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Infect. Immun. doi:10.1128/IAI.00249-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Invasion pathways and malaria severity in Kenyan Plasmodium falciparum clinical isolates

Institute of Immunology and Infection Research, University of Edinburgh, EH9 3JT, UK; London School of Hygiene and Tropical Medicine, UK and KEMRI/Wellcome Laboratories, Kilifi, Kenya

^* To whom correspondence should be addressed. Email: Alex.Rowe{at}ed.ac.uk.

	Abstract

Invasion of erythrocytes by P. falciparum occurs by multiple pathways that can be studied in vitro by examining invasion into erythrocytes treated with enzymes such as neuraminidase, trypsin and chymotrypsin. We have studied the invasion pathways used by 31 Kenyan P. falciparum isolates from children with uncomplicated or severe malaria. Six distinct invasion profiles were detected, out of eight possible profiles. The majority of isolates (23/31) showed neuraminidase-resistant, trypsin-sensitive invasion, characteristic of the pathway mediated by an unknown parasite ligand and erythrocyte receptor "X". The neuraminidase-sensitive, trypsin-sensitive phenotype consistent with invasion mediated by the parasite ligand EBA-175 binding to glycophorin A, that was the commonest invasion profile in a previous study of Gambian field isolates, was seen in only 3/31 Kenyan isolates. No particular invasion profile was associated with severe falciparum malaria and there was no significant difference in inhibition by the various enzyme treatments in isolates from children with severe malaria compared to isolates from children with uncomplicated malaria (P>0.1, all enzymes, Mann Whitney U). These results do not support the hypothesis that differences in invasion phenotypes play an important role in malaria virulence and indicate that considerable gaps remain in our knowledge of the molecular basis of invasion pathways in natural P. falciparum infections.

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