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Sickle-cell Anemia as an Agents of Natural Selection.

Anthony Allison stated that disease is an agent of natural selection. Referring to Sickle-cell anemia and malaria. What is sickle-cell anemia and why is it referred as an agent of natural selection. Describe the geography of the association between the two and its relationship.

Sickle-cell Anemia as an Agents of Natural Selection.

The paper comprehensively discusses sickle-cell anemia as an agent of natural selection. It specifically define sickle-cell anemia, it also give the reason why sickle-cell anemia is an agent of natural selection. Lastly, this research paper describes the geography and association between sickle-cell anemia and malaria.  Anthony Allison (1954) postulated that “disease is an agent of natural selection.” It is important to note that the human population show significant genetic and biological dissimilarities.

Sickle-cell disease refers to the genetic disorder affecting hemoglobin. Sickle hemoglobin exhibits a devastating propensity to shrink as rods in red blood cells during the removal of oxygen in the normal process of blood circulation i.e. hemoglobin become polymerized on deoxygenation (Serjeant 1974). The resultant rods alter the cells, making them less pliable, rigid and stiff and inept to transverse smaller blood vessels. Some red blood cells become distorted into a sickle-shaped rather than round. It thus leads to vasocclusion of the medium and small-sized blood vessels, injuring the inner lining of blood vessels and thus causing ischemia (Serjeant 1974).

There exist many genotypes of sickle-cell anemia, and homozygous sickle disease or sickle-cell anemia is among the most prevalent and undoubtedly the most life-threatening or severe form of sickle cell disease. The disease result from the inheritance of the sickle-cell gene (the HbS gene) from both parents (Serjeant 1974). Sickle-cell anemia also known as homozygous sickle cell (SS) disease is an agent of natural selection. Natural selection refers to the propensity for particular traits to decrease or increase in incidence in a given population dependent on the reproductive feat of those showing them (Karlsson 2014). In other words, it is the tendency or the process by which the organisms that are most fit to their environment survive, as well as, reproduce at higher rates (Karlsson 2014).

In the 1950s, Dr. Anthony Allison (1954) established a unique association between Malaria, which is a highly infectious parasitic disease, and sickle-cell anemia (a genetic disease). The discovery is certainly the best-understood case of natural selection in which important molecules, the selective force, as well as, the adaptive mutation were all identified. Anthony Allison (1954) found out that the sickle-cell allele protects against Malaria. It does so by compromising the capacity of Malaria parasite (Plasmodium falciparum) to replicate or rather reproduce.

Sickle-cell anemia (Homozygous sickle cell) is an agent of natural selection because the HbS gene has a protective effect against malaria in the presence of the sickle-cell allele in the heterozygous state (Allison, 291). More specifically, individuals who have sickle-cell anemia carry the genetic burden that enables people to live in regions of the world that are endemic to malaria. Homozygous persons have two of the same alleles of a specific gene. On the other hand, if the alleles are not similar, the person is said to be heterozygous for that particular gene. In geographical locations where malaria is rampant,  the manifestation of the sickle cell allele in the heterozygous (AS) state increases the survival fitness of persons. In other words, people who are heterozygous for the sickle-cell allele are at a selective advantage in malaria-prone regions and do not suffer sickle-cell anemia.

Allison (1954) found out that the sickle-cell allele can be advantageous in one environment and disadvantageous in a different environment. In a geographical location where Malaria is prevalent, persons who carry the sickle-cell allele have a selective benefit because they are protected against Malaria. Dr. Allison indicates that natural selection is advantageous in the case of increased frequency of the sickle-cell allele, in regions such as near Lake Victoria or the coastal part of East Africa. Additionally, in locations where the malaria parasite is widespread, homozygous persons for the sickle-cell allele, as well as, persons who are homozygous for the normal allele are placed at a selective disadvantage.

Allison (1954) also discovered that in areas where Malaria is not widespread, in places such as East African highlands, the Sickle-cell allele is not favorable. In areas such as East African Highland, persons who are heterozygous for the sickle-cell allele do not have a selective advantage because protection against a malaria parasite occurs at the expense of increased sickle-cell disease within the population.

In conclusion, Sickle-cell anemia and malaria are critical challenges to hematology, as well as, to infectious disease medicine respectively. The two diseases are evidently some of the primary public health challenges and problems. Different from malaria that is a parasite-caused disease and transmitted by a mosquito, sickle cell disease is inherited from both parents. The paper has analyzed the association between malaria and sickle-cell anemia. The paper has also described the reason why sickle-cell anemia is called an agent of natural selection and the geography of the association between malaria and sickle-cell anemia.

Work Cited.

Allison, Anthony C. “Protection Afforded by Sickle-Cell Trait against Sub-tertian Malarial Infection.” British Medical Journal 1, no. 4857 (February 6, 1954): 290–294.

Karlsson, Elinor K., Dominic P. Kwiatkowski, and Pardis C. Sabeti. “Natural Selection and Infectious Disease in Human Populations.” Nature Reviews Genetics 15.6 (2014): 379. Publisher Provided Full Text Searching File. Web. 28 Nov. 2015.

Serjeant, Graham R. “Sickle-Cell Disease.” Lancet 350.9079 (1997): 724. Business Source Complete. Web. 28 Nov. 2015.

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