Evidence map›Paper›PMID 39841324›Full record

ArticleBiochemical genetics2026

Haplotypes of Chloroquine Resistance Marker Genes Among Uncomplicated Malaria Cases in Lagos, Nigeria.

Uche Thecla Igbasi, Wellington Aghoghavia Oyibo, Jun-Hu Chen, Hong Quan, Sunday Aremu Omilabu, Shen-Bo Chen, Hai-Mo Shen, Xiao-Nong Zhou

Abstract read
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Article in Biochemical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Uche Thecla IgbasiCentre for Infectious Disease Research, Microbiology Department, Nigerian Institute of Medical Research, 6 Edmund Crescent, Yaba, Lagos, Nigeria. eyiuche2001@yahoo.com.ORCID http://orcid.org/0000-0002-8424-6838
Wellington Aghoghavia OyiboCentre for Malaria Diagnosis, NTD Research, Training, and Policy/ANDI Centre of Excellence for Malaria Diagnosis, College of Medicine, University of Lagos, Lagos, Nigeria.
Jun-Hu ChenKey Laboratory of Parasite and Vector Biology of the Chinese Ministry of Health, Chinese Center for Disease Control and Prevention, WHO Collaborating Centre for Tropical Diseases, National Institute of Parasitic Diseases, Shanghai, 200025, People's Republic of China.
Hong QuanKey Laboratory of Parasite and Vector Biology of the Chinese Ministry of Health, Chinese Center for Disease Control and Prevention, WHO Collaborating Centre for Tropical Diseases, National Institute of Parasitic Diseases, Shanghai, 200025, People's Republic of China.
Sunday Aremu OmilabuDepartment of Medical Microbiology and Parasitology, College of Medicine, University of Lagos, Lagos, Nigeria.
Shen-Bo ChenKey Laboratory of Parasite and Vector Biology of the Chinese Ministry of Health, Chinese Center for Disease Control and Prevention, WHO Collaborating Centre for Tropical Diseases, National Institute of Parasitic Diseases, Shanghai, 200025, People's Republic of China.
Hai-Mo ShenKey Laboratory of Parasite and Vector Biology of the Chinese Ministry of Health, Chinese Center for Disease Control and Prevention, WHO Collaborating Centre for Tropical Diseases, National Institute of Parasitic Diseases, Shanghai, 200025, People's Republic of China.
Xiao-Nong ZhouKey Laboratory of Parasite and Vector Biology of the Chinese Ministry of Health, Chinese Center for Disease Control and Prevention, WHO Collaborating Centre for Tropical Diseases, National Institute of Parasitic Diseases, Shanghai, 200025, People's Republic of China.

Funding

the National Research and Development Plan of China Grant No. 2018YFE0121600
6 · The paper itself

Abstract

Drug resistance resulting from mutations in Plasmodium falciparum, that caused the failure of previously effective malaria drugs, has continued to threaten the global malaria elimination goal. This study describes the profiles of P. falciparum chloroquine resistance transporter (Pfcrt) and P. falciparum multidrug resistance 1 (Pfmdr1), the genetic markers associated with 4-aminoquinoline resistance, among P. falciparum isolates from Lagos, Nigeria. Genomic DNA was extracted from the dried blood spot samples obtained from individuals with microscopically confirmed P. falciparum infection in health facilities and communities in Lagos State, Nigeria. The DNA was amplified using nested polymerase chain reaction, and sequence analysis was performed to identify single nucleotide polymorphisms in the pfcrt and pfmdr1 genes. The study showed that 82.4% (178) of the isolates had pfmdr1 wild-type, while mutations were observed at codons N86Y (11.6%) and D1246Y (3.2%). Other mutations seen were at codons Y23S (0.5%), E130K (2.3%), and S149P (0.5%). 30.8% (64) of the isolates had pfcrt wild-type (CVMNK), while 62.0% (129) had CVIET (mutant) haplotype. Other pfcrt haplotypes detected include; CVIDT (1.9%); CVMDT (1.4%); CVIKT (1.0%); CVINT (0.5%); CVMET (0.5%); CVMKT (0.5%); CVMNT (1.0%); and CVMEK (0.5%). The findings underscore the presence of uncommon pfcrt haplotypes and a high prevalence of drug-resistant pfcrt haplotypes (CVIET), alongside a high prevalence of wild-type pfmdr in Lagos. This study highlights the need for ongoing surveillance of these genetic markers to provide data that can inform decisions on malaria case management and preserve the efficacy of artemisinin combination therapies (ACTs) in Nigeria.

Indexed as

ATP-Binding Cassette, Sub-Family C ProteinsChloroquineDrug ResistanceHaplotypesMalaria, FalciparumMembrane Transport ProteinsPlasmodium falciparumProtozoan ProteinsAntimalarialsChildChild, PreschoolFemaleGenetic MarkersHumansMaleMutationAntimalarialsATP-Binding Cassette, Sub-Family C ProteinsChloroquineGenetic MarkersMdr1 protein, Plasmodium falciparumMembrane Transport ProteinsPfCRT protein, Plasmodium falciparumProtozoan ProteinsAntimalarial drug resistanceChloroquine resistance transporter geneLagosMultidrug resistance-1 geneMutation

Identifiers

PMID39841324

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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.