Evidence map›Paper›PMID 20418946›Full record

ArticlePloS one2010

Microevolution of group A streptococci in vivo: capturing regulatory networks engaged in sociomicrobiology, niche adaptation, and hypervirulence.

Ramy K Aziz, Rita Kansal, Bruce J Aronow, William L Taylor, Sarah L Rowe, Michael Kubal, Gursharan S Chhatwal, Mark J Walker, Malak Kotb

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
7.3field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Immunomodulating Enzymes fromMicroorganisms · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
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  12. Article
  13. Article
  14. Article
  15. Article
  16. Streptococcal collagen-like protein A and general stress protein 24 are immunomodulating virulence factors of group A Streptococcus.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    Article
  17. Article
  18. Article
  19. Tracing the evolutionary history of the pandemic group A streptococcal M1T1 clone.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
    Article
  20. 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

9 authors at 6 institutions in 4 countries.

Ramy K AzizResearch Services, Veterans Affairs Medical Center, Memphis, Tennessee, United States of America. ramy.aziz@salmonella.org
Rita Kansal
Bruce J Aronow
William L Taylor
Sarah L Rowe
Michael Kubal
Gursharan S Chhatwal
Mark J Walker
Malak Kotb
University of Chicago · USUniversity of Tennessee Health Science Center · USVeterans Health Administration · USCincinnati Children's Hospital Medical Center · USHelmholtz Centre for Infection Research · DEUniversity of Wollongong · AU

Funding

Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Alexander Miethke · 2007 to 2026
$24.4M
IMMUNOPATHOGENESIS OF GROUP A STREPTOCOCCAL INFECTIONSR01AI040198 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KANSAL, RITA · 1998 to 2007
$2.0M
NIAID NIH HHS AI40198-06NIAID NIH HHS R01 AI040198NIDDK NIH HHS P30 DK078392NIDDK NIH HHS P30DK078392
6 · The paper itself

Abstract

The onset of infection and the switch from primary to secondary niches are dramatic environmental changes that not only alter bacterial transcriptional programs, but also perturb their sociomicrobiology, often driving minor subpopulations with mutant phenotypes to prevail in specific niches. Having previously reported that M1T1 Streptococcus pyogenes become hypervirulent in mice due to selection of mutants in the covRS regulatory genes, we set out to dissect the impact of these mutations in vitro and in vivo from the impact of other adaptive events. Using a murine subcutaneous chamber model to sample the bacteria prior to selection or expansion of mutants, we compared gene expression dynamics of wild type (WT) and previously isolated animal-passaged (AP) covS mutant bacteria both in vitro and in vivo, and we found extensive transcriptional alterations of pathoadaptive and metabolic gene sets associated with invasion, immune evasion, tissue-dissemination, and metabolic reprogramming. In contrast to the virulence-associated differences between WT and AP bacteria, Phenotype Microarray analysis showed minor in vitro phenotypic differences between the two isogenic variants. Additionally, our results reflect that WT bacteria's rapid host-adaptive transcriptional reprogramming was not sufficient for their survival, and they were outnumbered by hypervirulent covS mutants with SpeB(-)/Sda(high) phenotype, which survived up to 14 days in mice chambers. Our findings demonstrate the engagement of unique regulatory modules in niche adaptation, implicate a critical role for bacterial genetic heterogeneity that surpasses transcriptional in vivo adaptation, and portray the dynamics underlying the selection of hypervirulent covS mutants over their parental WT cells.

Indexed as

Gene Expression Regulation, BacterialGene Regulatory NetworksSelection, GeneticAnimalsBiological EvolutionHost-Pathogen InteractionsMiceStreptococcus pyogenesVirulence

Identifiers

PMID20418946
PMCPMC2854683
OpenAlexW1964697420

What OpenQuestion holds

Textmetadata
LicenceCC0
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.