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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. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-06-2136v1 104/9/2961    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Cortés, A. Articles by Reeder, J. C. Search for Related Content PubMed PubMed Citation Articles by Cortés, A. Articles by Reeder, J. C. Related Collections Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS Ability of Plasmodium falciparum to invade Southeast Asian ovalocytes varies between parasite lines Alfred Cortés, Ariadna Benet, Brian M. Cooke, John W. Barnwell, and John C. Reeder From the Molecular Parasitology Laboratory, Papua New Guinea Institute of Medical Research, Madang, Papua New Guinea; Department of Microbiology, Monash University, Victoria, Australia; Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Chamblee, GA; and Papua New Guinea Institute of Medical Research, Goroka, Papua New Guinea. Plasmodium falciparum, the causative agent of the most lethal form of human malaria, uses 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 Southeast 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A.-M. Deans, S. Nery, D. J. Conway, O. Kai, K. Marsh, and J. A. Rowe Invasion Pathways and Malaria Severity in Kenyan Plasmodium falciparum Clinical Isolates Infect. Immun., June 1, 2007; 75(6): 3014 - 3020. [Abstract] [Full Text] [PDF] A. BENET, T. Y. KHONG, A. URA, R. SAMEN, K. LORRY, M. MELLOMBO, L. TAVUL, K. BAEA, S. J. ROGERSON, and A. CORTES PLACENTAL MALARIA IN WOMEN WITH SOUTH-EAST ASIAN OVALOCYTOSIS. Am J Trop Med Hyg, October 1, 2006; 75(4): 597 - 604. [Abstract] [Full Text] [PDF]

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