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Beta-globin gene haplotypes and selected Malaria-associated variants among black Southern African populations

Partial carrier-resistance to Plasmodium falciparum malaria conferred by the sickle cell (HbS) mutation has resulted in the local amplification and positive selection of sickle cell disease (SCD) in malaria-endemic regions and particularly in sub-Saharan Africa (SSA). The present study investigated...

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Detalles Bibliográficos
Autores principales: Pule, G. D., Chimusa, E. R., Mnika, K., Mhandire, K., Kampira, E., Dandara, C., Wonkam, A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cambridge University Press 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5870409/
https://www.ncbi.nlm.nih.gov/pubmed/29868223
http://dx.doi.org/10.1017/gheg.2017.14
Descripción
Sumario:Partial carrier-resistance to Plasmodium falciparum malaria conferred by the sickle cell (HbS) mutation has resulted in the local amplification and positive selection of sickle cell disease (SCD) in malaria-endemic regions and particularly in sub-Saharan Africa (SSA). The present study investigated the β-globin gene haplotypes, and selected malaria-associated variants among three cohorts of Bantu-speaking individuals from Malawi, Zimbabwe and South Africa compared with reports with data from others SSA populations. The data suggest a south-ward frequency decrease of malaria-associated variants in SSA linked to the evolutionary dynamics of various African populations’ genomes through selective pressure of malaria. These selected genomics differences, positive selection of SCD in malaria-endemic regions among ‘Bantus’ from various part of Africa emphasise the evidence of the dissociation between genetics, anthropology and culture. The present study also showed a relatively prevalent Benin haplotype, which is mostly found in West Africa, among Southern African Blacks and very low Bantu haplotype, which could suggest a major migration route, of Southern Africa Bantu, along the African west coast, post-occurrence of the Sickle cell mutation, which date remain to be fully elucidated.