ArticleMalaria journal2026
Molecular surveillance of antimalarial drug resistance markers in the pfcrt, pfmdr1 and pfmrp1 genes of Plasmodium falciparum isolates from southeastern Iran.
Article in Malaria journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
The trial behind it
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe emergence and spread of Plasmodium falciparum resistance to artemisinin and its partner drugs pose a major challenge to malaria elimination efforts. Continuous monitoring of resistance-associated molecular markers provides valuable insights into the emergence of resistant genotypes and their geographical distribution.
methodsIn this study, we investigated mutations linked to antimalarial drug resistance in the pfcrt, pfmdr1, and pfmrp1 genes among 100 P. falciparum isolates collected from southeastern Iran during 2022-2023 and compared the findings with data from the same region a decade earlier. Point mutations were genotyped using PCR-RFLP.
resultsMolecular analysis demonstrated a high prevalence (95%) of the pfcrt K76T mutation. In pfmdr1, no mutations were observed at codons 1034, 1042, or 1246; however, the N86Y and Y184F mutations were detected in 3.75% and 51.25% of isolates, respectively. Comparative analysis between the previous (2007-2010) and current (2022-2023) studies revealed a significant increase in the wild-type allele for N86Y and the mutant allele for Y184F. In pfmrp1, mutations at H191Y, S437A, I876V, and F1390I were identified in 68.75%, 85%, 78.75%, and 46.25% of isolates, respectively, while no mutation was observed at K1466R. The predominant pfmdr1 haplotype shifted from wild-type (50%) in the previous study to the single-mutation haplotype N
conclusionsThe persistence of the pfcrt K76T mutant allele despite the withdrawal of Chloroquine from the treatment policy in Iran may be attributable to the co-endemicity of P. vivax in the study area. The increasing prevalence of the N
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.