New loci for genetic resistance to malaria in humans

The pathogenic species belonging to this genus include P. ovale, P. Malariae, P. falciparum, P. vivax and P. Knowlesi. The severe form of the condition is the one caused by P. falcipurum which is prevalent in the Sub-Saharan Africa. Some overlapping clinical syndromes that indicates the severe form includes severe anaemia (SA) and cerebral malaria (CM) (World Health Organisation, 2000). The essay below refers to GWAS approach to develop the strategies applied in the development of control for infectious diseases in humans. According to Kwiatkowski (2005), the disease has been identified as a potent type in the human population. This is because genetic traits such as sickle cell variants have been proven to protect people from malaria. Some highly variant genes offer resistance to malaria e.g. sickle cell haemoglobin variant (Hb-S) and Glucose-6-phosphate dehydrogenase (G6PDH). This affirms that malaria resistance among humans is genetic (Hedrick, 2011). The response to the malarial parasite of the human body varies i.e. some people may succumb upon infection while others may survive. This variation is caused by genetic factors (Mackinnon et al., 2005). The prevalence of the disease has led to an increase in mutation in the human body to counter the negative effects of the disease. Snow et al., (2005) alludes that the malaria form caused by P. falcipurum in endemic areas has led to a strong selective pressure among the human population. … Studies on the genetic make-up of the human body have been enhanced by construction of a complete human genome. Enhanced genomic studies have been conducted globally to understand the variant traits of diseases and conditions such as diabetes and/or malaria. The genome wide studies include studies related to genome linkage and association. Genome-wide association studies are involved in the identification of the pathways influencing malaria, especially the severe form of malaria. Human chromosome 10 (10p15.3-14) and chromosome 13 (13q) have been identified by Timmann et al. (2012) to possess pronounced linkages to the severe malaria forms. Genome-wide association studies links individuals with common genetic variants to a host of diseases and traits. Hirschorn and Daly (2005) deduce that the studies are characterised by a survey across the genome sets of Single Nucleotide Polymorphism (SNP) for most of the common genetic variation that causes diseases or exposes an individual to disease vulnerability. Additionally, these studies contribute in the identification of the variants contributing to the disease on focus. The genome-wide analysis identifies the factors that influence health and disease. Contrary to the linkage studies where markers associated with the genome must segregate with diseases in families, the GWAS studies focuses on the analysis of genome for possible genetic variants causing the disease (Hirschorn and Daly, 2005). Timmann et al., (2012) asserts that resistance to malaria has not been comprehensively established. The GWAS studies are appropriate for identifying the variants for the genetic resistance in the body. The GWAS studies involve the application of