Evidence map›Paper›PMID 24465177›Full record

ArticlePLoS biology2014

Limiting damage during infection: lessons from infection tolerance for novel therapeutics.

Pedro F Vale, Andy Fenton, Sam P Brown

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
9.3field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 122 citations in OpenAlex.

  1. Article
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  7. Autophagy induced by taurolidine protects against polymicrobial sepsis by promoting both host resistance and disease tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Review
  9. Article
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  12. Host Susceptibility ModulatesFrontiers in microbiology · 2021
    Article
  13. Evolution of Human Respiratory Virus Epidemics.medRxiv : the preprint server for health sciences · 2020
    Article
  14. Article
  15. Article
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  18. Review
  19. Article
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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

3 authors at 2 institutions in 1 country.

Pedro F ValeCentre for Immunity, Infection, and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh, United Kingdom ; Institute of Evolutionary Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, United Kingdom.
Andy FentonInstitute of Integrative Biology, University of Liverpool, Liverpool, United Kingdom.
Sam P BrownCentre for Immunity, Infection, and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh, United Kingdom ; Institute of Evolutionary Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, United Kingdom.
Centre for Immunity, Infection and Evolution · GBUniversity of Liverpool · GB

Funding

Wellcome Trust 082273/Z/07/ZWellcome Trust 095831
6 · The paper itself

Abstract

The distinction between pathogen elimination and damage limitation during infection is beginning to change perspectives on infectious disease control, and has recently led to the development of novel therapies that focus on reducing the illness caused by pathogens (‘‘damage limitation’’)rather than reducing pathogen burdens directly (‘‘pathogen elimination’’). While beneficial at the individual host level, the population consequences of these interventions remain unclear. To address this issue,we present a simple conceptual framework for damage limitation during infection that distinguishes between therapies that are either host-centric (pro-tolerance) or pathogen-centric (anti-virulence). We then draw on recent developments from the evolutionary ecology of disease tolerance to highlight some potential epidemiological and evolutionary responses of pathogens to medical interventions that target the symptoms of infection. Just as pathogens are known to evolve in response to antimicrobial and vaccination therapies, we caution that claims of ‘‘evolution-proof’’ anti-virulence interventions may be premature, and further, that in infections where virulence and transmission are linked, reducing illness without reducing pathogen burden could have non-trivial epidemiological and evolutionary consequences that require careful examination.

Indexed as

Models, StatisticalAnti-Inflammatory Agents, Non-SteroidalAspirinBacterial AdhesionBacterial InfectionsBacterial ToxinsBiological EvolutionColony Count, MicrobialDrugs, InvestigationalHost-Pathogen InteractionsHumansIbuprofenImmune ToleranceQuorum SensingViral LoadVirulenceAnti-Inflammatory Agents, Non-SteroidalAspirinBacterial ToxinsDrugs, InvestigationalIbuprofenVirulence Factors

Identifiers

PMID24465177
PMCPMC3897360
OpenAlexW2086608992

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.