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Blood, 1 November 2004, Vol. 104, No. 9, pp. 2961-2966.
Prepublished online as a Blood First Edition Paper on July 20, 2004; DOI 10.1182/blood-2004-06-2136.
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Submitted June 4, 2004
Accepted June 21, 2004
Ability of Plasmodium falciparum to invade South-East Asian ovalocytes varies between parasite lines
Alfred Cortes*, Ariadna Benet, Brian M Cooke, John W Barnwell, and John C Reeder
Molecular Parasitology Laboratory, Papua New Guinea Institute of Medical Research, Madang, Madang Province, Papua New Guinea
Department of Microbiology, Monash University, Clayton, Victoria, Australia
Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Chamblee, GA, USA
Papua New Guinea Institute of Medical Research, Goroka, EHP, Papua New Guinea
* Corresponding author; email: acortes{at}nimr.mrc.ac.uk.
Plasmodium falciparum, the causative agent of the most lethal form of human malaria, utilizes multiple ligand-receptor interactions to invade host red blood cells (RBCs). We studied the invasion of P. falciparum into abnormal RBCs from humans carrying the South-East Asian ovalocytosis (SAO) trait. One particular parasite line, 3D7-A, invaded these cells efficiently, whereas all other lines studied invaded SAO RBCs to only about 20% of the extent of normal (non-SAO) cells. This result is consistent with the clinical observation that SAO individuals can experience high density P. falciparum infections, and provides an explanation for previous discrepant results on invasion of SAO RBCs. Characterization of the invasion phenotype of 3D7-A revealed that efficient invasion of SAO RBCs was paralleled by relatively efficient invasion of normal RBCs treated with either neuraminidase, trypsin or chymotrypsin and a novel capacity to invade normal RBCs treated sequentially with both neuraminidase and trypsin. Our results suggest that only parasites able to use some particular invasion pathways can invade SAO RBCs efficiently in culture. A similar situation might occur in the field.
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