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Background  Resistance to all available anti-malarial drugs has emerged and spread including artemisinin derivatives and their partner drugs. Several genes involved in artemisinin and partner drugs resistance, such as  pfcrt ,  pfmdr1 ,  pfK13  or  pfpm2 , have been identified. However, these genes do not properly explain anti-malarial drug resistance, and more particularly clinical failures observed in Africa. Mutations in genes encoding for  Plasmodium falciparum  proteins, such as  P. falciparum  Acetyl-CoA transporter (PfACT),  P. falciparum  UDP-galactose transporter (PfUGT) and  P. falciparum  cyclic amine resistance locus (PfCARL) have recently been associated to resistance to imidazolopiperazines and other unrelated drugs.    Methods  Mutations on  pfugt ,  pfact  and  pfcarl  were characterized on 86 isolates collected in Dakar, Senegal and 173 samples collected from patients hospitalized in France after a travel in African countries from 2015 and 2016 to assess their potential association with ex vivo susceptibility to chloroquine, quinine, lumefantrine, monodesethylamodiaquine, mefloquine, dihydroartemisinin, artesunate, doxycycline, pyronaridine and piperaquine.    Results  No mutations were found on the genes  pfugt  and  pfact . None of the  pfcarl  described mutations were identified in these samples from Africa. The K784N mutation was found in one sample and the K734M mutation was identified on 7.9% of all samples for  pfcarl.  The only significant differences in ex vivo susceptibility according to the K734M mutation were observed for pyronaridine for African isolates from imported malaria and for doxycycline for Senegalese parasites.    Conclusion  No evidence was found of involvement of these genes in reduced susceptibility to standard anti-malarial drugs in African  P. falciparum  isolates.

malaria journal

Low polymorphisms in pfact, pfugt and pfcarl genes in African Plasmodium falciparum isolates and absence of association with susceptibility to common anti-malarial drugs