Emergence of FY*Anull in a Plasmodium vivax-endemic region of Papua New Guinea

被引:150
作者
Zimmerman, PA
Woolley, I
Masinde, GL
Miller, SM
McNamara, DT
Hazlett, F
Mgone, CS
Alpers, MP
Genton, B
Boatin, BA
Kazura, JW
机构
[1] Case Western Reserve Univ, Sch Med, Div Geog Med, Cleveland, OH 44106 USA
[2] Papua New Guinea Inst Med Res, Madang, Papua N Guinea
[3] Swiss Trop Inst, Dept Epidemiol & Publ Hlth, CH-4002 Basel, Switzerland
[4] Onchocerciasis Control Programme, Ouagadougou, Burkina Faso
关键词
D O I
10.1073/pnas.96.24.13973
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 greater than or equal to 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.
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页码:13973 / 13977
页数:5
相关论文
共 29 条
[11]  
LIVINGSTONE FB, 1984, HUM BIOL, V56, P413
[12]   DUFFY BLOOD-GROUP DETERMINANTS - THEIR ROLE IN SUSCEPTIBILITY OF HUMAN AND ANIMAL ERYTHROCYTES TO PLASMODIUM-KNOWLESI MALARIA [J].
MASON, SJ ;
MILLER, LH ;
SHIROISHI, T ;
DVORAK, JA ;
MCGINNISS, MH .
BRITISH JOURNAL OF HAEMATOLOGY, 1977, 36 (03) :327-335
[13]   RESISTANCE FACTOR TO PLASMODIUM-VIVAX IN BLACKS - DUFFY-BLOOD-GROUP GENOTYPE, FYFY [J].
MILLER, LH ;
MASON, SJ ;
CLYDE, DF ;
MCGINNISS, MH .
NEW ENGLAND JOURNAL OF MEDICINE, 1976, 295 (06) :302-304
[14]   A NEW HUMAN DUFFY BLOOD-GROUP SPECIFICITY DEFINED BY A MURINE MONOCLONAL-ANTIBODY - IMMUNOGENETICS AND ASSOCIATION WITH SUSCEPTIBILITY TO PLASMODIUM-VIVAX [J].
NICHOLS, ME ;
RUBINSTEIN, P ;
BARNWELL, J ;
DECORDOBA, SR ;
ROSENFIELD, RE .
JOURNAL OF EXPERIMENTAL MEDICINE, 1987, 166 (03) :776-785
[15]  
Oron-Karni V, 1998, AM J HEMATOL, V58, P306, DOI 10.1002/(SICI)1096-8652(199808)58:4<306::AID-AJH10>3.0.CO
[16]  
2-5
[17]  
SERJEANTSON SW, 1992, HUMAN BIOL PAPUA NEW, P198
[18]   PRESENCE OF DUFFY BLOOD GROUP GENE FYB DEMONSTRATED IN MELANESIANS [J].
SIMMONS, RT ;
GAJDUSEK, DC ;
GORMAN, JG ;
KIDSON, C ;
HORNABRO.RW .
NATURE, 1967, 213 (5081) :1148-&
[19]   Arg89Cys substitution results ins very low membrane expression of the Duffy antigen/receptor for chemokines in Fyx individuals [J].
Tournamille, C ;
Le van Kim, C ;
Gane, P ;
Le Pennec, PY ;
Roubinet, F ;
Babinet, J ;
Cartron, JP ;
Colin, Y .
BLOOD, 1998, 92 (06) :2147-2156
[20]   MOLECULAR-BASIS AND PCR-DNA TYPING OF THE FYA/FYB BLOOD-GROUP POLYMORPHISM [J].
TOURNAMILLE, C ;
KIM, CLV ;
GANE, P ;
CARTRON, JP ;
COLIN, Y .
HUMAN GENETICS, 1995, 95 (04) :407-410