Gene Mutation Increases Artemesin Resistance of Malaria Parasite (Plasmodium falciparum) in Africa

Early indicators of the malaria parasite in Africa developing resistance to the most effective drug available have been confirmed, according to new research published in an open-access article in the May 2015 issue of Antimicrobial Agents and Chemotherapy. The article is titled “The Mu Subunit of Plasmodium falciparum Clathrin-Associated Adaptor Protein 2 Modulates in vitro Parasite Response to Artemisinin and Quinine.” Researchers at the London School of Hygiene & Tropical Medicine found Plasmodium falciparum malaria parasites with a mutation to the gene Ap2mu were less sensitive to the anti-malarial drug artemisinin. A study in 2013, also led by the School, suggested an initial link between a mutation in the ap2mu gene and low levels of malaria parasites remaining in the blood of Kenyan children after they had been treated. However, further research was needed to confirm if these genetic characteristics represented an early step towards resistance. In the new study, researchers genetically altered the malaria parasite in the laboratory to mutate ap2mu in the same way that had been observed in Kenya. They found the altered parasite was significantly less susceptible, requiring 32% more drug to be killed by artemisinin. The genetically altered parasite was also 42.4% less susceptible to the traditional antimalarial drug, quinine. Earlier this year, a different research group discovered mutations in the gene kelch13 that were linked to reduced susceptibility to artemisinin combination treatment in South East Asia. Historically, resistance to antimalarial medicines has emerged in South East Asia and then spread to Africa. But these new findings suggest a different route to drug resistance may be developing independently in Africa. Lead researcher Dr.
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