{"title":"尼日利亚恶性疟原虫分离株Pfatpase-6基因的分子谱分析","authors":"Deborah Adedire, Chiamaka Iwegbulam, Roland Funwei, Temitope Owoeye, Zainab Kashim-Bello, Adeola Orogade, Catherine Falade, Oyekanmi Nash","doi":"10.53771/ijlsra.2023.4.1.0153","DOIUrl":null,"url":null,"abstract":"Anti-malarial drug resistance is one of the biggest public health burdens confronting global malaria control programmes. The emergence of P. falciparum chloroquine resistance transporter and multi-drug resistance mutant genes had devastating effects on the therapeutic efficacy of chloroquine when it was the drug of choice for malaria treatment. The artemisinins have proven to be an excellent therapeutic alternative to fill the void in chemotherapeutic options left by resistance mechanisms. The sarco/endoplasmic reticulum Ca2+-ATPase ortholog of P. falciparum (PfATPase-6) has been suggested as one of the targets of the artemisinins. Consequently, Pfatpase-6 gene polymorphisms are being investigated as markers of artemisinin resistance elsewhere. The present study assessed the molecular profile of the current prevalence of four P. falciparum candidate artemisinin resistance biomarkers L263E, E431K, A623E, and S769N in the Pfatpase-6 gene in 113 samples of P. falciparum isolates collected from Ibadan, Oyo State, Nigeria between 2017 and 2018. The frequency of occurrence of E431K mutation was 17% from collected samples. No A623E, L263E and S769N were detected. The result suggests that resistance to artemisinin has either not yet been selected in Nigeria or other genes mutations might be responsible for such, if at all","PeriodicalId":14144,"journal":{"name":"International Journal of Life Science Research Archive","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Molecular profile of Pfatpase-6 gene from Plasmodium falciparum isolates in Nigeria\",\"authors\":\"Deborah Adedire, Chiamaka Iwegbulam, Roland Funwei, Temitope Owoeye, Zainab Kashim-Bello, Adeola Orogade, Catherine Falade, Oyekanmi Nash\",\"doi\":\"10.53771/ijlsra.2023.4.1.0153\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Anti-malarial drug resistance is one of the biggest public health burdens confronting global malaria control programmes. The emergence of P. falciparum chloroquine resistance transporter and multi-drug resistance mutant genes had devastating effects on the therapeutic efficacy of chloroquine when it was the drug of choice for malaria treatment. The artemisinins have proven to be an excellent therapeutic alternative to fill the void in chemotherapeutic options left by resistance mechanisms. The sarco/endoplasmic reticulum Ca2+-ATPase ortholog of P. falciparum (PfATPase-6) has been suggested as one of the targets of the artemisinins. Consequently, Pfatpase-6 gene polymorphisms are being investigated as markers of artemisinin resistance elsewhere. The present study assessed the molecular profile of the current prevalence of four P. falciparum candidate artemisinin resistance biomarkers L263E, E431K, A623E, and S769N in the Pfatpase-6 gene in 113 samples of P. falciparum isolates collected from Ibadan, Oyo State, Nigeria between 2017 and 2018. The frequency of occurrence of E431K mutation was 17% from collected samples. No A623E, L263E and S769N were detected. The result suggests that resistance to artemisinin has either not yet been selected in Nigeria or other genes mutations might be responsible for such, if at all\",\"PeriodicalId\":14144,\"journal\":{\"name\":\"International Journal of Life Science Research Archive\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-01-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Journal of Life Science Research Archive\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.53771/ijlsra.2023.4.1.0153\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Life Science Research Archive","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.53771/ijlsra.2023.4.1.0153","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Molecular profile of Pfatpase-6 gene from Plasmodium falciparum isolates in Nigeria
Anti-malarial drug resistance is one of the biggest public health burdens confronting global malaria control programmes. The emergence of P. falciparum chloroquine resistance transporter and multi-drug resistance mutant genes had devastating effects on the therapeutic efficacy of chloroquine when it was the drug of choice for malaria treatment. The artemisinins have proven to be an excellent therapeutic alternative to fill the void in chemotherapeutic options left by resistance mechanisms. The sarco/endoplasmic reticulum Ca2+-ATPase ortholog of P. falciparum (PfATPase-6) has been suggested as one of the targets of the artemisinins. Consequently, Pfatpase-6 gene polymorphisms are being investigated as markers of artemisinin resistance elsewhere. The present study assessed the molecular profile of the current prevalence of four P. falciparum candidate artemisinin resistance biomarkers L263E, E431K, A623E, and S769N in the Pfatpase-6 gene in 113 samples of P. falciparum isolates collected from Ibadan, Oyo State, Nigeria between 2017 and 2018. The frequency of occurrence of E431K mutation was 17% from collected samples. No A623E, L263E and S769N were detected. The result suggests that resistance to artemisinin has either not yet been selected in Nigeria or other genes mutations might be responsible for such, if at all