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Mutations in the propeller domain of  Plasmodium falciparum kelch 13  ( Pfk13 ) gene are associated with artemisinin resistance in Southeast Asia. Artemisinin resistance is defined by increased ring survival rate and delayed parasite clearance half-life in patients. Additionally, an amplification of the  Plasmodium falciparum plasmepsin II  gene ( pfpm2 ), encoding a protease involved in hemoglobin degradation, has been found to be associated with reduced in vitro susceptibility to piperaquine in Cambodian  P. falciparum  parasites and with dihydroartemisinin–piperaquine failures in Cambodia. The World Health Organization (WHO) has recommended the use of these two genes to track the emergence and the spread of the resistance to dihydroartemisinin–piperaquine in malaria endemic areas. Although the resistance to dihydroartemisinin–piperaquine has not yet emerged in Africa, few reports on clinical failures suggest that  k13  and  pfpm2  would not be the only genes involved in artemisinin and piperaquine resistance. It is imperative to identify molecular markers or drug resistance genes that associate with artemisinin and piperaquine in Africa.  K13  polymorphisms and  Pfpm2  copy number variation analysis may not be sufficient for monitoring the emergence of dihydroartemisinin–piperaquine resistance in Africa. But, these markers should not be ruled out for tracking the emergence of resistance.

malaria journal

Are k13 and plasmepsin II genes, involved in Plasmodium falciparum resistance to artemisinin derivatives and piperaquine in Southeast Asia, reliable to monitor resistance surveillance in Africa?