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Dynamics of Asymptomatic Plasmodium vivax Infections and Duffy Binding Protein Polymorphisms in Relation to Parasitemia Levels in Papua New Guinean Children

The interaction between Plasmodium vivax Duffy binding protein II (PvDBPII) and human erythrocyte Duffy antigen is necessary for blood stage infections. However, PvDBPII is highly polymorphic. We recently observed that certain recombinant DBPII variants bind better to erythrocytes in vitro. To examine the hypothesis that haplotypes with enhanced binding have increased parasitemia levels, we followed 206 Papua New Guinean children biweekly for six months with a total of 713 P. vivax samples genotyped. Twenty-seven PvDBPII haplotypes were identified, and 3 haplotypes accounted for 57% of the infections. The relative frequencies of dominant haplotypes remained stable throughout the study. There was no significant association with PvDBPII alleles or haplotypes with P. vivax parasitemia. The dominant haplotype (26% of samples), however, corresponded to a high-binding haplotype. Thus, common haplotypes are not likely to have arisen from increased fitness as measured by greater parasitemia levels. The restricted number of common haplotypes increases the feasibility of a PvDBPII-based vaccine.

Received March 23, 2007. Accepted for publication June 22, 2007.

Acknowledgments We thank the study participants for their time; the teachers at the Mugil and Megiar Schools for their participation; the nurses of the New Guinea Institute for Medical Research (IMR) at the Mugil Health center for assistance; the IMR staff for collecting samples during the follow-ups and preparing microscopic sections for analysis; Daniel Tisch for statistical advice; and Arlene Dent for helpful comments on the manuscript.

Financial support: This study was supported by a grant from the Veteran’s Affairs Research Service and funds from the Papua New Guinean Government. Jennifer L. Cole-Tobian was supported by the ID/GeoMed Training Grant (T32-AI-07024) during this study.

^* Address correspondence to Jennifer L. Cole-Tobian, or Christopher L. King, Center for Global Health and Disease, Case Western Reserve University, Wolstein Research Building 4-101, 10900 Euclid Avenue, Cleveland, OH 44106. E-mail: jtobian{at}gmail.com or cxk21{at}case.edu

Authors’ addresses: Jennifer L. Cole-Tobian, Center for Global Health and Disease, Case Western Reserve University, Wolstein Research Building 4-101, 10900 Euclid Avenue, Cleveland, OH 44106. Pascal Michon, Elijah Dabod, and Ivo Mueller, Papua New Guinea Institute of Medical Research, PO Box 378, Madang 511, Papua New Guinea. Christopher L. King, Center for Global Health and Disease, Case Western Reserve University, Wolstein Research Building 4-132 10900 Euclid Avenue, Cleveland, OH 44106 and Louis Stokes Veterans Affairs Medical Center, 10701 East Boulevard, Cleveland, OH 44106.

Reprint requests: Christopher L. King, Center for Global Health and Disease, Case Western Reserve University, Wolstein Research Building 4-132, 10900 Euclid Avenue, Cleveland, OH 44106 and Research Department, Veterans Affairs Medical Center, 10701 East Boulevard, Cleveland, OH 44106, Telephone: 216-368-4817, Fax: 216-368-4825, E-mail: christopher.king{at}case.edu.