1989;Snounou et al 1989).…”

Polymorphism of the Merozoite Surface Protein-1 Block 2 Region in Plasmodium Falciparum Isolates from Symptomatic Individual Living in Rural Area of Senegal

“…pattern, it appeared clearly that the single infection was more frequent than the double and triple infection was not found in our study. Differences in transmission level over time and anti-malarial immunity known to be strain specific [28], could partly explained the differences in the distribution of the different alleles over year. In a given locality, the parasite genetic pool may be relatively stable, perhaps related to the stable parasite life cycle; thus, the distribution of alleles may be determined randomly so that certain alleles will predominate by chance.…”

Genetic polymorphism of the serine rich antigen N-terminal region in Plasmodium falciparum field isolates from Brazil

“…As a result and because of the emergence of resistance of both the parasite and the mosquito vector to drugs and insecticides, respectively, a malaria vaccine is one of the most powerful potential tools to be added to those classically used to control malaria transmission. Consequently, different antigens expressed during the asexual cycle of the malaria parasite and their encoding genes have been characterized in the last years , SallenaveSales et al 2000, Magesa et al 2002. The gene codifying to the serine rich antigen (SERA), a protein also known as p126 or serine-rich protein (SERP), which is located in the parasitophorous vacuole of trophozoites and schizonts, has been also target of interest to several groups.…”