Evidence map›Paper›PMID 24786281›Full record

ArticlePLoS genetics2014

Heterogeneity in the frequency and characteristics of homologous recombination in pneumococcal evolution.

Rafal Mostowy, Nicholas J Croucher, William P Hanage, Simon R Harris, Stephen Bentley, Christophe Fraser

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
7.1field-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

55 citing papers in PubMed, 84 citations in OpenAlex.

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  19. Comparative Virulence and Genomic Analysis ofFrontiers in microbiology · 2020
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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

6 authors at 3 institutions in 2 countries.

Rafal MostowyDepartment of Infectious Disease Epidemiology, Imperial College London, St Mary's Campus, London, United Kingdom.
Nicholas J CroucherDepartment of Infectious Disease Epidemiology, Imperial College London, St Mary's Campus, London, United Kingdom; Center for Communicable Disease Dynamics, Harvard School of Public Health, Boston, Massachusetts, United States of America; The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, United Kingdom.
William P HanageCenter for Communicable Disease Dynamics, Harvard School of Public Health, Boston, Massachusetts, United States of America.
Simon R HarrisThe Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, United Kingdom.
Stephen BentleyThe Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, United Kingdom; Department of Medicine, University of Cambridge, Addenbrookes Hospital, Cambridge, United Kingdom.
Christophe FraserDepartment of Infectious Disease Epidemiology, Imperial College London, St Mary's Campus, London, United Kingdom.
Center for Disease Dynamics, Economics & Policy · USImperial College London · GBWellcome Sanger Institute · GB

Funding

Understanding and controlling antibiotic resistanceU54GM088558 · NIGMS · HARVARD SCHOOL OF PUBLIC HEALTH · PI LIPSITCH, MARC · 2009 to 2018
$26.4M
Medical Research Council MR/K010174/1NIGMS NIH HHS U54 GM088558NIGMS NIH HHS U54GM088558Wellcome Trust
6 · The paper itself

Abstract

The bacterium Streptococcus pneumoniae (pneumococcus) is one of the most important human bacterial pathogens, and a leading cause of morbidity and mortality worldwide. The pneumococcus is also known for undergoing extensive homologous recombination via transformation with exogenous DNA. It has been shown that recombination has a major impact on the evolution of the pathogen, including acquisition of antibiotic resistance and serotype-switching. Nevertheless, the mechanism and the rates of recombination in an epidemiological context remain poorly understood. Here, we proposed several mathematical models to describe the rate and size of recombination in the evolutionary history of two very distinct pneumococcal lineages, PMEN1 and CC180. We found that, in both lineages, the process of homologous recombination was best described by a heterogeneous model of recombination with single, short, frequent replacements, which we call micro-recombinations, and rarer, multi-fragment, saltational replacements, which we call macro-recombinations. Macro-recombination was associated with major phenotypic changes, including serotype-switching events, and thus was a major driver of the diversification of the pathogen. We critically evaluate biological and epidemiological processes that could give rise to the micro-recombination and macro-recombination processes.

Indexed as

Evolution, MolecularGenetic HeterogeneityRecombination, GeneticDrug Resistance, MicrobialGenes, BacterialModels, GeneticStreptococcus pneumoniae

Identifiers

PMID24786281
PMCPMC4006708
OpenAlexW2123692448

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.