Abstract
In humans, infections contribute highly to mortality and morbidity rates worldwide. Malaria tropica is one of the major infectious diseases globally and is caused by the protozoan parasite Plasmodium falciparum. Plasmodia have accompanied human beings since the emergence of humankind. Due to its pathogenicity, malaria is a powerful selective force on the human genome. Genetic epidemiology approaches such as family and twin studies, candidate gene studies, and disease-association studies have identified a number of genes that mediate relative protection against the severest forms of the disease. New molecular approaches, including genome-wide association studies, have recently been performed to expand our knowledge on the functional effect of human variation in malaria. For the future, a systematic determination of gene-dosage effects and expression profiles of protective genes might unveil the functional impact of structural alterations in these genes on either side of the host-parasite interaction.
Highlights
Malaria is a disease caused by Apicomplexa parasites of the genus Plasmodium, and is transmitted by the bite of an infected female Anopheles mosquito
copy number variation (CNV) are a feature of the parasite-host interaction in malaria
Whereas the parasite perspective of malaria has been under intense investigation, especially regarding drug response and resistance, the host side has so far received less attention
Summary
Malaria is a disease caused by Apicomplexa parasites of the genus Plasmodium, and is transmitted by the bite of an infected female Anopheles mosquito. This finding indicates the influence of many other unexplored protective genes, each individually resulting in small population effects Genetic markers such as single nucleotide polymorphisms (SNPs) are a valuable tool to study risk assessment and progression of infectious diseases. Common genetic variants located in the human MBL2 gene locus impact the stability and the serum level of the resulting protein, which influences the predisposition and clinical outcome of various infectious diseases of bacterial and parasitic origin [27,28]. Various studies link the human genetic variations of the HLA genes, whose protein products are responsible for antigen presentation to the immune system, to disease progression and outcome. CNV could be the starting point of a new round in the arms race between parasites and the human immune system
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