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Base-pair substitution that causes sickle cell anemia. The gene defect is a single nucleotide mutation of the β-globin gene, which results in glutamate being substituted by valine at position 6 of the β-globin chain. [62] Hemoglobin S with this mutation is referred to as HbS, as opposed to the normal adult HbA.
Hemoglobin D conditions such as homozygous and HbD/HbA heterozygous do not require medical intervention. HbD/HbS and HbD-thalassemia conditions are managed like the typical cases of sickle cell anemia and thalassemia. [29] In case of sickle cell anemia, daily treatment with penicillin recommended up to five years of age. [35]
With sickle cell disease — also called sickle cell anemia — red blood cells take on a folded or sickle shape that can clog tiny blood vessels and cause progressive organ damage and pain, and ...
The mutation is the result of histidine 112 being replaced with aspartic acid in the protein's polypeptide sequence. [1] Additionally, within one of the mutated alpha chains, there are substitutes at 114 and 118, two points on the amino acid chain. [2] This mutation can cause sickle cell anemia. [3]
That has been the case for Kayla Smith Owens, 25, of Chesapeake Beach, Maryland, who started experiencing mild symptoms of sickle cell disease pain and fatigue until around age 12, during puberty.
The sickle cell trait provides a survival advantage against malaria fatality over people with normal hemoglobin in regions where malaria is endemic. The trait is known to cause significantly fewer deaths due to malaria, especially when Plasmodium falciparum is the causative organism.
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