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• W2969593979 abstract "<ns4:p><ns4:bold>Background:</ns4:bold> The human malaria parasite <ns4:italic>Plasmodium falciparum</ns4:italic> has evolved complex drug evasion mechanisms to all available antimalarials. To date, the combination of amodiaquine-artesunate is among the drug of choice for treatment of uncomplicated malaria. In this combination, a short acting, artesunate is partnered with long acting, amodiaquine for which resistance may emerge rapidly especially in high transmission settings. Here, we used a rodent malaria parasite <ns4:italic>Plasmodium berghei </ns4:italic>ANKA as a surrogate of <ns4:italic>P. falciparum</ns4:italic> to investigate the mechanisms of amodiaquine resistance.</ns4:p><ns4:p> <ns4:bold>Methods</ns4:bold>: We used serial technique to select amodiaquine resistance by submitting the parasites to continuous amodiaquine pressure. We then employed the 4-Day Suppressive Test to monitor emergence of resistance and determine the cross-resistance profiles. Finally, we genotyped the resistant parasite by PCR amplification, sequencing and relative quantitation of mRNA transcript of targeted genes.</ns4:p><ns4:p> <ns4:bold>Results:</ns4:bold> Submission of <ns4:italic>P. berghei</ns4:italic> ANKA to amodiaquine pressure yielded resistant parasite within thirty-six passages. The effective dosage that reduced 90% of parasitaemia (ED<ns4:sub>90</ns4:sub>) of sensitive line and resistant line were 4.29mg/kg and 19.13mg/kg, respectively. After freezing at -80ºC for one month, the resistant parasite remained stable with an ED<ns4:sub>90</ns4:sub> of 18.22mg/kg. Amodiaquine resistant parasites are also resistant to chloroquine (6fold), artemether (10fold), primaquine (5fold), piperaquine (2fold) and lumefantrine (3fold). Sequence analysis of <ns4:italic>Plasmodium berghei chloroquine resistant transporter</ns4:italic> revealed His95Pro mutation. No variation was identified in <ns4:italic>Plasmodium berghei multidrug resistance gene-1 (Pbmdr1), Plasmodium berghei deubiquitinating enzyme-1</ns4:italic> or <ns4:italic>Plasmodium berghei Kelch13 domain</ns4:italic> nucleotide sequences. Amodiaquine resistance is also accompanied by high mRNA transcripts of key transporters; <ns4:italic>Pbmdr1</ns4:italic>, <ns4:italic>V-type/H+ pumping pyrophosphatase-2</ns4:italic> and <ns4:italic>sodium hydrogen ion exchanger-1 </ns4:italic>and Ca<ns4:sup>2+</ns4:sup>/H<ns4:sup>+</ns4:sup> antiporter.</ns4:p><ns4:p> <ns4:bold>Conclusions:</ns4:bold> Selection of amodiaquine resistance yielded stable “multidrug-resistant’’ parasites and thus may be used to study common resistance mechanisms associated with other antimalarial drugs. Genome wide studies may elucidate other functionally important genes controlling AQ resistance in <ns4:italic>P. berghei</ns4:italic>.</ns4:p>" @default.
• W2969593979 created "2019-08-29" @default.
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• W2969593979 date "2017-06-20" @default.
• W2969593979 modified "2023-09-24" @default.
• W2969593979 title "Amodiaquine resistance in Plasmodium berghei is associated with PbCRT His95Pro mutation, loss of chloroquine, artemisinin and primaquine sensitivity, and high transcript levels of key transporters" @default.
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• W2969593979 doi "https://doi.org/10.12688/wellcomeopenres.11768.1" @default.
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