Abstract
Hemoglobinopathies, including sickle cell disease (SCD) and thalassemia, are inherited disorders that affect hemoglobin structure and function, leading to significant health implications. However, these genetic conditions also confer a degree of protection against malaria, particularly Plasmodium falciparum, the most virulent malaria parasite. This comprehensive review examines the relationship between hemoglobinopathies and malaria protection, exploring how genetic mutations in hemoglobin subunits influence susceptibility to malaria. Sickle cell trait (HbAS) provides notable protection against severe malaria, with mechanisms including reduced parasite growth, enhanced immune clearance, and microvascular obstruction. Although homozygous sickle cell disease (HbSS) does not confer protection and leads to severe complications, the high prevalence of HbS in malaria-endemic regions underscores an evolutionary balance. Thalassemia, both alpha and beta types, also offers partial malaria protection by altering the red blood cell environment, though the precise mechanisms remain less understood. Additionally, other hemoglobin variants, such as hemoglobin C (HbC) and hemoglobin E (HbE), demonstrate varying degrees of malaria resistance. The review highlights the evolutionary and epidemiological evidence supporting the protective effects of these genetic traits, emphasizing their role in malaria-endemic regions. Public health implications include the need for genetic counseling and targeted malaria control strategies. Future research directions include elucidating mechanistic pathways, exploring regional variations, and assessing the impact on malaria vaccine efficacy. By integrating insights from hemoglobinopathy research into public health interventions, more effective malaria control strategies can be developed, ultimately improving health outcomes for affected populations. Keywords: Hemoglobinopathies, Sickle Cell Disease, Thalassemia, Malaria Protection, Plasmodium falciparum.
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