Unlike malaria species from other evolutionary lineages, the seven characterized species of the Laverania are unique for their expression of EMP1 on the surface of infected RBCs where it binds to molecules on the host endothelial surface and enables the infected cell to adhere to blood vessel walls, thus sequestering the parasites from the peripheral circulation and avoiding destruction in the spleen. falciparum is the sole human-infective member of a subgenus of Plasmodium that infects apes called the Laverania. The contribution of RIFINs, STEVORs and PfMC-2TMs to cytoadherence is unclear, however PfEMP1 has been shown to be the major cytoadhesive molecule and is thought to be the primary virulence determinant of P. falciparum erythrocyte membrane protein 1). falciparum MaurerвЂ™s cleft-2 transmembrane domain proteins) and PfEMP1 ( P. The virulence of this species is due in large part to the cytoadhesive properties of infected RBCs that result from the placement on the RBC surface of parasite encoded variable antigens, included proteins referred to as RIFIN (repetitive interspersed family), STEVOR (subtelomeric variant open reading frame), PfMC-2TM ( P. Of the five parasite species that infect humans, by far the most virulent is P. The influence of malaria on human evolution is thought to have been substantial, and infection by Plasmodium parasites has been proposed to have played a significant role in shaping the human genome. This stage of the infection is associated with a massive increase in parasite numbers and can lead to severe anemia, extensive inflammation and vascular occlusion that can disrupt circulation. Malaria parasites exhibit multiple morphological states as they transition between their mosquito vectors and their vertebrate hosts, but all symptoms of the disease result from asexual replication of the parasites within the circulating red blood cells (RBCs) of the infected individual. There are five species that infect humans and cause malaria, a disease that can be severe, resulting in significant morbidity and mortality within human populations in tropical and subtropical regions of the world. These changes likely underlie the chronic nature of these infections as well as their exceptional virulence.Д®ukaryotic parasites of the genus Plasmodium infect a broad range of vertebrate species, including birds, reptiles and mammals. These observations suggest that changes in transmission dynamics selected for significant alterations in the transcriptional regulatory mechanisms that mediate antigenic variation in the parasite lineage that includes P. We hypothesize that these changes originated at a time of dramatic climatic change on the African continent that is predicted to have led to significant changes in transmission dynamics, thus selecting for patterns of antigenic variation that enabled lengthier, more chronic infections. In addition, two uniquely conserved var genes that have been proposed to play a role in coordinating transcriptional switching similarly arose uniquely within this clade. falciparum evolved distinct subsets of var genes distinguishable by different upstream transcriptional regulatory regions that have been associated with different expression profiles and virulence properties. Unlike the other members of the Laverania, the clade that gave rise to P. Here we show that the common ancestor of the branch of the Laverania lineage that includes the human parasite underwent a remarkable change in the organization and structure of elements linked to the complex transcriptional regulation displayed by the var gene family. By changing which var gene is expressed, parasites avoid immune recognition, a process called antigenic variation that underlies the chronic nature of malaria infections. These proteins are encoded by a large, multicopy gene family called var, with each var gene encoding a different form of the protein. The exceptional virulence of this species to humans can be largely attributed to a family of variant surface antigens placed by the parasites onto the surface of infected red blood cells that mediate adherence to the vascular endothelium. falciparum being the only member that infects humans.

This unicellular organism is a member of a subgenus of Plasmodium called the Laverania that infects apes, with P.

The most severe form of human malaria is caused by the protozoan parasite Plasmodium falciparum.

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