Evolution of Genetic Resistance/Susceptibility to Malaria Infection

摘要: Severe malaria infection still kills more than 2.7 million people across the globe every year. Of few infections which has shaped human genome over millennia through process of natural selection, left its imprints on genome. Genetic studies malarial resistance started in late 1940s with demonstration protection against carriers several haemoglobinopathy genes and further increasing prevalence such malarious areas world. As parasites pass a significant period life inside red cell, many cell proteins their were studied for polymorphic variants offers infection. Total absence Plasmodium vivax Western Africa linkage total Duffy antigen is case point. Subsequently as rational extension above idea, association or susceptibility to severe relation innate immunity, adoptive cytokine genes, adhesion molecules, coagulation proteins, involved systemic inflammatory reactions etc. Innumerable have shown various kinds association. However, at present interest shifted towards wide Present review stops short presents snapshot view infection. Key Concepts: The immune system man evolved fight pathogens like parasite. Pathogens exerted intense selective pressures evolution man. Key elements adaptive system, receptors major histocompatibility complex show evidence pressures. Mutation key genetic mechanism underlying co-evolution pathogens. Evolutionary adaptation involves aspects modification Innate Immune system. Owing cycle parasite specific requirements nutrition need during growth, vulnerability increases due changes Nutrient (haemoglobin), Host Enzyme (Oxidant damage), specialised entry into cells (Red cells, Hepatocytes) ability adhere Key (Endothelium). Product metabolism (Hemozoin) exerts strong immunomodulatory effect. As from different regions world selection pressure population groups endowment (polymorphisms), this resulted resistant molecules parts world. Keywords: falciparum malaria; vivax malaria; red cell; haemoglobin; polymorphisms; HLA antigens; cytokine genes; adhesion molecules; endothelial cells; toll receptors; haemozoin; immunomodulation