HB S [β6(A3)GLU→VAL, GAG>GTG] AND β-GLOBIN GENE CLUSTER HAPLOTYPE DISTRIBUTION IN MAURITANIA

被引：9
|
作者：
Veten, Fatimetou M. [1 ]
Abdelhamid, Isselmou O. [2 ]
Meiloud, Ghlana M. [1 ]
Ghaber, Sidi M. [2 ]
Salem, Mohamed L. [2 ]
Abbes, Salem [3 ]
Houmeida, Ahmed O. [1 ]
机构：
[1] Fac Sci & Tech, Dept Biol, Nouakchott, Mauritania
[2] Ctr Hosp Natl, Dept Biochim & Hematol, Nouakchott, Mauritania
[3] Inst Pasteur Tunis, Lab Hematol Mol & Cellulaire, Tunis, Tunisia
来源：
HEMOGLOBIN | 2012年 / 36卷 / 04期
关键词：
Hemoglobin (Hb); Hb S; Population; beta(S) Haplotypes; Frequency; Mauritania; HEMOGLOBINOPATHIES; EPIDEMIOLOGY; POPULATION; ORIGIN;
D O I：
10.3109/03630269.2012.688782
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Of 1050 Mauritanian blood donors screened from the two main racial groups, i.e., the Moors and Black Africans, 60 were found to carry Hb S [beta 6(A3) Glu -> Val, GAG>GTG], giving a global frequency of 5.71%. The prevalence observed in the Black African Mauritanians (10.69%) is almost five times that found in the Moor group (2.25%). Four of the five main beta(S) haplotypes were detected in this study: Senegal (77.8%), Benin (8.8%), Arab-Indian (5.5%) and Bantu (4.4%). These data showed that Hb S is a serious public health problem in Mauritania. They also confirm the ethnic heterogeneity of the Mauritanian population.
引用
收藏
页码：311 / 315
页数：5
相关论文
共 36 条
  • [31] DNAse I hypersensitive site 3′ to the β-globin gene cluster contains a TAA insertion specific for βs-benin haplotype
    Bordin, S
    Alberto, FL
    Crespi, VG
    Duarte, ASS
    Bassères, DS
    Melo, MB
    Saad, STO
    Costa, FF
    BRITISH JOURNAL OF HAEMATOLOGY, 1998, 102 (01) : 47 - 47
  • [32] Effect of A3[6]beta(Glu->Val) mutation on reactivity of the CysF9[93]beta sulfhydryl group of human haemoglobin S
    Okonjo, KO
    Akenova, YA
    Aboluwoye, CO
    Nwozo, S
    Akhigbe, FU
    Babalola, JO
    Babarinde, NA
    JOURNAL OF THE CHEMICAL SOCIETY-FARADAY TRANSACTIONS, 1996, 92 (10): : 1739 - 1746
  • [33] Compound Heterozygosity for Hemoglobin S [β6(A3)Glu6Val] and Hemoglobin Korle-Bu [β73(E17)Asp73Asn]
    Akl, Pascale S.
    Kutlar, Ferdane
    Young, Andrew N.
    AMERICAN JOURNAL OF CLINICAL PATHOLOGY, 2009, 132 (03) : 463 - 464
  • [34] FIVE VARIANTS OF THE β-GLOBIN GENE WITHOUT CLINICAL OR HEMATOLOGICAL EFFECTS: Hb MARYLAND [β47(CD6)Asp→His], Hb KENT [β37(C3)Trp→Cys], Hb VISAYAN [β136(H14)Gly→Cys], Hb CUTLERVILLE [β138(H16)Ala→Val] AND Hb HORNCHURCH [β43(CD2)Glu→Lys]
    Hoyer, James D.
    Kaur, Prabhjot
    Kozak, Elizabeth A.
    Lum, Sophia
    Alter, David N.
    HEMOGLOBIN, 2008, 32 (05) : 471 - 477
  • [35] A New δ Chain Variant, Hb A2-Tunis [δ46(CD5)Gly → Glu; HBD: c.140G>A], Observed in a Tunisian Family in Association with a Compound Heterozygosity for Hb C [β6(A3)Glu → Lys; HBB: c.19G>A] β0-Thalassemia [IVS-I-1 (β143, G>A); HBB: c.92+1G>A]
    Moumni, Imen
    Zorai, Amine
    Mahjoub, Sonia
    Mosbahi, Ikbel
    Chaouechi, Dorra
    Benromdhane, Neila
    Abbes, Salem
    HEMOGLOBIN, 2014, 38 (02) : 88 - 90
  • [36] Strategy for Identification by Mass Spectrometry of a New Human Hemoglobin Variant with Two Mutations in Cis in the -Globin Chain: Hb S-Clichy [6(A3)GluVal; 8(A5)LysThr]
    Zanella-Cleon, Isabelle
    Prehu, Claude
    Joly, Philippe
    Riou, Jean
    Becchi, Michel
    Wajcman, Henri
    Francina, Alain
    HEMOGLOBIN, 2009, 33 (3-4) : 177 - 187
1234