Malaria is a common tropical disease caused by a protozoan P. falciparum which is largely transmitted through mosquito bites. The protozoa then infect the red blood cells of the victim and multiply thereby becoming available for transfer to other susceptible individuals via mosquito bites. According to Tapper (134), malaria is a disease that has existed in Africa and other tropical regions for several millennia. Overtime, the persistence presence of Malaria particularly in central and Western Africa began to form a selective pressure, thereby not only influencing the genetic development individuals resistant to the disease but also enhancing their survivability. On the other hand, Sickle cell is known to affect the hemoglobin and hemoglobin molecules referred to as hemoglobin S (Hgb. AS) are typical among fellows with this specific hemoglobinopathy. Consequently, the protection against malaria seen in carriers of sickle cell anemia is considered to be a form of genetic trade off.A number of researchers have asserted that Hgb. AS mutation which provides a certain level of prevention against malaria never developed as straight response towards the malaria parasite. Instead, it developed by chance. Individuals without the mutation residing in places that are endemic for malaria remained at a higher risk of contracting the malaria parasite followed by the development of this given infectious disease. Symptoms like enlarged spleens and high fevers were common among the affected individuals. Besides, it was observed that carriers of HGB. AS had higher chances of survival whenever malaria struck in comparison with the Hgb. AA carriers who always died during their first year of life if infected with malaria.Although the exact mechanism of how Sickle cell allele(S) impairs the development of Malaria is not yet fully known, it is widely believed that the infection of sickle cell trait red blood cells by P. falciparum often deform them in a way that they are marked as abnormal by macrophages before they are subsequently removed from the circulation and destroyed in the spleen together with the parasite (Ferreira 342). Other studies have suggested that the conditions in sickle cell trait erythrocytes may directly kill the Malaria parasites thereby impairing their proliferation. For example, some ultrastructural studies have revealed that incubating P. falciparum parasites at low oxygen tension similar to
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Tapper, Melbourne. In The Blood: Sickle Cell Anemia and the Politics of Race. University of Pennsylvania Press, 2009.Print.
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