Plasmodium falciparum malaria remains a devastating public health problem. Recent discoveries have shed light on the origin and evolution of Plasmodium parasites and their interactions with their vertebrate and mosquito hosts. P.
View Article and Find Full Text PDFBackground: The var genes of the human malaria parasite Plasmodium falciparum are highly polymorphic loci coding for the erythrocyte membrane proteins 1 (PfEMP1), which are responsible for the cytoaherence of P. falciparum infected red blood cells to the human vasculature. Cytoadhesion, coupled with differential expression of var genes, contributes to virulence and allows the parasite to establish chronic infections by evading detection from the host's immune system.
View Article and Find Full Text PDFBackground: The human malaria parasite Plasmodium falciparum survives pressures from the host immune system and antimalarial drugs by modifying its genome. Genetic recombination and nucleotide substitution are the two major mechanisms that the parasite employs to generate genome diversity. A better understanding of these mechanisms may provide important information for studying parasite evolution, immune evasion and drug resistance.
View Article and Find Full Text PDFOver the past decade, attempts to explain the unusual size and prevalence of low-complexity regions (LCRs) in the proteins of the human malaria parasite Plasmodium falciparum have used both neutral and adaptive models. This past research has offered conflicting explanations for LCR characteristics and their role in, and influence on, the evolution of genome structure. Here we show that P.
View Article and Find Full Text PDFProtein sequences frequently contain regions composed of a reduced number of amino acids. Despite their presence in about half of all proteins and their unusual prevalence in the malaria parasite Plasmodium falciparum, the function and evolution of such low-complexity regions (LCRs) remain unclear. Here we show that LCR abundance and amino acid composition depend largely, but not exclusively, on genomic A+T content and obey power-law growth dynamics.
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