Author:
- INTRODUCTION
- MATERIALS AND METHODS
- RESULTS
- Characteristics of Buritis, Colina, and Ribeirinha.
- Relationship between years of residence in the endemic area and malaria history.
- Anti-PvRBP1 and anti-PvDBP-RII seroprevalence in three communities of Rondônia.
- Magnitude of IgG responses.
- Multivariate logistic regression analysis of total IgG antibody reactivity according to gender, age, and indices of malaria exposure.
- Seroprevalence and malaria exposure.
- IgG subclass distribution of anti-PvDBP-RII and anti-PvRBP1 antibodies.
- IgG subclass levels and months since last known malaria episode.
- DISCUSSION
ProCite
RefWorks
Reference Manager
BibTeX
Zotero
EndNote
-
1
Mendis K, Sina BJ, Marchesini P, Carter R, 2001. The neglected burden of Plasmodium vivax malaria. Am J Trop Med Hyg 64 :97 –106.
-
2
Breman JG, 2001. The ears of the hippopotamus: manifestations, determinants, and estimates of the malaria burden. Am J Trop Med Hyg 64 :1–11.
-
3
Moorthy VS, Good MF, Hill AV, 2004. Malaria vaccine developments. Lancet 363 :150–156.
-
4
Ballou WR, Arevalo-Herrera M, Carucci D, Richie TL, Corradin G, Diggs C, Druilhe P, Giersing BK, Saul A, Heppner DG, Kester KE, Lanar DE, Lyon J, Hill AV, Pan W, Cohen JD, 2004. Update on the clinical development of candidate malaria vaccines. Am J Trop Med Hyg 71 :239–247.
-
5
Sina B, 2002. Focus on Plasmodium vivax.Trends Parasitol 18 :287–289.
-
6
Wertheimer SP, Barnwell JW, 1989. Plasmodium vivax interaction with the human Duffy blood group glycoprotein: identification of a parasite receptor-like protein. Exp Parasitol 69 :340–350.
-
7
Fang XD, Kaslow DC, Adams JH, Miller LH, 1991. Cloning of the Plasmodium vivax Duffy receptor. Mol Biochem Parasitol 44 :125–132.
-
8
Adams JH, Hudson DE, Torii M, Ward GE, Wellems TE, Aikawa M, Miller LH, 1990. The Duffy receptor family of Plasmodium knowlesi is located within the micronemes of invasive malaria merozoites. Cell 63 :141–153.
-
9
Sim BK, Toyoshima T, Haynes JD, Aikawa M, 1992. Localization of the 175-kilodalton erythrocyte binding antigen in micronemes of Plasmodium falciparum merozoites. Mol Biochem Parasitol 51 :157–159.
-
10
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.
-
11
Chitnis CE, Miller LH, 1994. Identification of the erythrocyte binding domains of Plasmodium vivax and Plasmodium knowlesi proteins involved in erythrocyte invasion. J Exp Med 180 :497–506.
-
12
Cole-Tobian J, King CL, 2003. Diversity and natural selection in Plasmodium vivax Duffy binding protein gene. Mol Biochem Parasitol 127 :121–132.
-
13
Michon P, Fraser T, Adams JH, 2000. Naturally acquired and vaccine-elicited antibodies block erythrocyte cytoadherence of the Plasmodium vivax Duffy binding protein. Infect Immun 68 :3164–3171.
-
14
Galinski MR, Medina CC, Ingravallo P, Barnwell JW, 1992. A reticulocyte-binding protein complex of Plasmodium vivax merozoites. Cell 69 :1213–1226.
-
15
Galinski MR, Xu M, Barnwell JW, 2000. Plasmodium vivax reticulocyte binding protein-2 (PvRBP-2) shares structural features with PvRBP-1 and the Plasmodium yoelii 235 kDa rhop-try protein family. Mol Biochem Parasitol 108 :257–262.
-
16
Galinski MR, Barnwell JW, 1996. Plasmodium vivax: merozoites, invasion of reticulocytes and considerations for vaccine development. Parasitol Today 12 :20–29.
-
17
Rayner JC, Galinski MR, Ingravallo P, Barnwell JW, 2000. Two Plasmodium falciparum genes express merozoite proteins that are related to Plasmodium vivax and Plasmodium yoelii adhesive proteins involved in host cell selection and invasion. Proc Natl Acad Sci U S A 97 :9648–9653.
-
18
Rayner JC, Vargas-Serrato E, Huber CS, Galinski MR, Barnwell JW, 2001. A Plasmodium falciparum homologue of Plasmodium vivax reticulocyte binding protein (PvRBP1) defines a trypsin-resistant erythrocyte invasion pathway. J Exp Med 194 :1571–1581.
-
19
Triglia T, Thompson J, Caruana SR, Delorenzi M, Speed T, Cowman AF, 2001. Identification of proteins from Plasmodium falciparum that are homologous to reticulocyte binding proteins in Plasmodium vivax.Infect Immun 69 :1084–1092.
-
20
Rayner JC, Tran TM, Corredor V, Huber CS, Barnwell JW, Galinski MR, 2005. Dramatic difference in diversity between Plasmodium falciparum and Plasmodium vivax reticulocyte binding-like genes. Am J Trop Med Hyg 72 :666–674.
-
21
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.
-
22
Bouharoun-Tayoun H, Druilhe P, 1992. Plasmodium falciparum malaria: evidence for an isotype imbalance which may be responsible for delayed acquisition of protective immunity. Infect Immun 60 :1473–1481.
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Banic DM, de Oliveira-Ferreira J, Pratt-Riccio LR, Conseil V, Goncalves D, Fialho RR, Gras-Masse H, Daniel-Ribeiro CT, Camus D, 1998. Immune response and lack of immune response to Plasmodium falciparum P126 antigen and its amino-terminal repeat in malaria-infected humans. Am J Trop Med Hyg 58 :768–774.
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Banic DM, Goldberg AC, Pratt-Riccio LR, De Oliveira-Ferreira J, Santos F, Gras-Masse H, Camus D, Kalil J, Daniel-Ribeiro CT, 2002. Human leukocyte antigen class II control of the immune response to p126-derived amino terminal peptide from Plasmodium falciparum.Am J Trop Med Hyg 66 :509–515.
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Xainli J, Cole-Tobian JL, Baisor M, Kastens W, Bockarie M, Yazdani SS, Chitnis CE, Adams JH, King CL, 2003. Epitope-specific humoral immunity to Plasmodium vivax Duffy binding protein. Infect Immun 71 :2508–2515.
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COMPARISON OF IgG REACTIVITIES TO PLASMODIUM VIVAX MEROZOITE INVASION ANTIGENS IN A BRAZILIAN AMAZON POPULATION
TUAN M. TRAN
TUAN M. TRAN
Emory Vaccine Center & Yerkes National Primate Research Center, Emory University, Atlanta, Georgia; Department of Immunology, Institute Oswaldo Cruz, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil; Fundação Nacional de Saúde, Ministry of Health, Rondônia, Brazil; Malaria Research Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India; Malaria Branch, Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; Department of Medicine, Division of Infectious Diseases, Emory University, Atlanta, Georgia
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JOSELI OLIVEIRA-FERREIRA
JOSELI OLIVEIRA-FERREIRA
Emory Vaccine Center & Yerkes National Primate Research Center, Emory University, Atlanta, Georgia; Department of Immunology, Institute Oswaldo Cruz, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil; Fundação Nacional de Saúde, Ministry of Health, Rondônia, Brazil; Malaria Research Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India; Malaria Branch, Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; Department of Medicine, Division of Infectious Diseases, Emory University, Atlanta, Georgia
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ALBERTO MORENO
ALBERTO MORENO
Emory Vaccine Center & Yerkes National Primate Research Center, Emory University, Atlanta, Georgia; Department of Immunology, Institute Oswaldo Cruz, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil; Fundação Nacional de Saúde, Ministry of Health, Rondônia, Brazil; Malaria Research Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India; Malaria Branch, Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; Department of Medicine, Division of Infectious Diseases, Emory University, Atlanta, Georgia
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FATIMA SANTOS
FATIMA SANTOS
Emory Vaccine Center & Yerkes National Primate Research Center, Emory University, Atlanta, Georgia; Department of Immunology, Institute Oswaldo Cruz, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil; Fundação Nacional de Saúde, Ministry of Health, Rondônia, Brazil; Malaria Research Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India; Malaria Branch, Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; Department of Medicine, Division of Infectious Diseases, Emory University, Atlanta, Georgia
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SYED S. YAZDANI
SYED S. YAZDANI
Emory Vaccine Center & Yerkes National Primate Research Center, Emory University, Atlanta, Georgia; Department of Immunology, Institute Oswaldo Cruz, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil; Fundação Nacional de Saúde, Ministry of Health, Rondônia, Brazil; Malaria Research Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India; Malaria Branch, Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; Department of Medicine, Division of Infectious Diseases, Emory University, Atlanta, Georgia
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CHETAN E. CHITNIS
CHETAN E. CHITNIS
Emory Vaccine Center & Yerkes National Primate Research Center, Emory University, Atlanta, Georgia; Department of Immunology, Institute Oswaldo Cruz, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil; Fundação Nacional de Saúde, Ministry of Health, Rondônia, Brazil; Malaria Research Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India; Malaria Branch, Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; Department of Medicine, Division of Infectious Diseases, Emory University, Atlanta, Georgia
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JOHN D. ALTMAN
JOHN D. ALTMAN
Emory Vaccine Center & Yerkes National Primate Research Center, Emory University, Atlanta, Georgia; Department of Immunology, Institute Oswaldo Cruz, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil; Fundação Nacional de Saúde, Ministry of Health, Rondônia, Brazil; Malaria Research Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India; Malaria Branch, Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; Department of Medicine, Division of Infectious Diseases, Emory University, Atlanta, Georgia
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ESMERALDA V-S. MEYER
ESMERALDA V-S. MEYER
Emory Vaccine Center & Yerkes National Primate Research Center, Emory University, Atlanta, Georgia; Department of Immunology, Institute Oswaldo Cruz, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil; Fundação Nacional de Saúde, Ministry of Health, Rondônia, Brazil; Malaria Research Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India; Malaria Branch, Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; Department of Medicine, Division of Infectious Diseases, Emory University, Atlanta, Georgia
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JOHN W. BARNWELL
JOHN W. BARNWELL
Emory Vaccine Center & Yerkes National Primate Research Center, Emory University, Atlanta, Georgia; Department of Immunology, Institute Oswaldo Cruz, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil; Fundação Nacional de Saúde, Ministry of Health, Rondônia, Brazil; Malaria Research Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India; Malaria Branch, Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; Department of Medicine, Division of Infectious Diseases, Emory University, Atlanta, Georgia
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MARY R. GALINSKI
MARY R. GALINSKI
Emory Vaccine Center & Yerkes National Primate Research Center, Emory University, Atlanta, Georgia; Department of Immunology, Institute Oswaldo Cruz, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil; Fundação Nacional de Saúde, Ministry of Health, Rondônia, Brazil; Malaria Research Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India; Malaria Branch, Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; Department of Medicine, Division of Infectious Diseases, Emory University, Atlanta, Georgia
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Naturally acquired antibody reactivity to two major Plasmodium vivax vaccine candidates was investigated in 294 donors from three malaria-endemic communities of Rondônia state, Brazil. Antibody recognition of recombinantly expressed antigens covering five different regions of P. vivax reticulocyte binding protein 1 (PvRBP1) and region II of P. vivax Duffy binding protein (PvDBP-RII) were compared. Positive IgG responses to these antigens were significantly related to the level of malaria exposure in terms of past infections and years of residence in the endemic area when corrected for age. The highest prevalence of anti-PvRBP1 total IgG antibodies corresponded to the amino acid regions denoted PvRBP1431-748 (41%) and PvRBP1733-1407 (47%). Approximately one-fifth of positively responding sera had titers of at least 1:1,600. Total IgG responses to PvDBP-RII were more prevalent (67%), of greater magnitude, and acquired more rapidly than those to individual PvRBP1 antigens. Responses to both PvRBP1 and PvDBP-RII were biased toward the cytophilic subclasses IgG1 and IgG3. These data provide the first insights on acquired antibody responses to PvRBP1 and a comparative view with PvDBP-RII that may prove valuable for understanding protective immune responses to these two vaccine candidates as they are evaluated as components of multitarget blood-stage vaccines.
Author Notes
- INTRODUCTION
- MATERIALS AND METHODS
- RESULTS
- Characteristics of Buritis, Colina, and Ribeirinha.
- Relationship between years of residence in the endemic area and malaria history.
- Anti-PvRBP1 and anti-PvDBP-RII seroprevalence in three communities of Rondônia.
- Magnitude of IgG responses.
- Multivariate logistic regression analysis of total IgG antibody reactivity according to gender, age, and indices of malaria exposure.
- Seroprevalence and malaria exposure.
- IgG subclass distribution of anti-PvDBP-RII and anti-PvRBP1 antibodies.
- IgG subclass levels and months since last known malaria episode.
- DISCUSSION
ProCite
RefWorks
Reference Manager
BibTeX
Zotero
EndNote
-
1
Mendis K, Sina BJ, Marchesini P, Carter R, 2001. The neglected burden of Plasmodium vivax malaria. Am J Trop Med Hyg 64 :97 –106.
-
2
Breman JG, 2001. The ears of the hippopotamus: manifestations, determinants, and estimates of the malaria burden. Am J Trop Med Hyg 64 :1–11.
-
3
Moorthy VS, Good MF, Hill AV, 2004. Malaria vaccine developments. Lancet 363 :150–156.
-
4
Ballou WR, Arevalo-Herrera M, Carucci D, Richie TL, Corradin G, Diggs C, Druilhe P, Giersing BK, Saul A, Heppner DG, Kester KE, Lanar DE, Lyon J, Hill AV, Pan W, Cohen JD, 2004. Update on the clinical development of candidate malaria vaccines. Am J Trop Med Hyg 71 :239–247.
-
5
Sina B, 2002. Focus on Plasmodium vivax.Trends Parasitol 18 :287–289.
-
6
Wertheimer SP, Barnwell JW, 1989. Plasmodium vivax interaction with the human Duffy blood group glycoprotein: identification of a parasite receptor-like protein. Exp Parasitol 69 :340–350.
-
7
Fang XD, Kaslow DC, Adams JH, Miller LH, 1991. Cloning of the Plasmodium vivax Duffy receptor. Mol Biochem Parasitol 44 :125–132.
-
8
Adams JH, Hudson DE, Torii M, Ward GE, Wellems TE, Aikawa M, Miller LH, 1990. The Duffy receptor family of Plasmodium knowlesi is located within the micronemes of invasive malaria merozoites. Cell 63 :141–153.
-
9
Sim BK, Toyoshima T, Haynes JD, Aikawa M, 1992. Localization of the 175-kilodalton erythrocyte binding antigen in micronemes of Plasmodium falciparum merozoites. Mol Biochem Parasitol 51 :157–159.
-
10
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.
-
11
Chitnis CE, Miller LH, 1994. Identification of the erythrocyte binding domains of Plasmodium vivax and Plasmodium knowlesi proteins involved in erythrocyte invasion. J Exp Med 180 :497–506.
-
12
Cole-Tobian J, King CL, 2003. Diversity and natural selection in Plasmodium vivax Duffy binding protein gene. Mol Biochem Parasitol 127 :121–132.
-
13
Michon P, Fraser T, Adams JH, 2000. Naturally acquired and vaccine-elicited antibodies block erythrocyte cytoadherence of the Plasmodium vivax Duffy binding protein. Infect Immun 68 :3164–3171.
-
14
Galinski MR, Medina CC, Ingravallo P, Barnwell JW, 1992. A reticulocyte-binding protein complex of Plasmodium vivax merozoites. Cell 69 :1213–1226.
-
15
Galinski MR, Xu M, Barnwell JW, 2000. Plasmodium vivax reticulocyte binding protein-2 (PvRBP-2) shares structural features with PvRBP-1 and the Plasmodium yoelii 235 kDa rhop-try protein family. Mol Biochem Parasitol 108 :257–262.
-
16
Galinski MR, Barnwell JW, 1996. Plasmodium vivax: merozoites, invasion of reticulocytes and considerations for vaccine development. Parasitol Today 12 :20–29.
-
17
Rayner JC, Galinski MR, Ingravallo P, Barnwell JW, 2000. Two Plasmodium falciparum genes express merozoite proteins that are related to Plasmodium vivax and Plasmodium yoelii adhesive proteins involved in host cell selection and invasion. Proc Natl Acad Sci U S A 97 :9648–9653.
-
18
Rayner JC, Vargas-Serrato E, Huber CS, Galinski MR, Barnwell JW, 2001. A Plasmodium falciparum homologue of Plasmodium vivax reticulocyte binding protein (PvRBP1) defines a trypsin-resistant erythrocyte invasion pathway. J Exp Med 194 :1571–1581.
-
19
Triglia T, Thompson J, Caruana SR, Delorenzi M, Speed T, Cowman AF, 2001. Identification of proteins from Plasmodium falciparum that are homologous to reticulocyte binding proteins in Plasmodium vivax.Infect Immun 69 :1084–1092.
-
20
Rayner JC, Tran TM, Corredor V, Huber CS, Barnwell JW, Galinski MR, 2005. Dramatic difference in diversity between Plasmodium falciparum and Plasmodium vivax reticulocyte binding-like genes. Am J Trop Med Hyg 72 :666–674.
-
21
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.
-
22
Bouharoun-Tayoun H, Druilhe P, 1992. Plasmodium falciparum malaria: evidence for an isotype imbalance which may be responsible for delayed acquisition of protective immunity. Infect Immun 60 :1473–1481.
-
23
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