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Sickle Cell Anemia

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Sickle Cell Anemia

Postby p3la » Mon Oct 22, 2007 7:32 pm

What would you expect to happen to the frequency of the sickle cell allele in a population which historically had a high incidence of malaria but in which malaria had been eradicated?

This was on my midterm a week ago and it's still bothering me. I answered it the following way, please input your thoughts.

The frequency of the sickle cell allele would be higher due to the fact that natural selection acts on populations with high levels of malaria by selecting the sickle cell allele. The reason for this is because the heterozygote HbAHbS is resistant to malaria unlike normal blood (HbAHbA) and sickling blood HbSHbS. For this reason as well it will be prevalent in certain human population because natural selection has acted to increase its frequency in order to eradicate malaria. So if the malaria was eradicated it would mean that a lot of that population is a carrier (HbAHbS - malaria resistant) and there will be some with sickling blood.
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Postby mith » Mon Oct 22, 2007 7:58 pm

The question is asking you to compare the frequency of the historic population to the present day population.

Note that the selecting factor, malaria, is gone; the present day population is comparable to other non-malaria populations in terms of selection factors.

So, how will the frequency of non-malaria afflicted populations compare with malaria afflicted populations?
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Postby Darby » Fri Oct 26, 2007 2:52 pm

Also keep in mind that there are two selecting factors - when malaria is around, it's a positive selection factor for sickle-cell, but the sickle-cell itself is a negative selection factor. Take away the malaria, and what's left-?
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Postby blcr11 » Fri Oct 26, 2007 6:36 pm

I don’t think it’s a simple trait kind of thing. There are a number of different gene polymorphs that confer some kind of resistance to the most severe symptoms and death from malaria. HbS or alpha-thalassaemia confer resistance to death from complications of P falciprum infections, but having both traits is either no different or even slightly worse than having no resistance marker at all. And resistence to complications doesn’t mean that these individuals are immune to infection, only that they suffer fewer of the more severe symptoms of malaria. I’m not sure it’s always clear why. I think it’s also true what others are saying, that only in the presence of significant malarial infection is there any advantage to having the sickle-cell trait. In the absence of any malaria, there should be at least a mild selection against it. I don’t think the presence of the trait would, in itself, eliminate malaria since the life-cycle of the parasite is not interrupted in any way and transmission is still possible. It’s just that some infected individuals don’t get as sick from their disease. Try some of the following:

1: Williams TN.
Human red blood cell polymorphisms and malaria.
Curr Opin Microbiol. 2006 Aug;9(4):388-94. Epub 2006 Jul 3. Review.
PMID: 16815736 [PubMed - indexed for MEDLINE]

2: Kwiatkowski DP.
How malaria has affected the human genome and what human genetics can teach us
about malaria.
Am J Hum Genet. 2005 Aug;77(2):171-92. Epub 2005 Jul 6. Review.
PMID: 16001361 [PubMed - indexed for MEDLINE]

3: Min-Oo G, Gros P.
Erythrocyte variants and the nature of their malaria protective effect.
Cell Microbiol. 2005 Jun;7(6):753-63. Review.
PMID: 15888079 [PubMed - indexed for MEDLINE]

4: Roberts DJ, Williams TN.
Haemoglobinopathies and resistance to malaria.
Redox Rep. 2003;8(5):304-10. Review.
PMID: 14962371 [PubMed - indexed for MEDLINE]

5: Weatherall DJ, Miller LH, Baruch DI, Marsh K, Doumbo OK, Casals-Pascual C,
Roberts DJ.
Malaria and the red cell.
Hematology Am Soc Hematol Educ Program. 2002;:35-57. Review.
PMID: 12446418 [PubMed - indexed for MEDLINE]

6: Destro Bisol G.
Genetic resistance to malaria, oxidative stress and hemoglobin oxidation.
Parassitologia. 1999 Sep;41(1-3):203-4. Review.
PMID: 10697857 [PubMed - indexed for MEDLINE]

7: Giardina B, Messana I, Scatena R, Castagnola M.
The multiple functions of hemoglobin.
Crit Rev Biochem Mol Biol. 1995;30(3):165-96. Review.
PMID: 7555018 [PubMed - indexed for MEDLINE]

8: Nagel RL.
Innate resistance to malaria: the intraerythrocytic cycle.
Blood Cells. 1990;16(2-3):321-39; discussion 340-9. Review.
PMID: 2257317 [PubMed - indexed for MEDLINE]

9: Teo CG, Wong HB.
The innate resistance of thalassaemia to malaria: a review of the evidence and
possible mechanisms.
Singapore Med J. 1985 Dec;26(7):504-9. Review. No abstract available.
PMID: 2422762 [PubMed - indexed for MEDLINE]
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