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Infection and Immunity, May 2005, p. 2841-2847, Vol. 73, No. 5
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.5.2841-2847.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Judith N. Bulmer,5
Lars Hviid,3
Kojo Yeboah-Antwi,4,
Betty R. Kirkwood,1 and
Eleanor M. Riley2
Department of Epidemiology and Population Health,1 Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, London, WC1E 7HT, United Kingdom,2 Centre for Medical Parasitology, Copenhagen University Hospital (Rigshospitalet) and Institute for Medical Microbiology and Immunology, University of Copenhagen, Copenhagen, Denmark,3 Kintampo Health Research Centre, Ghana Health Service, PO Box 200, Brong Ahafo, Ghana,4 Department of Pathology, University of Newcastle, Royal Victoria Infirmary, Newcastle upon Tyne, NE3 4PH, United Kingdom5
Received 29 October 2004/ Returned for modification 8 December 2004/ Accepted 23 January 2005
Recent evidence suggests that pregnancy-associated malaria (PAM), associated with maternal anemia and low birth weight, results from preferential sequestration of parasitized red blood cells (pRBC) in the placenta via binding of variant surface antigens (VSA) expressed on the surface of pRBC to chondroitin sulfate A (CSA). The VSA mediating CSA binding (VSACSA) and thus sequestration of pRBC in the placenta are antigenically distinct from those that mediate pRBC sequestration elsewhere in the body, and it has been suggested that VSACSA are relatively conserved and may thus constitute an attractive target for vaccination against PAM. Using flow cytometry, levels of antibody to VSA and VSACSA expressed on the surface of red blood cells infected with Plasmodium falciparum isolates were measured during pregnancy and lactation in Ghanaian primigravid women enrolled in a trial of maternal vitamin A supplementation. Antibody responses to VSACSA were detected within the first trimester of pregnancy and increased with increasing duration of pregnancy, and they seemed to be isolate specific, indicating that different CSA-adherent parasite lines express antigenically distinct VSA and thus may not be as antigenically conserved as has been previously suggested. Levels of anti-VSACSA were not significantly associated with placental malarial infection determined by histology, indicating that primary immune responses to VSACSA may not be sufficient to eradicate placental parasitemia in primigravidae.
Sadly, Paul Arthur died before completion of this study.
Present address: Malaria Consortium, West Africa Officer, Unicef House, 4-8 Rangoon Close, Cantonments, PO Box 5051, Accra, Ghana.
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