Mendis K, Sina BJ, Marchesini P, Carter R, 2001. The neglected burden of Plasmodium vivax malaria. Am J Trop Med Hyg 64 :97–106.
Sachs J, Malaney P, 2002. The economic and social burden of malaria. Nature 415 :680–685.
Nagel RL, 1990. Innate resistance to malaria: the intraerythrocytic cycle. Blood Cells 16 :321–339; discussion 340–349.
Doolan DL, Hoffman SL, 1997. Pre-erythrocytic-stage immune effector mechanisms in Plasmodium spp. infections. Philos Trans R Soc Lond B Biol Sc 352 :1361–1367.
Hadley TJ, Lu ZH, Wasniowska K, Martin AW, Peiper SC, Hesselgesser J, Horuk R, 1994. Postcapillary venule endothelial cells in kidney express a multispecific chemokine receptor that is structurally and functionally identical to the erythroid isoform, which is the Duffy blood group antigen. J Clin Invest 94 :985–991.
Miller LH, Mason SJ, Dvorak JA, McGinniss MH, Rothman IK, 1975. Erythrocyte receptors for (Plasmodium knowlesi) malaria: Duffy blood group determinants. Science 189 :561–563.
Cutbush M, Mollison PL, 1950. The Duffy blood group system. Heredity 4 :383–389.
Chown B, Lewis M, Kaita H, 1965. The Duffy Blood Group System in Caucasians: evidence for a new allele. Am J Hum Genet 17 :384–389.
Miller LH, Mason SJ, Clyde DF, McGinniss MH, 1976. The resistance factor to Plasmodium vivax in blacks. The Duffy-blood-group genotype, FyFy. N Engl J Med 295 :302–304.
Gelpi AP, King MC, 1976. Duffy blood group and malaria. Science 191 :1284.
Hamblin MT, Di Rienzo A, 2000. Detection of the signature of natural selection in humans: evidence from the Duffy blood group locus. Am J Hum Genet 66 :1669–1679.
Situación epidemiológica de las enfermedades transmitidas por vectores 2003–2004. Boletín Epidemiológico Semanal del Ministerio de Protección Social, República de Colombia, Febrero 22–28, 2004. Online Junio 16, 2005. Available from http://www.col.ops-oms.org/sivigila/2004/bole08_04.htm.
Roggero MA, Filippi B, Church P, Hoffman SL, Blum-Tirouvanziam U, Lopez JA, Esposito F, Matile H, Reymond CD, Fasel N, 1995. Synthesis and immunological characterization of 104-mer and 102-mer peptides corresponding to the N-and C-terminal regions of the Plasmodium falciparum CS protein. Mol Immunol 32 :1301–1309.
Singh S, Pandey K, Chattopadhayay R, Yazdani SS, Lynn A, Bharadwaj A, Ranjan A, Chitnis C, 2001. Biochemical, biophysical, and functional characterization of bacterially expressed and refolded receptor binding domain of Plasmodium vivax duffy-binding protein. J Biol Chem 276 :17111–17116.
Tournamille C, Colin Y, Cartron JP, le van Kim C, 1995. Disruption of a GATA motif in the Duffy gene promoter abolishes erythroid gene expression in Duffy-negative individuals. Nat Genet 10 :224–228.
Voller A, O’Neill P, 1971. Immunofluorescence method suitable for large-scale application to malaria. Bull World Health Organ 45 :524–529.
Herrera S, De Plata C, Gonzalez M, Perlaza BL, Bettens F, Corradin G, Arevalo-Herrera M, 1997. Antigenicity and immunogenicity of multiple antigen peptides (MAP) containing P. vivax CS epitopes in Aotus monkeys. Parasite Immunol 19 :161–170.
Guerin-Marchand C, Druilhe P, Galey B, Londono A, Patarapotikul J, Beaudoin RL, Dubeaux C, Tartar A, Mercereau-Puijalon O, Langsley G, 1987. A liver-stage-specific antigen of Plasmodium falciparum characterized by gene cloning. Nature 329 :164–167.
Ocana-Morgner C, Mota MM, Rodriguez A, 2003. Malaria blood stage suppression of liver stage immunity by dendritic cells. J Exp Med 197 :143–151.
Wipasa J, Xu H, Stowers A, Good MF, 2001. Apoptotic deletion of Th cells specific for the 19-kDa carboxyl-terminal fragment of merozoite surface protein 1 during malaria infection. J Immunol 167 :3903–3909.
Woolley IJ, Hotmire KA, Sramkoski RM, Zimmerman PA, Kazura JW, 2000. Differential expression of the Duffy antigen receptor for chemokines according to RBC age and FY genotype. Transfusion 40 :949–953.
|Past two years||Past Year||Past 30 Days|
|Full Text Views||470||126||2|
The Duffy antigen (Fy) is necessary for Plasmodium vivax invasion of human erythrocytes. Some populations have a highly prevalent Fy-negative phenotype; such persons are naturally protected from P. vivax blood infection but are expected to completely support the P. vivax pre-erythrocytic cycle, representing a valuable model for studying the immune response during these parasitic stages. We typed 214 individuals, mostly Afro-Colombians, from a P. vivax-endemic area for Fy expression and determined the antibody response to P. vivax pre-erythrocytic (sporozoites and CS) and blood-stage antigens (blood forms, P. vivax merozoite surface protein 1, and P. vivax Duffy binding protein [PvDBP]). Antibody titers to P. vivax circumsporozoite protein, P11, and N-terminal peptides and the number of responders were similar in Fy-negative and Fy-positive individuals. The number of responders to sporozoites, blood forms, and PvDBP were different between these groups. Thus, Fy-negative individuals from malaria-endemic areas can be used to study the immune response to the P. vivax liver phase without interference of the erythrocytic cycle.