Evidence map›Paper›PMID 27337450›Full record

ReviewMicrobiology spectrum2016

Artemisinin-Resistant Plasmodium falciparum Malaria.

Rick M Fairhurst, Arjen M Dondorp

Abstract readReview
In one paragraph

Review in Microbiology spectrum, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 4 pooled it
29.7field-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

145 citing papers in PubMed, 4 syntheses or guidelines pooled it, 308 citations in OpenAlex.

  1. Pooled it
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  11. Characterization of high-artemisinin yieldingBiochemistry and biophysics reports · 2026
    Article
  12. Article
  13. TheScience advances · 2026
    Article
  14. Review
  15. Article
  16. Article
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  20. Review

85 more citing papers are in PubMed but not listed here.

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 2 institutions in 3 countries.

Rick M FairhurstLaboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852.
Arjen M DondorpMahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok 10400, Thailand.
Mahidol Oxford Tropical Medicine Research Unit · THNational Institutes of Health · US

Funding

International Research in Cambodia: Tropical Medicine and Vector Research ZIAAI001066 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI YEK, CHRISTINA · 2009 to 2025
$10.8M
Malaria Pathogenesis and Human ImmunityZIAAI001000 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI FAIRHURST, RICK · 2009 to 2017
$9.3M
Malaria Pathogenesis and Human ImmunityZ01AI001000 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI FAIRHURST, RICK · 2007 to 2008
$826k
Intramural NIH HHS Z01 AI001000Wellcome Trust
6 · The paper itself

Abstract

For more than five decades, Southeast Asia (SEA) has been fertile ground for the emergence of drug-resistant Plasmodium falciparum malaria. After generating parasites resistant to chloroquine, sulfadoxine, pyrimethamine, quinine, and mefloquine, this region has now spawned parasites resistant to artemisinins, the world's most potent antimalarial drugs. In areas where artemisinin resistance is prevalent, artemisinin combination therapies (ACTs)-the first-line treatments for malaria-are failing fast. This worrisome development threatens to make malaria practically untreatable in SEA, and threatens to compromise global endeavors to eliminate this disease. A recent series of clinical, in vitro, genomics, and transcriptomics studies in SEA have defined in vivo and in vitro phenotypes of artemisinin resistance, identified its causal genetic determinant, explored its molecular mechanism, and assessed its clinical impact. Specifically, these studies have established that artemisinin resistance manifests as slow parasite clearance in patients and increased survival of early-ring-stage parasites in vitro; is caused by single nucleotide polymorphisms in the parasite's K13 gene, is associated with an upregulated "unfolded protein response" pathway that may antagonize the pro-oxidant activity of artemisinins, and selects for partner drug resistance that rapidly leads to ACT failures. In SEA, clinical studies are urgently needed to monitor ACT efficacy where K13 mutations are prevalent, test whether new combinations of currently available drugs cure ACT failures, and advance new antimalarial compounds through preclinical pipelines and into clinical trials. Intensifying these efforts should help to forestall the spread of artemisinin and partner drug resistance from SEA to sub-Saharan Africa, where the world's malaria transmission, morbidity, and mortality rates are highest.

Indexed as

AnimalsAnophelesAntimalarialsArtemisininsDrug ResistanceHumansMalaria, FalciparumMolecular EpidemiologyPlasmodium falciparumAntimalarialsartemisininArtemisinins

Identifiers

PMID27337450
PMCPMC4992992
OpenAlexW2467614481

What OpenQuestion holds

Textmetadata
LicenceTDM
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.