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Sickle haemoglobin, haemoglobin C and malaria mortality feedbacks.
Bronner P Gonçalves1, Sunetra Gupta2, Bridget S Penman3
1Department of Immunology and Infection, London School of Hygiene and Tropical Medicine, London, W1CE 7HT, UK. bronner.goncalves@lshtm.ac.uk.
Malaria Journal
|January 13, 2016
Summary
Sickle haemoglobin (HbS) and haemoglobin C (HbC) offer malaria protection. A feedback loop where malaria severity increases with HbS or HbC presence favors HbS, explaining its wider spread despite greater disease severity.
Area of Science:
- Population genetics
- Evolutionary biology
- Molecular genetics
Background:
- Sickle haemoglobin (HbS) and haemoglobin C (HbC) are genetic variants offering malaria protection.
- HbS is more widespread than HbC, despite HbS homozygosity causing more severe disease (sickle cell anemia) than HbC homozygosity.
- The differing geographical distributions may relate to varying malaria protection levels in heterozygotes or parasite transmission dynamics.
Purpose of the Study:
- To investigate the evolutionary dynamics of HbS and HbC.
- To understand the role of malaria selection in the differential success of these alleles.
Main Methods:
- Utilized a population genetic model.
- Simulated evolutionary consequences based on malaria selection strength correlated with allele frequencies.
Main Results:
- Positive correlation between malaria selection pressure and HbS or HbC frequency facilitates HbS allele success.
- HbS demonstrated an advantage in competitive interactions between the two alleles under these conditions.
Conclusions:
- A feedback mechanism, where variant haemoglobins intensify malaria selection, likely contributed to HbS's global prevalence over HbC.
- This mechanism helps explain HbS's success despite its higher associated blood disorder cost.
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