Evidence map›Paper›PMID 31119263›Full record

ReviewBriefings in functional genomics2019

The genomic architecture of antimalarial drug resistance.

Annie N Cowell, Elizabeth A Winzeler

Open access · hybridAbstract readReview
In one paragraph

Review in Briefings in functional genomics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 3 pooled it
10.2field-weighted citation impact, top 1% 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

46 citing papers in PubMed, 3 syntheses or guidelines pooled it, 110 citations in OpenAlex.

  1. Pooled it
  2. A Dual, Systematic Approach to Malaria Diagnostic Biomarker Discovery.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2022
    Pooled it
  3. Pooled it
  4. Review
  5. Review
  6. Review
  7. Mapping Plasmodium falciparum mutations in Africa: A critical review of emerging drug resistance and implications for malaria control.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2025
    Review
  8. Review
  9. Plasmodium falciparum isolates: ex vivo drug response.The Journal of antimicrobial chemotherapy · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Health science reports · 2024
    Article
  18. Article
  19. Genetic variation of theFrontiers in parasitology · 2024
    Article
  20. Review
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

2 authors at 1 institution in 1 country.

Annie N CowellDivision of Infectious Diseases and Global Health, Department of Medicine, University of California, San Diego, Gilman Dr., La Jolla, CA, USA.
Elizabeth A WinzelerDivision of Host-Microbe Systems & Therapeutics, Department of Pediatrics, University of California, San Diego, Gilman Dr., La Jolla, CA, USA.
University of California, San Diego · US

Funding

Discovery of chemically validated malaria liver stage targetsR01AI090141 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WINZELER, ELIZABETH A · 2011 to 2019
$3.4M
Defining the targets of broad intervention antimalarial agentsR01AI103058 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WINZELER, ELIZABETH A · 2013 to 2016
$2.6M
NIAID NIH HHS R01 AI090141NIAID NIH HHS R01 AI103058
6 · The paper itself

Abstract

Plasmodium falciparum and Plasmodium vivax, the two protozoan parasite species that cause the majority of cases of human malaria, have developed resistance to nearly all known antimalarials. The ability of malaria parasites to develop resistance is primarily due to the high numbers of parasites in the infected person's bloodstream during the asexual blood stage of infection in conjunction with the mutability of their genomes. Identifying the genetic mutations that mediate antimalarial resistance has deepened our understanding of how the parasites evade our treatments and reveals molecular markers that can be used to track the emergence of resistance in clinical samples. In this review, we examine known genetic mutations that lead to resistance to the major classes of antimalarial medications: the 4-aminoquinolines (chloroquine, amodiaquine and piperaquine), antifolate drugs, aryl amino-alcohols (quinine, lumefantrine and mefloquine), artemisinin compounds, antibiotics (clindamycin and doxycycline) and a napthoquinone (atovaquone). We discuss how the evolution of antimalarial resistance informs strategies to design the next generation of antimalarial therapies.

Indexed as

AminoquinolinesAnti-Bacterial AgentsAntimalarialsArtemisininsAtovaquoneDrug ResistanceDrug Resistance, MultipleFolic Acid AntagonistsHumansMalariaPlasmodium falciparumPlasmodium vivaxQuinineAminoquinolinesAnti-Bacterial AgentsAntimalarialsartemisininArtemisininsAtovaquoneFolic Acid AntagonistsQuinineartemisinindrug resistancemalariaPlasmodium falciparumPlasmodium vivax

Identifiers

PMID31119263
PMCPMC6859814
OpenAlexW2982424451

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.