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Abstract
Plasmodium falciparum causes the most severe form of malaria in humans. The adhesion of the infected erythrocytes (IEs) to endothelial receptors (sequestration) and to uninfected erythrocytes (rosetting) are considered major elements in the pathogenesis of the disease. Both sequestration and rosetting appear to involve particular members of several IE variant surface antigens (VSAs) as ligands, interacting with multiple vascular host receptors, including the ABO blood group antigens. In this study, we subjected genetically distinct P. falciparum parasites to in vitro selection for increased IE adhesion to ABO antigens in the absence of potentially confounding receptors. The selection resulted in IEs that adhered stronger to pure ABO antigens, to erythrocytes, and to various human cell lines than their unselected counterparts. However, selection did not result in marked qualitative changes in transcript levels of the genes encoding the best-described VSA families, PfEMP1 and RIFIN. Rather, overall transcription of both gene families tended to decline following selection. Furthermore, selection-induced increases in the adhesion to ABO occurred in the absence of marked changes in immune IgG recognition of IE surface antigens, generally assumed to target mainly VSAs. Our study sheds new light on our understanding of the processes and molecules involved in IE sequestration and rosetting.
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1 University of Ghana, Department of Immunology, Noguchi Memorial Institute for Medical Research, Legon, Ghana (GRID:grid.8652.9) (ISNI:0000 0004 1937 1485); Rigshospitalet, Centre for Medical Parasitology, Department of Clinical Microbiology, Copenhagen, Denmark (GRID:grid.475435.4)
2 University of Copenhagen, Centre for Medical Parasitology, Department of Immunology and Microbiology, Faculty of Health and Medical Sciences, Copenhagen, Denmark (GRID:grid.5254.6) (ISNI:0000 0001 0674 042X)
3 Rigshospitalet, Centre for Medical Parasitology, Department of Clinical Microbiology, Copenhagen, Denmark (GRID:grid.475435.4)
4 University of Ghana, Department of Immunology, Noguchi Memorial Institute for Medical Research, Legon, Ghana (GRID:grid.8652.9) (ISNI:0000 0004 1937 1485)
5 Rigshospitalet, Department of Infectious Diseases, Copenhagen, Denmark (GRID:grid.475435.4); University of Copenhagen, Centre for Medical Parasitology, Department of Immunology and Microbiology, Faculty of Health and Medical Sciences, Copenhagen, Denmark (GRID:grid.5254.6) (ISNI:0000 0001 0674 042X)
6 Rigshospitalet, Centre for Medical Parasitology, Department of Clinical Microbiology, Copenhagen, Denmark (GRID:grid.475435.4); University of Copenhagen, Centre for Medical Parasitology, Department of Immunology and Microbiology, Faculty of Health and Medical Sciences, Copenhagen, Denmark (GRID:grid.5254.6) (ISNI:0000 0001 0674 042X)