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Journal articles on the topic 'Antimalarials Dihydropteroate Synthase'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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1

Khim, Nimol, Christiane Bouchier, Marie-Thérèse Ekala, et al. "Countrywide Survey Shows Very High Prevalence of Plasmodium falciparum Multilocus Resistance Genotypes in Cambodia." Antimicrobial Agents and Chemotherapy 49, no. 8 (2005): 3147–52. http://dx.doi.org/10.1128/aac.49.8.3147-3152.2005.

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ABSTRACT Cambodia is located in an area of resistance to multiple antimalarials and has been the first country to implement the systematic use of an artesunate-mefloquine combination as first-line treatment for Plasmodium falciparum malaria. Little is known, however, about the prevalence of resistance mutations within the natural parasite populations, impeding rational drug policy in this context. Using direct sequencing of PCR products, we have analyzed sequence polymorphism of the dihydrofolate reductase-thymidylate synthase, dihydropteroate synthetase, and multidrug resistance 1 genes in a
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2

Nduati, Eunice, Sonya Hunt, Eddy M. Kamau, and Alexis Nzila. "2,4-Diaminopteridine-Based Compounds as Precursors for De Novo Synthesis of Antifolates: a Novel Class of Antimalarials." Antimicrobial Agents and Chemotherapy 49, no. 9 (2005): 3652–57. http://dx.doi.org/10.1128/aac.49.9.3652-3657.2005.

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ABSTRACT We have tested the hypothesis that 2,4-diamino-6-hydroxymethyl-pteridine (DAP), 2,4-diaminopteroic acid (DAPA), and 2,4 diamino-N10-methyl-pteroic acid (DAMPA) could be converted into aminopterin (from DAP and DAPA) and methotrexate (from DAMPA), both of which are potent inhibitors of dihydrofolate reductase, a proven drug target for Plasmodium falciparum. DAP, DAPA, and DAMPA inhibited parasite growth in the micromolar range; DAMPA was the most active, with 50% inhibitory concentrations in vitro of 446 ng/ml against the antifolate-sensitive strain and 812 ng/ml against the highly res
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3

Chotpatiwetchkul, Warot, Kanokthip Boonyarattanakalin, Duangkamol Gleeson, and M. Paul Gleeson. "Exploring the catalytic mechanism of dihydropteroate synthase: elucidating the differences between the substrate and inhibitor." Organic & Biomolecular Chemistry 15, no. 26 (2017): 5593–601. http://dx.doi.org/10.1039/c7ob01272a.

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QM/MM calculations are reported that help elucidate the reaction mechanism of DHPS, a validated antimicrobial and antimalarial target that has become increasingly compromised due to disease resistance.
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4

Lucchi, Naomi W., Sheila Akinyi Okoth, Franklin Komino, et al. "Increasing Prevalence of a Novel Triple-Mutant Dihydropteroate Synthase Genotype in Plasmodium falciparum in Western Kenya." Antimicrobial Agents and Chemotherapy 59, no. 7 (2015): 3995–4002. http://dx.doi.org/10.1128/aac.04961-14.

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ABSTRACTThe molecular basis of sulfadoxine-pyrimethamine (SP) resistance lies in a combination of single-nucleotide polymorphisms (SNPs) in two genes coding forPlasmodium falciparumdihydrofolate reductase (Pfdhfr) andP. falciparumdihydropteroate synthase (Pfdhps), targeted by pyrimethamine and sulfadoxine, respectively. The continued use of SP for intermittent preventive treatment in pregnant women in many African countries, despite SP's discontinuation as a first-line antimalarial treatment option due to high levels of drug resistance, may further increase the prevalence of SP-resistant paras
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5

Winstanley, P. A., E. K. Mberu, I. S. Szwandt, A. M. Breckenridge, and W. M. Watkins. "In vitro activities of novel antifolate drug combinations against Plasmodium falciparum and human granulocyte CFUs." Antimicrobial Agents and Chemotherapy 39, no. 4 (1995): 948–52. http://dx.doi.org/10.1128/aac.39.4.948.

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The potency of antimalarial dihydrofolate reductase inhibitors, alone and in synergistic combination with dihydropteroate synthetase inhibitors, against the Kenyan K39 strain of Plasmodium falciparum (pyrimethamine resistant) and against normal replicating human bone marrow cells in in vitro culture has been studied. Therapeutic indices and rank order of synergistic potency were derived. Trimethoprim, pyrimethamine, and the quinazolines WR159412 and WR158122 had the smallest therapeutic indices (1.39, 4.38, 2.56, and 90.0, respectively), while the three triazines clociguanil, WR99210, and chlo
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6

Abugri, James, Felix Ansah, Kwaku P. Asante, Comfort N. Opoku, Lucas A. Amenga-Etego, and Gordon A. Awandare. "Prevalence of chloroquine and antifolate drug resistance alleles in Plasmodium falciparum clinical isolates from three areas in Ghana." AAS Open Research 1 (December 3, 2018): 1. http://dx.doi.org/10.12688/aasopenres.12825.2.

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Background: The emergence and spread of resistance in Plasmodium falciparum to chloroquine (CQ) necessitated the change from CQ to artemisinin-based combination therapies (ACTs) as first-line drug for the management of uncomplicated malaria in Ghana in 2005. Sulphadoxine-pyrimethamine (SP) which was the second line antimalarial drug in Ghana, was now adopted for intermittent preventive treatment of malaria in pregnancy (IPTp). Methods: To examine the prevalence of molecular markers associated with CQ and antifolate drug resistance in Ghana, we employed restriction fragment length polymorphism
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7

Talawanich, Yuwadee, Sumalee Kamchonwongpaisan, Worachart Sirawaraporn, and Yongyuth Yuthavong. "Use of bacterial surrogates as a tool to explore antimalarial drug interaction: Synergism between inhibitors of malarial dihydrofolate reductase and dihydropteroate synthase." Acta Tropica 149 (September 2015): 64–69. http://dx.doi.org/10.1016/j.actatropica.2015.05.011.

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8

Pearce, Richard J., Chris Drakeley, Daniel Chandramohan, Frank Mosha, and Cally Roper. "Molecular Determination of Point Mutation Haplotypes in the Dihydrofolate Reductase and Dihydropteroate Synthase of Plasmodium falciparum in Three Districts of Northern Tanzania." Antimicrobial Agents and Chemotherapy 47, no. 4 (2003): 1347–54. http://dx.doi.org/10.1128/aac.47.4.1347-1354.2003.

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ABSTRACT The antimalarial combination of sulfadoxine and pyrimethamine (SP) was introduced as first-line treatment for uncomplicated malaria in Tanzania during 2001 following 18 years of second-line use. The genetic determinants of in vitro resistance to the two drugs individually are shown to be point mutations at seven sites in the dihydrofolate reductase gene (dhfr) conferring resistance to pyrimethamine and five sites in the dihydropteroate synthase (dhps) gene conferring resistance to sulfadoxine. Different combinations of mutations within each gene confer differing degrees of insensitivi
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9

Karema, Corine, Mallika Imwong, Caterina I. Fanello, et al. "Molecular Correlates of High-Level Antifolate Resistance in Rwandan Children with Plasmodium falciparum Malaria." Antimicrobial Agents and Chemotherapy 54, no. 1 (2009): 477–83. http://dx.doi.org/10.1128/aac.00498-09.

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ABSTRACT Antifolate drugs have an important role in the treatment of malaria. Polymorphisms in the genes encoding the dihydrofolate reductase and dihydropteroate synthetase enzymes cause resistance to the antifol and sulfa drugs, respectively. Rwanda has the highest levels of antimalarial drug resistance in Africa. We correlated the efficacy of chlorproguanil-dapsone plus artesunate (CPG-DDS+A) and amodiaquine plus sulfadoxine-pyrimethamine (AQ+SP) in children with uncomplicated malaria caused by Plasmodium falciparum parasites with p fdhfr and p fdhps mutations, which are known to confer redu
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10

Lumb, Vanshika, Manoj K. Das, Neeru Singh, Vas Dev, Wajihullah Khan, and Yagya D. Sharma. "Multiple Origins of Plasmodium falciparum Dihydropteroate Synthetase Mutant Alleles Associated with Sulfadoxine Resistance in India." Antimicrobial Agents and Chemotherapy 55, no. 6 (2011): 2813–17. http://dx.doi.org/10.1128/aac.01151-10.

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ABSTRACTWith the spread of chloroquine (CQ)-resistant malaria in India, sulfadoxine-pyrimethamine (SP) alone or in combination with artesunate is used as an alternative antimalarial drug. Due to continuous drug pressure, thePlasmodium falciparumparasite is exhibiting resistance to antifolates because of mutations in candidate genes dihydrofolate reductase (dhfr) and dihydropteroate synthetase (dhps). Our earlier study on flanking microsatellite markers ofdhfrmutant alleles from India had shown a single origin of the pyrimethamine resistance and some minor haplotypes which shared haplotypes wit
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11

Noisang, Chaturong, Wieland Meyer, Nongyao Sawangjaroen, John Ellis, and Rogan Lee. "Molecular Detection of Antimalarial Drug Resistance in Plasmodium vivax from Returned Travellers to NSW, Australia during 2008–2018." Pathogens 9, no. 2 (2020): 101. http://dx.doi.org/10.3390/pathogens9020101.

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To monitor drug resistance in Plasmodium vivax, a multidrug resistance 1 (Pvmdr1) gene and a putative transporter protein (Pvcrt-o) gene were used as molecular markers for chloroquine resistance. The biomarkers, the dihydrofolate reductase (Pvdhfr) gene and the dihydropteroate synthetase (Pvdhps) gene, were also used for the detection of resistance to sulphadoxine-pyrimethamine (SP); this drug is often accidentally used to treat P. vivax infections. Clinical blood samples (n = 120) were collected from patients who had been to one of eight malaria-endemic countries and diagnosed with P. vivax i
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12

McCollum, Andrea M., Kristen Mueller, Leopoldo Villegas, Venkatachalam Udhayakumar, and Ananias A. Escalante. "Common Origin and Fixation of Plasmodium falciparum dhfr and dhps Mutations Associated with Sulfadoxine-Pyrimethamine Resistance in a Low-Transmission Area in South America." Antimicrobial Agents and Chemotherapy 51, no. 6 (2007): 2085–91. http://dx.doi.org/10.1128/aac.01228-06.

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ABSTRACT Recent studies indicated that sensitive parasites could increase in frequency in a population when drugs are removed, suggesting that the life span of affordable antimalarial drugs could be expanded. We studied 97 samples from Bolivar State, Venezuela, an area where sulfadoxine-pyrimethamine (SP) has not been used for 8 years due to its ineffectiveness. We characterized point mutations in two genes that have been implicated in resistance to SP, dihydrofolate reductase (dhfr) and dihydropteroate synthase (dhps). We also assayed neutral microsatellite markers around the dhfr (chromosome
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13

Marks, Florian, Christian G. Meyer, Jürgen Sievertsen, et al. "Genotyping of Plasmodium falciparum Pyrimethamine Resistance by Matrix-Assisted Laser Desorption-Ionization Time-of-Flight Mass Spectrometry." Antimicrobial Agents and Chemotherapy 48, no. 2 (2004): 466–72. http://dx.doi.org/10.1128/aac.48.2.466-472.2004.

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ABSTRACT Increasing resistance, recrudescences, and treatment failure have led to the replacement of chloroquine with the combination of pyrimethamine (PYR) and sulfadoxine (SDX) as the first-line antimalarial drugs for treatment of uncomplicated Plasmodium falciparum malaria in several areas where this disease is endemic. The development of resistance to PYR-SDX is favored by incomplete treatment courses or by subtherapeutic levels in plasma. PYR-SDX resistance has been associated with several single-nucleotide polymorphisms (SNPs) in the P. falciparum dihydrofolate reductase (pfdhfr) and the
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14

Alifrangis, Michael, Thor G. Theander, Bruno Mmbando, et al. "Five-Year Surveillance of Molecular Markers of Plasmodium falciparum Antimalarial Drug Resistance in Korogwe District, Tanzania: Accumulation of the 581G Mutation in the P. falciparum Dihydropteroate Synthase Gene." American Journal of Tropical Medicine and Hygiene 80, no. 4 (2009): 523–27. http://dx.doi.org/10.4269/ajtmh.2009.80.523.

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15

Turkiewicz, Anna, Emilia Manko, Colin J. Sutherland, Ernest Diez Benavente, Susana Campino, and Taane G. Clark. "Genetic diversity of the Plasmodium falciparum GTP-cyclohydrolase 1, dihydrofolate reductase and dihydropteroate synthetase genes reveals new insights into sulfadoxine-pyrimethamine antimalarial drug resistance." PLOS Genetics 16, no. 12 (2020): e1009268. http://dx.doi.org/10.1371/journal.pgen.1009268.

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Plasmodium falciparum parasites resistant to antimalarial treatments have hindered malaria disease control. Sulfadoxine-pyrimethamine (SP) was used globally as a first-line treatment for malaria after wide-spread resistance to chloroquine emerged and, although replaced by artemisinin combinations, is currently used as intermittent preventive treatment of malaria in pregnancy and in young children as part of seasonal malaria chemoprophylaxis in sub-Saharan Africa. The emergence of SP-resistant parasites has been predominantly driven by cumulative build-up of mutations in the dihydrofolate reduc
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16

Torrevillas, Brandi K., Sarah M. Garrison, Alexander J. McKeeken, et al. "Plasmodium falciparum DHFR and DHPS Mutations Are Associated With HIV-1 Co-Infection and a Novel DHPS Mutation I504T Is Identified in Western Kenya." Frontiers in Cellular and Infection Microbiology 10 (November 26, 2020). http://dx.doi.org/10.3389/fcimb.2020.600112.

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Antifolate resistance is significant in Kenya and presumed to result from extensive use and cross-resistance between antifolate antimalarials and antibiotics, including cotrimoxazole/Bactrim used for HIV-1 chemotherapy. However, little is known about antifolate-resistant malaria in the context of newly diagnosed HIV-1 co-infection prior to administration of HIV-1 chemotherapy. Blood samples from a cross-sectional study of asymptomatic adult Kenyans enrolled during voluntary HIV testing were analyzed by PCR for Plasmodium spp. More than 95% of volunteers with identifiable parasite species (132
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17

Heidari, Aliehsan, and Hossein Keshavarz. "The Drug Resistance of Plasmodium falciparum and P. vivax in Iran: A Review Article." Iranian Journal of Parasitology, June 2, 2021. http://dx.doi.org/10.18502/ijpa.v16i2.6265.

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Background: One of the main obstacles to malaria control in the world has been the emergence of resistance in Plasmodium falciparum to chloroquine and other antimalarial drugs. This study aimed to review studies in Iran on resistance in P. falciparum and P. vivax to drugs, and to reveal the mechanisms and molecular markers of resistance of these two species.
 Methods: The databases of PubMed, Scopus, Google Scholar, Magiran, and reputable Iranian journals were searched to find published studies on the resistance in P. falciparum and P. vivax to antimalarial drugs in Iran.
 Results: T
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18

Wamae, Kevin, Dorcas Okanda, Leonard Ndwiga, et al. "No Evidence of Plasmodium falciparum k13 Artemisinin Resistance-Conferring Mutations over a 24-Year Analysis in Coastal Kenya but a Near Complete Reversion to Chloroquine-Sensitive Parasites." Antimicrobial Agents and Chemotherapy 63, no. 12 (2019). http://dx.doi.org/10.1128/aac.01067-19.

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ABSTRACT Antimalarial drug resistance is a substantial impediment to malaria control. The spread of resistance has been described using genetic markers, which are important epidemiological tools. We carried out a temporal analysis of changes in allele frequencies of 12 drug resistance markers over 2 decades of changing antimalarial drug policy in Kenya. We did not detect any of the validated kelch 13 (k13) artemisinin resistance markers; nonetheless, a single k13 allele, K189T, was maintained at a stable high frequency (>10%) over time. There was a distinct shift from chloroquine-resistant
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