Two Novel Loci for Genetic Resistance in Malaria - Essay Example

Severe forms of malaria are caused by P. falciparum, a prevalent parasite in Sub-Saharan Africa. Malaria has been mentioned in literature as a potent form of natural selection among human populations (Kwiatkowski, 2005). This has been evident in malaria prone regions where, for instance, sickle cell variants in human populations have been shown to be refractive against malaria infection. Other genes which are known to confer genetic resistance against malaria include Glucose-6-phosphate dehydrogenase (G6PDH) deficiency and ?

-thalassemias variants. In Africa and Asia, genetic resistance against most prevalent malaria form, severe falciparum malaria is conferred by variants of hemoglobin and G6PDH deficiency. The structure adopted by the sickle cell variant of hemoglobin may not offer optimum environment for the malaria parasites to flourish as compared to the normal hemoglobin. Genetic Resistance in Malaria Genes involved in malaria resistance include the sickle cell genes for hemoglobin where the heterozygote form confers malarial resistance (Kwiatkowski, 2005).

In addition, Glucose-6-phosphate dehydrogenase (G6PDH) deficient individuals are also refractory to malaria infections. This confirms that malaria resistance among humans has a genetic element which according to Hedrick (2011) is evolutionarily significant. It is important to note that these malaria resistance genes such as the ABO, HLA and G6PDH are highly variant. Human host response to malarial parasite is different especially for P. falciparum. Some individuals may succumb to infection whereas others may survive.

This varied refractoriness may be attributed to genetic factors which account for around 25% of the risk of severe malaria (Mackinnon et al., 2005). Thus, among the population where malaria cases are prevalent, malaria has exerted significant pressure on the human genome to select mutations that are known to confer genetic resistance (Tishkoff and Williams, 2002). Besides sickle cell and Glucose-6-phosphate dehydrogenase (G6PDH) deficiency, other mutations such as Duffy mutations and ?- thalassemias also confer genetic resistance to malaria.

In endemic areas especially Sub-Saharan Africa, malaria caused by Plasmodium falciparum has imposed strong selective pressure amongst the population (Snow et al., 2005). Factors mentioned in literature linked to this susceptibility environmental, host genetics and parasite virulence (Mackinnon et al., 2005). These factors may interplay to determine the course of the disease. The advent of the completed human genome has heralded a new dawn in the understanding of major diseases and the potential susceptibility to these diseases as a result of one’s genetic make-up.

Apart from the known genetic resistance variants known to protect against malaria, G6PDH and sickle cell trait, molecular biology technologies which have engaged data from the complete human genome have contributed to the progressive discovery of genes and/or gene loci that influence the susceptibility to disease both directly or indirectly. Genes that confer resistance to malaria, for instance, may alter the normal interaction between the parasite and host or in other cases may modulate the development of immune response towards the pathogen.

These polymorphisms may exist in the population as processes of natural selection and co-adaptation take place. Several malaria parasites infections