Evidence map›Paper›PMID 40200353›Full record

ArticleTropical medicine and health2025

Mutational profile of pfdhfr, pfdhps, pfmdr1, pfcrt and pfk13 genes of P. falciparum associated with resistance to different antimalarial drugs in Osun state, southwestern Nigeria.

Alexandra Martín Ramírez, Akeem Abiodun Akindele, Vicenta González Mora, Luz García, Nicole Lara, Eva de la Torre-Capitán Matías, Irene Molina de la Fuente, Sulaiman Adebayo Nassar, Thuy-Huong Ta-Tang, Agustín Benito and 1 more

Abstract read
In one paragraph

Article in Tropical medicine and health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Polymorphisms of theParasite epidemiology and control · 2026
    Article
  3. Article
  4. Article
4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Alexandra Martín RamírezCentro de Investigación Biomédica en Red de Enfermedades Infecciosas, Instituto de Salud Carlos III, Madrid, Spain. a.martin@isciii.es.
Akeem Abiodun AkindeleMedical Laboratory Science Department, Ladoke Akintola University of Technology, Ogbomoso, Nigeria.
Vicenta González MoraNational Centre of Tropical Medicine, Institute of Health Carlos III, Madrid, Spain.
Luz GarcíaNational Centre of Tropical Medicine, Institute of Health Carlos III, Madrid, Spain.
Nicole LaraComplutense University of Madrid, Madrid, Spain.
Eva de la Torre-Capitán MatíasAlcala University, Madrid, Spain.
Irene Molina de la FuenteCentro de Investigación Biomédica en Red de Enfermedades Infecciosas, Instituto de Salud Carlos III, Madrid, Spain.
Sulaiman Adebayo NassarMedical Laboratory Science Department, Ladoke Akintola University of Technology, Ogbomoso, Nigeria.
Thuy-Huong Ta-TangCentro de Investigación Biomédica en Red de Enfermedades Infecciosas, Instituto de Salud Carlos III, Madrid, Spain.
Agustín BenitoCentro de Investigación Biomédica en Red de Enfermedades Infecciosas, Instituto de Salud Carlos III, Madrid, Spain.
Pedro BerzosaCentro de Investigación Biomédica en Red de Enfermedades Infecciosas, Instituto de Salud Carlos III, Madrid, Spain. pberzosa@isciii.es.

Funding

CIBER-Consorcio Centro de Investigación Biomédica en Red CB21/13/00120Instituto de Salud Carlos III, Ministerio de Ciencia, Innovación y Universidades and by the Spanish Strategic Health Action (AESI-ISCIII) P121CIII/00034
6 · The paper itself

Abstract

backgroundNigeria accounts for the greatest burden of malaria disease globally. Malaria control requires an effective treatment after diagnosis. The efficacy of antimalarial drugs can be assessed through the analysis of genetic changes associated with reduced drug sensitivity.

methodsThis study includes the analysis of the markers associated with artemisinin (pfk13), sulfadoxine-pyrimethamine (pfdhfr and pfdhps), and chloroquine and its derivatives (pfmdr1 and pfcrt) resistances, in blood samples collected from asymptomatic children in south-western Nigeria.

resultsThe 25.95% of samples showed a number of mutations in pfk13 gene. Among those, the validated, C580Y, and the candidate, R515K, mutations by WHO were detected. Twenty-seven pfdhps different haplotypes were observed, with the haplotype ISGKAA as the most prevalent (18.80%), followed by IFGKAA (12.78%) and IAGKAA (11.28%). The VAGKGS was the most common haplotype carrying the I431V mutation (10.53%). Combinations of alleles in pfdhfr and pfdhps genes provided a 40.98% of samples with the partially resistant haplotype (IRNG). No samples exhibited the 'fully resistant' or 'super resistant' pfdhprf-pfdhps combinations, but one sample contained mutations at pfdhfr 51I, 59R, and 108N with pfdhps 431V, 436A, A437G and 540E. The analysis of pfcrt 72-76 variants disclosed a 12.12% of samples with the mutant-type (CVIET). No double mutant pfmdr1 haplotypes 86Y/1246Y (YY) were detected, nor was the haplotype formed by the alleles 86Y pfmdr1 + pfcrt 76 T (YT).

conclusionsThere was no evidence of parasite genomes harbouring multilocus mutations conferring multidrug resistance, although evidence of a validated (C580Y) and a candidate (R515K) mutation in pfk13 gene, high frequency pfdhfr mutant alleles and high variability of pfdhps haplotypes were found in this study, which provides a baseline information essential in monitoring P. falciparum resistances.

Indexed as

Antimalarial drug resistanceDrug-resistant P. falciparumMalariaNigeriaPfcrtPfdhfrPfdhpspfk13pfmdr1

Identifiers

PMID40200353
PMCPMC11977893

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.