%0 Journal Article
%T Molecular Investigation of Genetic Signatures of Selection in <i>Plasmodium falciparum</i> Actin-Binding Protein Coronin, Cysteine Desulfurase, and Plasmepsin 2 Gene in Mbita Field Isolates, Western Kenya
%A Houdou Diarra
%A Edward E. Makhulu
%A Peter O. Odhiambo
%A Robinson M. Irekwa
%A Johnson Kinyua
%A Jeremy K. Herren
%A Victor A. Mobegi
%J Open Journal of Genetics
%P 120-144
%@ 2162-4461
%D 2021
%I Scientific Research Publishing
%R 10.4236/ojgen.2021.114011
%X <b><span style=\"font-family:Verdana;\">Background:</span></b><i><span style=\"font-family:Verdana;\"> Plasmodium falciparum</span></i><span style=\"font-family:;\" \"=\"\"><span style=\"font-family:Verdana;\"> (</span><i><span style=\"font-family:Verdana;\">Pf</span></i><span style=\"font-family:Verdana;\">) resistance to antimalarial drugs is
a major impediment to malaria control. The </span><i><span style=\"font-family:Verdana;\">Pf</span></i><span style=\"font-family:Verdana;\">.</span><i><span style=\"font-family:Verdana;\">Kelch 13</span></i><span style=\"font-family:Verdana;\"> (</span><i><span style=\"font-family:Verdana;\">PfK13</span></i><span style=\"font-family:Verdana;\">) gene has been largely reported to be associated with
artemisinin resistance. However, recent studies have shown artemisinin
resistance without </span><i><span style=\"font-family:Verdana;\">Kech13 </span></i><span style=\"font-family:Verdana;\">mutations
suggesting the implication of others genes in artemisinin resistance. In this
current study, we focused on mutations in </span><i><span style=\"font-family:Verdana;\">Pf.</span></i><span style=\"font-family:Verdana;\">actin-binding
protein coronin, </span><i><span style=\"font-family:Verdana;\">Pf.</span></i><span style=\"font-family:Verdana;\">c</span><span><span style=\"font-family:Verdana;\">ysteine</span><i> </i><span style=\"font-family:Verdana;\">desulfurase
and </span><i><span style=\"font-family:Verdana;\">Pf</span></i><span style=\"font-family:Verdana;\">.plasmepsin 2 gene, three
putative candidates recently were reported to be</span><span style=\"color:red;\"> </span><span style=\"font-family:Verdana;\">involved
in artemisinin, lumefantrine and piperaquine resistance respectively. </span><b><span style=\"font-family:Verdana;\">Method: </span></b><span style=\"font-family:Verdana;\">Archived blood samples previously collected from asymptomatic school
children from December 2016 to October 2018 were used in this study. Genomic
DNA was extracted using ISOL</span></span><span style=\"font-family:Verdana;\">ATE II Genomic DNA kit. After PCR
amplification, amplicons were purified and sequenced by capillary sequencing.
Reads were analyzed for the identification of point mutations previously
reported to be involved in drug selection. </span><b><span style=\"font-family:Verdana;\">Results:</span></b><span style=\"font-family:Verdana;\"> Mutations R100K, and
G50E involved in reduced artemisinin susceptibility were detected in </span><i><span style=\"font-family:Verdana;\">Pfcoronin</span></i><span
%K &lt
%K i&gt
%K Plasmodium falciparum&lt
%K /i&gt
%K Mutations
%K Artemisinin
%K Lumefantrine
%K Piperaquine
%U http://www.scirp.org/journal/PaperInformation.aspx?PaperID=114048