The continuous Plasmodium falciparum kelch13 (PfK13) genetic alterations conferring resistance to artemisinin-based combination therapies and partner drugs pose a significant threat to effective treatment and control of P. falciparum infection in developing countries. This review evaluates the emergence and epidemiology of the PfK13 mutation associated with artemisinin resistance in the sub-Saharan Africa (SSA) population. Despite empirical control and artemisinin combination therapy, the PfK13 gene mutation, previously described in Southeast Asia, has been reported in the SSA. Eight of these validated markers, including P553L, M476I, C580Y, A675V, P574L, R561H, R622I, and F446I, were reported among the SSA population. Novel and unvalidated markers, such as P615S, M472I, F434S, A578S, P570L, Y558C, K563R, A569T, I684N, M472I, and C473F spread among the population with low frequency. We provide insight into the emergence and spread of validated and unvalidated PfK13 mutations among the SSA population, which could lead to high artemisinin resistance. Investigating the verified PfK13 mutations will improve prophylactic strategies, prognostic diagnosis and guide effective population-based surveillance for effective P. falciparum malaria control in SSA.
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Emergence of chloroquine-sensitive
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Artemisinin resistance (ART) has been confirmed in Greater Mekong Sub-region countries. Currently, C580Y mutation on Pfkelch13 gene is known as the molecular marker for the detection of ART. Rapid and accurate detection of ART in field study is essential to guide malaria containment and elimination interventions. A simple method for collection of malaria-infected blood is to spot the blood on filter paper and is fast and easy for transportation and storage in the field study. This study aims to evaluate LAMP-SNP assay for C580Y mutation detection by introducing an extra mismatched nucleotide at the 3’ end of the FIP primer. The LAMP-SNP assay was performed in a water bath held at a temperature of 56°C for 45 min. LAMP-SNP products were interpreted by both gel-electrophoresis and HNB-visualized changes in color. The method was then tested with 120 P. falciparum DNA from dried blood spot samples. In comparing the LAMP-SNP assay results with those from DNA sequencing of the clinical samples, the 2 results fully agreed to detect C580Y. The sensitivity and specificity of the LAMP-SNP assay showed 100%. There were no cross-reactions with other Plasmodium species and other Pfkelch13 mutations. The LAMP-SNP assay performed in this study was rapid, reliable, and useful in detecting artemisinin resistance in the field study.
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Prevalence of drug resistance associated mutations in Plasmodium vivax against sulphadoxine-pyrimethamine in southern Pakistan Afsheen Raza, Najia K Ghanchi, Muhammad Shahzeb Khan, Mohammad Asim Beg Malaria Journal.2013;[Epub] CrossRef
Blood Stage of Plasmodium vivax in Central China Is Still Susceptible to Chloroquine Plus Primaquine Combination Therapy Eun-Taek Han, Yaobao Liu, Feng Lu, Qi Gao, Jun Cao, Guoding Zhu, Huayun Zhou The American Journal of Tropical Medicine and Hygiene.2013; 89(1): 184. CrossRef
The use of sulfadoxine and pyrimethamine (SP) for treatment of vivax malaria is uncommon in most malarious areas, but Plasmodium vivax isolates are exposed to SP because of mixed infections with other Plasmodium species. As P. vivax is the most prevalent species of human malaria parasites in Iran, monitoring of resistance of the parasite against the drug is necessary. In the present study, 50 blood samples of symptomatic patients were collected from 4 separated geographical regions of south-east Iran. Point mutations at residues 57, 58, 61, and 117 were detected by the PCR-RFLP method. Polymorphism at positions 58R, 117N, and 117T of P. vivax dihydrofolate reductase (Pvdhfr) gene has been found in 12%, 34%, and 2% of isolates, respectively. Mutation at residues F57 and T61 was not detected. Five distinct haplotypes of the Pvdhfr gene were demonstrated. The 2 most prevalent haplotypes were F57S58T61S117 (62%) and F57S58T61N117 (24%). Haplotypes with 3 and 4 point mutations were not found. The present study suggested that P. vivax in Iran is under the pressure of SP and the sensitivity level of the parasite to SP is diminishing and this fact must be considered in development of malaria control programs.
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Molecular evaluation of pvdhfr and pvmdr-1 mutants in Plasmodium vivax isolates after treatment with sulfadoxine/pyrimethamine and chloroquine in Iran during 2001–2016 Mahdi Parsaei, Ahmad Raeisi, Adel Spotin, Abbas Shahbazi, Mahmoud Mahami-Oskouei, Teimour Hazratian, Alireza Salimi Khorashad, Jalal Zaman, Ahad Bazmani, Sedighe Sarafraz Infection, Genetics and Evolution.2018; 64: 70. CrossRef
Mutational Analysis of Plasmodium vivax dhfr Gene Among Cases in South East of Iran Hadi Mirahmadi, Maryam Rafee, Jalal Zaman, Ahmad Mehravaran, Reza Shafiei Jundishapur Journal of Microbiology.2017;[Epub] CrossRef
MOLECULAR SURVEILLANCE OF Plasmodium vivax AND Plasmodium falciparum DHFR MUTATIONS IN ISOLATES FROM SOUTHERN IRAN Khojasteh SHARIFI-SARASIABI, Ali HAGHIGHI, Bahram KAZEMI, Niloofar TAGHIPOUR, Ehsan Nazemalhosseini MOJARAD, Latif GACHKAR Revista do Instituto de Medicina Tropical de São Paulo.2016;[Epub] CrossRef
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