Evidence map›Paper›PMID 28954914›Full record

ReviewProceedings. Biological sciences2017

Reversing resistance: different routes and common themes across pathogens.

Richard C Allen, Jan Engelstädter, Sebastian Bonhoeffer, Bruce A McDonald, Alex R Hall

Open access · hybridAbstract readReview
In one paragraph

Review in Proceedings. Biological sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Tripartite Loops Reverse Antibiotic Resistance.Molecular biology and evolution · 2025
    Article
  4. Article
  5. Review
  6. Theoretical considerations and empirical predictions of the pharmaco- and population dynamics of heteroresistance.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Assessing the predictability of fungicide resistance evolution through in vitro selection.Journal of plant diseases and protection : scientific journal of the German Phytomedical Society (DPG) · 2024
    Article
  8. Article
  9. Natural selection has driven the recurrent loss of an immunity gene that protectsProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  10. Article
  11. Review
  12. Genomics ofFrontiers in microbiology · 2020
    Article
  13. Quantifying the impact of treatment history on plasmid-mediated resistance evolution in human gut microbiota.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  14. Article
  15. Resistance Gene Carriage Predicts Growth of Natural and ClinicalApplied and environmental microbiology · 2019
    Article
  16. Article
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

5 authors at 2 institutions in 2 countries.

Richard C AllenInstitute of Integrative Biology, ETH Zürich, CH-8092 Zurich, Switzerland richard.allen@env.ethz.ch.ORCID http://orcid.org/0000-0001-6012-7888
Jan EngelstädterSchool of Biological Sciences, The University of Queensland, Brisbane, Queensland 4072, Australia.ORCID http://orcid.org/0000-0003-3340-918X
Sebastian BonhoefferInstitute of Integrative Biology, ETH Zürich, CH-8092 Zurich, Switzerland.ORCID http://orcid.org/0000-0001-8052-3925
Bruce A McDonaldInstitute of Integrative Biology, ETH Zürich, CH-8092 Zurich, Switzerland.ORCID http://orcid.org/0000-0002-5332-2172
Alex R HallInstitute of Integrative Biology, ETH Zürich, CH-8092 Zurich, Switzerland alex.hall@env.ethz.ch.ORCID http://orcid.org/0000-0002-3654-1373
ETH Zurich · CHThe University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resistance spreads rapidly in pathogen or pest populations exposed to biocides, such as fungicides and antibiotics, and in many cases new biocides are in short supply. How can resistance be reversed in order to prolong the effectiveness of available treatments? Some key parameters affecting reversion of resistance are well known, such as the fitness cost of resistance. However, the population biological processes that actually cause resistance to persist or decline remain poorly characterized, and consequently our ability to manage reversion of resistance is limited. Where do susceptible genotypes that replace resistant lineages come from? What is the epidemiological scale of reversion? What information do we need to predict the mechanisms or likelihood of reversion? Here, we define some of the population biological processes that can drive reversion, using examples from a wide range of taxa and biocides. These processes differ primarily in the origin of revertant genotypes, but also in their sensitivity to factors such as coselection and compensatory evolution that can alter the rate of reversion, and the likelihood that resistance will re-emerge upon re-exposure to biocides. We therefore argue that discriminating among different types of reversion allows for better prediction of where resistance is most likely to persist.

Indexed as

Evolution, MolecularGenetics, PopulationDisinfectantsDrug Resistance, MicrobialGenetic FitnessGenotypeDisinfectantsantimicrobialsbiocidesfungicidesreversing resistance

Identifiers

PMID28954914
PMCPMC5627214
OpenAlexW2757070126

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.