Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people
Malaria therapy, experimental, and epidemiological studies have shown that erythrocyte Duffy blood group-negative people, largely of African ancestry, are resistant to erythrocyte Plasmodium vivax infection. These findings established a paradigm that the Duffy antigen is required for P. vivax erythr...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 107; no. 13; pp. 5967 - 5971 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
National Academy of Sciences
30.03.2010
National Acad Sciences |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0027-8424 1091-6490 1091-6490 |
| DOI | 10.1073/pnas.0912496107 |
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| Abstract | Malaria therapy, experimental, and epidemiological studies have shown that erythrocyte Duffy blood group-negative people, largely of African ancestry, are resistant to erythrocyte Plasmodium vivax infection. These findings established a paradigm that the Duffy antigen is required for P. vivax erythrocyte invasion. P. vivax is endemic in Madagascar, where admixture of Duffy-negative and Duffy-positive populations of diverse ethnic backgrounds has occurred over 2 millennia. There, we investigated susceptibility to P. vivax blood-stage infection and disease in association with Duffy blood group polymorphism. Duffy blood group genotyping identified 72% Duffy-negative individuals (FY*BES/*BES) in community surveys conducted at eight sentinel sites. Flow cytometry and adsorption-elution results confirmed the absence of Duffy antigen expression on Duffy-negative erythrocytes. P. vivax PCR positivity was observed in 8.8% (42/476) of asymptomatic Duffy-negative people. Clinical vivax malaria was identified in Duffy-negative subjects with nine P. vivax monoinfections and eight mixed Plasmodium species infections that included P. vivax (4.9 and 4.4% of 183 participants, respectively). Microscopy examination of blood smears confirmed blood-stage development of P. vivax, including gametocytes. Genotyping of polymorphic surface and microsatellite markers suggested that multiple P. vivax strains were infecting Duffy-negative people. In Madagascar, P. vivax has broken through its dependence on the Duffy antigen for establishing human blood-stage infection and disease. Further studies are necessary to identify the parasite and host molecules that enable this Duffy-independent P. vivax invasion of human erythrocytes. |
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| AbstractList | Malaria therapy, experimental, and epidemiological studies have shown that erythrocyte Duffy blood group-negative people, largely of African ancestry, are resistant to erythrocyte
Plasmodium vivax
infection. These findings established a paradigm that the Duffy antigen is required for
P. vivax
erythrocyte invasion.
P. vivax
is endemic in Madagascar, where admixture of Duffy-negative and Duffy-positive populations of diverse ethnic backgrounds has occurred over 2 millennia. There, we investigated susceptibility to
P. vivax
blood-stage infection and disease in association with Duffy blood group polymorphism. Duffy blood group genotyping identified 72% Duffy-negative individuals (
FY*B
ES
/*B
ES
) in community surveys conducted at eight sentinel sites. Flow cytometry and adsorption–elution results confirmed the absence of Duffy antigen expression on Duffy-negative erythrocytes.
P. vivax
PCR positivity was observed in 8.8% (42/476) of asymptomatic Duffy-negative people. Clinical vivax malaria was identified in Duffy-negative subjects with nine
P. vivax
monoinfections and eight mixed
Plasmodium
species infections that included
P. vivax
(4.9 and 4.4% of 183 participants, respectively). Microscopy examination of blood smears confirmed blood-stage development of
P. vivax
, including gametocytes. Genotyping of polymorphic surface and microsatellite markers suggested that multiple
P. vivax
strains were infecting Duffy-negative people. In Madagascar,
P. vivax
has broken through its dependence on the Duffy antigen for establishing human blood-stage infection and disease. Further studies are necessary to identify the parasite and host molecules that enable this Duffy-independent
P. vivax
invasion of human erythrocytes. Malaria therapy, experimental, and epidemiological studies have shown that erythrocyte Duffy blood group-negative people, largely of African ancestry, are resistant to erythrocyte Plasmodium vivax infection. These findings established a paradigm that the Duffy antigen is required for P. vivax erythrocyte invasion. P. vivax is endemic in Madagascar, where admixture of Duffy-negative and Duffy-positive populations of diverse ethnic backgrounds has occurred over 2 millennia. There, we investigated susceptibility to P. vivax blood-stage infection and disease in association with Duffy blood group polymorphism. Duffy blood group genotyping identified 72% Duffy-negative individuals (FY*B(ES)/*B(ES)) in community surveys conducted at eight sentinel sites. Flow cytometry and adsorption-elution results confirmed the absence of Duffy antigen expression on Duffy-negative erythrocytes. P. vivax PCR positivity was observed in 8.8% (42/476) of asymptomatic Duffy-negative people. Clinical vivax malaria was identified in Duffy-negative subjects with nine P. vivax monoinfections and eight mixed Plasmodium species infections that included P. vivax (4.9 and 4.4% of 183 participants, respectively). Microscopy examination of blood smears confirmed blood-stage development of P. vivax, including gametocytes. Genotyping of polymorphic surface and microsatellite markers suggested that multiple P. vivax strains were infecting Duffy-negative people. In Madagascar, P. vivax has broken through its dependence on the Duffy antigen for establishing human blood-stage infection and disease. Further studies are necessary to identify the parasite and host molecules that enable this Duffy-independent P. vivax invasion of human erythrocytes. Malaria therapy, experimental, and epidemiological studies have shown that erythrocyte Duffy blood group-negative people, largely of African ancestry, are resistant to erythrocyte Plasmodium vivax infection. These findings established a paradigm that the Duffy antigen is required for P. vivax erythrocyte invasion. P. vivax is endemic in Madagascar, where admixture of Duffy-negative and Duffy-positive populations of diverse ethnic backgrounds has occurred over 2 millennia. There, we investigated susceptibility to P. vivax blood-stage infection and disease in association with Duffy blood group polymorphism. Duffy blood group genotyping identified 72% Duffy-negative individuals (FY*BES/*BES) in community surveys conducted at eight sentinel sites. Flow cytometry and adsorption-elution results confirmed the absence of Duffy antigen expression on Duffy-negative erythrocytes. P. vivax PCR positivity was observed in 8.8% (42/476) of asymptomatic Duffy-negative people. Clinical vivax malaria was identified in Duffy-negative subjects with nine P. vivax monoinfections and eight mixed Plasmodium species infections that included P. vivax (4.9 and 4.4% of 183 participants, respectively). Microscopy examination of blood smears confirmed blood-stage development of P. vivax, including gametocytes. Genotyping of polymorphic surface and microsatellite markers suggested that multiple P. vivax strains were infecting Duffy-negative people. In Madagascar, P. vivax has broken through its dependence on the Duffy antigen for establishing human blood-stage infection and disease. Further studies are necessary to identify the parasite and host molecules that enable this Duffy-independent P. vivax invasion of human erythrocytes. Malaria therapy, experimental, and epidemiological studies have shown that erythrocyte Duffy blood group-negative people, largely of African ancestry, are resistant to erythrocyte Plasmodium vivax infection. These findings established a paradigm that the Duffy antigen is required for P. vivax erythrocyte invasion. P. vivax is endemic in Madagascar, where admixture of Duffy-negative and Duffy-positive populations of diverse ethnic backgrounds has occurred over 2 millennia. There, we investigated susceptibility to P. vivax blood-stage infection and disease in association with Duffy blood group polymorphism. Duffy blood group genotyping identified 72% Duffynegative individuals (FY*B...*B...) in community surveys conducted at eight sentinel sites. Flow cytometry and adsorption-elution results confirmed the absence of Duffy antigen expression on Duffy-negative erythrocytes. P. vivax PCR positivity was observed in 8.8% (42/476) of asymptomatic Duffy-negative people. Clinical vivax malaria was identified in Duffy-negative subjects with nine P. vivax monoinfections and eight mixed Plasmodium species infections that included P. vivax (4.9 and 4.4% of 183 participants, respectively). Microscopy examination of blood smears confirmed blood-stage development of P. vivax, including gametocytes. Genotyping of polymorphic surface and microsatellite markers suggested that multiple P. vivax strains were infecting Duffy-negative people. In Madagascar, P. vivax has broken through its dependence on the Duffy antigen for establishing human blood-stage infection and disease. Further studies are necessary to identify the parasite and host molecules that enable this Duffy-independent P. vivax invasion of human erythrocytes. (ProQuest: ... denotes formulae/symbols omitted.) Malaria therapy, experimental, and epidemiological studies have shown that erythrocyte Duffy blood group-negative people, largely of African ancestry, are resistant to erythrocyte Plasmodium vivax infection. These findings established a paradigm that the Duffy antigen is required for P. vivax erythrocyte invasion. P. vivax is endemic in Madagascar, where admixture of Duffy-negative and Duffy-positive populations of diverse ethnic backgrounds has occurred over 2 millennia. There, we investigated susceptibility to P. vivax blood-stage infection and disease in association with Duffy blood group polymorphism. Duffy blood group genotyping identified 72% Duffy-negative individuals (FY*B(ES)/*B(ES)) in community surveys conducted at eight sentinel sites. Flow cytometry and adsorption-elution results confirmed the absence of Duffy antigen expression on Duffy-negative erythrocytes. P. vivax PCR positivity was observed in 8.8% (42/476) of asymptomatic Duffy-negative people. Clinical vivax malaria was identified in Duffy-negative subjects with nine P. vivax monoinfections and eight mixed Plasmodium species infections that included P. vivax (4.9 and 4.4% of 183 participants, respectively). Microscopy examination of blood smears confirmed blood-stage development of P. vivax, including gametocytes. Genotyping of polymorphic surface and microsatellite markers suggested that multiple P. vivax strains were infecting Duffy-negative people. In Madagascar, P. vivax has broken through its dependence on the Duffy antigen for establishing human blood-stage infection and disease. Further studies are necessary to identify the parasite and host molecules that enable this Duffy-independent P. vivax invasion of human erythrocytes.Malaria therapy, experimental, and epidemiological studies have shown that erythrocyte Duffy blood group-negative people, largely of African ancestry, are resistant to erythrocyte Plasmodium vivax infection. These findings established a paradigm that the Duffy antigen is required for P. vivax erythrocyte invasion. P. vivax is endemic in Madagascar, where admixture of Duffy-negative and Duffy-positive populations of diverse ethnic backgrounds has occurred over 2 millennia. There, we investigated susceptibility to P. vivax blood-stage infection and disease in association with Duffy blood group polymorphism. Duffy blood group genotyping identified 72% Duffy-negative individuals (FY*B(ES)/*B(ES)) in community surveys conducted at eight sentinel sites. Flow cytometry and adsorption-elution results confirmed the absence of Duffy antigen expression on Duffy-negative erythrocytes. P. vivax PCR positivity was observed in 8.8% (42/476) of asymptomatic Duffy-negative people. Clinical vivax malaria was identified in Duffy-negative subjects with nine P. vivax monoinfections and eight mixed Plasmodium species infections that included P. vivax (4.9 and 4.4% of 183 participants, respectively). Microscopy examination of blood smears confirmed blood-stage development of P. vivax, including gametocytes. Genotyping of polymorphic surface and microsatellite markers suggested that multiple P. vivax strains were infecting Duffy-negative people. In Madagascar, P. vivax has broken through its dependence on the Duffy antigen for establishing human blood-stage infection and disease. Further studies are necessary to identify the parasite and host molecules that enable this Duffy-independent P. vivax invasion of human erythrocytes. |
| Author | Ratsimbasoa, Arsène Thonier, Vincent Barnadas, Céline Henry-Halldin, Cara Bertrand, Olivier Domarle, Olivier Picot, Julien Zimmerman, Peter A Carod, Jean-François Ménard, Didier Gray, Laurie R Bouchier, Christiane King, Christopher L Colin, Yves Grimberg, Brian T Mercereau-Puijalon, Odile |
| Author_xml | – sequence: 1 fullname: Ménard, Didier – sequence: 2 fullname: Barnadas, Céline – sequence: 3 fullname: Bouchier, Christiane – sequence: 4 fullname: Henry-Halldin, Cara – sequence: 5 fullname: Gray, Laurie R – sequence: 6 fullname: Ratsimbasoa, Arsène – sequence: 7 fullname: Thonier, Vincent – sequence: 8 fullname: Carod, Jean-François – sequence: 9 fullname: Domarle, Olivier – sequence: 10 fullname: Colin, Yves – sequence: 11 fullname: Bertrand, Olivier – sequence: 12 fullname: Picot, Julien – sequence: 13 fullname: King, Christopher L – sequence: 14 fullname: Grimberg, Brian T – sequence: 15 fullname: Mercereau-Puijalon, Odile – sequence: 16 fullname: Zimmerman, Peter A |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20231434$$D View this record in MEDLINE/PubMed https://pasteur.hal.science/pasteur-00741118$$DView record in HAL |
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| Notes | SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 Edited by Thomas E. Wellems, National Institutes of Health, Bethesda, MD, and approved February 22, 2010 (received for review October 29, 2009) Author contributions: D.M., C. Barnadas, A.R., C.L.K., O.M.-P., and P.A.Z. designed research; D.M., C. Barnadas, C. Bouchier, C.H.-H., L.R.G., A.R., V.T., J.-F.C., O.D., O.B., J.P., and B.T.G. performed research; C.H.-H., Y.C., C.L.K., and P.A.Z. contributed new reagents/analytic tools; D.M., C. Barnadas, C.H.-H., Y.C., O.B., C.L.K., O.M.-P., and P.A.Z. analyzed data; and D.M., C. Barnadas, Y.C., C.L.K., O.M.-P., and P.A.Z. wrote the paper. 1D.M. and C. Barnadas contributed equally to this work. |
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| SubjectTerms | Adolescent African Continental Ancestry Group African Continental Ancestry Group - genetics ancestry Antigens Asian Continental Ancestry Group Asian Continental Ancestry Group - genetics Base Sequence Biological Sciences Blood Blood groups Child Child, Preschool Cytometry DNA Primers DNA Primers - genetics Duffy Blood-Group System Duffy Blood-Group System - genetics Duffy Blood-Group System - immunology epidemiological studies Epidemiology Erythrocyte invasion Erythrocytes Erythrocytes - parasitology Female flow cytometry gametocytes Genetic Association Studies genetic markers Genotype & phenotype genotyping Host-Parasite Interactions Host-Parasite Interactions - genetics Host-Parasite Interactions - immunology Human health and pathology Humans Infections Infectious diseases Life Sciences Madagascar Madagascar - epidemiology Malaria Malaria, Vivax Malaria, Vivax - blood Malaria, Vivax - epidemiology Malaria, Vivax - genetics Male microscopy Molecular Sequence Data Molecules Parasites Parasitic protozoa people Plasmodium vivax Plasmodium vivax - genetics Plasmodium vivax - growth & development Plasmodium vivax - pathogenicity polymerase chain reaction therapeutics Vector-borne diseases |
| Title | Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people |
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