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Host immunity exerts strong selective pressure on pathogens. Population-level genetic analysis can identify signatures of this selection, but these signatures reflect the net selective effect of all hosts and vectors in a population. In contrast, analysis of pathogen diversity within hosts provides information on individual, host-specific selection pressures. Here, we combine these complementary approaches in an analysis of the malaria parasite Plasmodium falciparum using haplotype sequences from thousands of natural infections in sub-Saharan Africa. We find that parasite genotypes show preferential clustering within multi-strain infections in young children, and identify individual amino acid positions that may contribute to strain-specific immunity. Our results demonstrate that natural host defenses to P. falciparum act in an allele-specific manner to block specific parasite haplotypes from establishing blood-stage infections. This selection partially explains the extreme amino acid diversity of many parasite antigens and suggests that vaccines targeting such proteins should account for allele-specific immunity.

Aims:The frequency of the mutant gene for sickle cell is widely distributed in the sub-Saharan Africa, the Middle East, and the Indian subcontinent. There is epidemiologic evidence that sickle cell trait confers a survival advantage against malaria and that the selection pressure due to malaria has resulted in high frequencies of the mutant gene in areas of high malaria transmission. We carried out a study to look at the relationship between sickle cell trait, age, haemoglobin level, and malaria parasite density. Methods: We carried out a cross-sectional study between the months of October and December, 2004 in Kombewa Division of Kisumu West District, a P. falciparum malaria

Aims: Erythrocyte complement regulatory proteins, complement receptor 1 (CR1) and decay accelerating factor (CD55) protect red blood cells (RBCs) from complement mediated damage by controlling complement activation cascade and potentially protect RBCs from complement mediated damage that may occur when immune complexes are