Emergence of FY*A(null) in a Plasmodium vivax-endemic region of Papua New Guinea

Détails

ID Serval
serval:BIB_A2541037AB49
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Emergence of FY*A(null) in a Plasmodium vivax-endemic region of Papua New Guinea
Périodique
Proceedings of the National Academy of Sciences of the United States of America
Auteur(s)
Zimmerman  P. A., Woolley  I., Masinde  G. L., Miller  S. M., McNamara  D. T., Hazlett  F., Mgone  C. S., Alpers  M. P., Genton  B., Boatin  B. A., Kazura  J. W.
ISSN
0027-8424 (Print)
Statut éditorial
Publié
Date de publication
11/1999
Volume
96
Numéro
24
Pages
13973-7
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Nov 23
Résumé
In Papua New Guinea (PNG), numerous blood group polymorphisms and hemoglobinopathies characterize the human population. Human genetic polymorphisms of this nature are common in malarious regions, and all four human malaria parasites are holoendemic below 1500 meters in PNG. At this elevation, a prominent condition characterizing Melanesians is alpha(+)-thalassemia. Interestingly, recent epidemiological surveys have demonstrated that alpha(+)-thalassemia is associated with increased susceptibility to uncomplicated malaria among young children. It is further proposed that alpha(+)-thalassemia may facilitate so-called "benign" Plasmodium vivax infection to act later in life as a "natural vaccine" against severe Plasmodium falciparum malaria. Here, in a P. vivax-endemic region of PNG where the resident Abelam-speaking population is characterized by a frequency of alpha(+)-thalassemia >/=0.98, we have discovered the mutation responsible for erythrocyte Duffy antigen-negativity (Fy[a-b-]) on the FY*A allele. In this study population there were 23 heterozygous and no homozygous individuals bearing this new allele (allele frequency, 23/1062 = 0.022). Flow cytometric analysis illustrated a 2-fold difference in erythroid-specific Fy-antigen expression between heterozygous (FY*A/FY*A(null)) and homozygous (FY*A/FY*A) individuals, suggesting a gene-dosage effect. In further comparisons, we observed a higher prevalence of P. vivax infection in FY*A/FY*A (83/508 = 0.163) compared with FY*A/FY*A(null) (2/23 = 0.087) individuals (odds ratio = 2.05, 95% confidence interval = 0.47-8.91). Emergence of FY*A(null) in this population suggests that P. vivax is involved in selection of this erythroid polymorphism. This mutation would ultimately compromise alpha(+)-thalassemia/P. vivax-mediated protection against severe P. falciparum malaria.
Mots-clé
Animals Base Sequence DNA, Complementary Duffy Blood-Group System/*genetics *Endemic Diseases Flow Cytometry Gene Expression Genotype Humans Malaria, Vivax/epidemiology/*genetics Molecular Sequence Data Papua New Guinea/epidemiology Plasmodium vivax
Pubmed
Web of science
Création de la notice
28/01/2008 12:48
Dernière modification de la notice
03/03/2018 20:09
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