Evidence map›Paper›PMID 32933490›Full record

ArticleBMC infectious diseases2020

Distribution pattern of amino acid mutations in chloroquine and antifolate drug resistance associated genes in complicated and uncomplicated Plasmodium vivax isolates from Chandigarh, North India.

Hargobinder Kaur, Rakesh Sehgal, Archit Kumar, Praveen K Bharti, Devendra Bansal, Pradyumna K Mohapatra, Jagadish Mahanta, Ali A Sultan

Open access · goldAbstract read
In one paragraph

Article in BMC infectious diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
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

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.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 32 citations in OpenAlex.

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4 · The record

Corrections and comments

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

8 authors at 4 institutions in 2 countries.

Hargobinder KaurDepartment of Medical Parasitology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Rakesh SehgalDepartment of Medical Parasitology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. sehgalpgi@gmail.com.
Archit KumarDepartment of Virology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Praveen K BhartiNational Institute for Research in Tribal Health, Indian Council of Medical Research, Nagpur Road, Garha, Jabalpur, Madhya Pradesh, India.
Devendra BansalDepartment of Microbiology and Immunology, Weill Cornell Medicine - Qatar, Cornell University, Qatar Foundation, Education City, Doha, Qatar.
Pradyumna K MohapatraRegional Medical Research Centre, NE, Indian Council of Medical Research, Post Box no.105, Dibrugarh, Assam, India.
Jagadish MahantaRegional Medical Research Centre, NE, Indian Council of Medical Research, Post Box no.105, Dibrugarh, Assam, India.
Ali A SultanDepartment of Microbiology and Immunology, Weill Cornell Medicine - Qatar, Cornell University, Qatar Foundation, Education City, Doha, Qatar.
Post Graduate Institute of Medical Education and Research · INRegional Medical Research Centre · INWeill Cornell Medical College in Qatar · QAIndian Council of Medical Research · IN

Funding

Qatar National Research Fund NPRP 5 - 098 - 3 - 021
6 · The paper itself

Abstract

backgroundThe increasing antimalarial drug resistance is a significant hindrance to malaria control and elimination programs. For the last six decades, chloroquine (CQ) plus pyrimethamine remains the first-line treatment for P. vivax malaria. Regions where both P. falciparum and P. vivax co-exist, P. vivax is exposed to antifolate drugs due to either misdiagnosis or improper treatment that causes selective drug pressure to evolve. Therefore, the present study aims to estimate antimalarial drug resistance among the complicated and uncomplicated P. vivax patients.

methodsA total of 143 P. vivax malaria positive patients were enrolled in this study, and DNA was isolated from their blood samples. Pvcrt-o, Pvmdr-1, Pvdhps, and Pvdhfr genes were PCRs amplified, and drug resistance-associated gene mutations were analyzed. Statistical analysis of the drug resistance genes and population diversity was performed using MEGA vs. 7.0.21 and DnaSP v software.

resultsAmong the CQ resistance marker gene Pvcrt-o, the prevalence of K10 insertion was 17.5% (7/40) and 9.5% (7/73) of complicated and uncomplicated P vivax group isolates respectively. In Pvmdr-1, double mutant haplotype (M

conclusionThe study presents the situations of polymorphism in the antimalarial drug resistance-associated genes and emphasizes the need for regular surveillance. It is imperative for the development of suitable antimalarial drug policy in India.

Indexed as

AdolescentAntimalarialsATP-Binding Cassette, Sub-Family C ProteinsChildChild, PreschoolChloroquineDNA, ProtozoanDrug ResistanceFemaleFolic Acid AntagonistsHaplotypesHumansIndiaMalaria, VivaxMalePlasmodium vivaxAntimalarialsATP-Binding Cassette, Sub-Family C ProteinsChloroquineDNA, ProtozoanFolic Acid AntagonistsMdr1 protein, Plasmodium vivaxProtozoan ProteinsAntimalarial drug resistanceComplicated malariaNorth IndiaPlasmodium vivax

Identifiers

PMID32933490
PMCPMC7493319
OpenAlexW3085384851

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Registered trials

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