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A similar relationship exists between malaria and sickle-cell disease. One theory to explain this is that cells infected with the Plasmodium parasite are cleared more rapidly by the spleen . This phenomenon might give G6PD deficiency carriers an evolutionary advantage by increasing their fitness in malarial endemic environments.
A well-studied case is that of sickle cell anemia in humans, a hereditary disease that damages red blood cells. Sickle cell anemia is caused by the inheritance of an allele (HgbS) of the hemoglobin gene from both parents. In such individuals, the hemoglobin in red blood cells is extremely sensitive to oxygen deprivation, which results in ...
"Sickle Cell Anemia, a Molecular Disease" is a 1949 scientific paper by Linus Pauling, Harvey A. Itano, Seymour J. Singer and Ibert C. Wells that established sickle-cell anemia as a genetic disease in which affected individuals have a different form of the metalloprotein hemoglobin in their blood.
It is possible for a person to have both the gene for hemoglobin S (the form associated with sickle cell anemia) and the gene for hemoglobin C; this state is called hemoglobin SC disease, and is generally more severe than hemoglobin C disease, but milder than sickle cell anemia. [2]
Common causes include asplenia (post-splenectomy) or congenital absence of spleen (right atrial appendage isomerism). Spleens are also removed for therapeutic purposes in conditions like hereditary spherocytosis, trauma to the spleen, and autosplenectomy caused by sickle cell anemia.
An example of overdominance in humans is that of the sickle cell anemia.This condition is determined by a single polymorphism.Possessors of the deleterious allele have lower life expectancy, with homozygotes rarely reaching 50 years of age.
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