Sickle Cell Trait and Resistance to Malaria: A Review

Abstract

This paper explores the intricate relationship between sickle cell trait (SCT) and malaria, analyzing the dimensions of genetics, evolution, and molecular biology. Sickle cell trait is an inherited blood disorder that is prevalent amongst individuals of African descent. A point mutation in the HBB gene, results in the synthesis of both sickle hemoglobin (HbS) and normal hemoglobin (HbA). Despite the anomalous protein structure of the HBB gene, individuals generally lead a normal life. Malaria, a widespread endemic in tropical regions, is transmitted by Anopheles mosquitoes and poses a global health threat. The disease is caused by the Plasmodium parasite and presents a range of symptoms, making young children, the elderly, and pregnant women more vulnerable (Malaria: Causes, Symptoms, Diagnosis, Treatment & Prevention, 2017). The interaction between sickle cell trait and malaria reveals a compelling connection between evolution and adaptation. Individuals with SCT display at least 90% resistance to malaria due to the altered physiology of the red blood cells, which hinders parasite growth (Carter & Mendis, 2002). The resistance is ascribed to the enhanced immune system responses, which are heightened when sickle hemoglobin is present, creating an unfavorable environment for the parasite. These genetics and immunological processes elucidate the evolutionary forces shaping human populations. This paper synthesizes the current research on SCT and malaria to underscore the intricate interplay between genetics, epidemiology, and evolution. Further research in genetics will allow for a more complex understanding of disease susceptibility and the human species as a whole.