Evidence map›Paper›PMID 20814186›Full record

ArticleJournal of innate immunity2010

Parameters governing invasive disease propensity of non-M1 serotype group A streptococci.

Peter G Maamary, Martina L Sanderson-Smith, Ramy K Aziz, Andrew Hollands, Jason N Cole, Fiona C McKay, Jason D McArthur, Joshua K Kirk, Amanda J Cork, Rachael J Keefe and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of innate immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. StreptococcusVirulence · 2023
    Article
  3. Article
  4. Review
  5. Frontiers in cellular and infection microbiology · 2020
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Association between polymorphisms in the csrRS two-component regulatory system and invasive group A streptococcal infection.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2014
    Article
  18. Review
  19. Article
  20. Review
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

18 authors at 8 institutions in 4 countries.

Peter G MaamarySchool of Biological Sciences, University of Wollongong, Wollongong, NSW, Australia.
Martina L Sanderson-Smith
Ramy K Aziz
Andrew Hollands
Jason N Cole
Fiona C McKay
Jason D McArthur
Joshua K Kirk
Amanda J Cork
Rachael J Keefe
Rita G Kansal
Hongmin Sun
William L Taylor
Gursharan S Chhatwal
David Ginsburg
Victor Nizet
Malak Kotb
Mark J Walker
University of Wollongong · AUCairo University · EGHelmholtz Centre for Infection Research · DEHoward Hughes Medical Institute · USUniversity of Cincinnati · USUniversity of Missouri · USUniversity of Montana · USUniversity of Tennessee Health Science Center · US

Funding

TRANSGENIC MODELS FOR THE STUDY OF FACTOR V FUNCTIONP01HL057346 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAUFMAN, RANDAL J. · 1997 to 2013
$19.9M
GAS Switch from Colonizing Bacterium to Invasive PathogenR01AI077780 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI NIZET, VICTOR · 2008 to 2019
$3.8M
NHLBI NIH HHS P01 HL057346NIAID NIH HHS AI077780NIAID NIH HHS R01 AI077780
6 · The paper itself

Abstract

Group A Streptococcus (GAS) causes rare but life-threatening syndromes of necrotizing fasciitis and toxic shock-like syndrome in humans. The GAS serotype M1T1 clone has globally disseminated, and mutations in the control of virulence regulatory sensor kinase (covRS) operon correlate with severe invasive disease. Here, a cohort of non-M1 GAS was screened to determine whether mutation in covRS triggers systemic dissemination in divergent M serotypes. A GAS disease model defining parameters governing invasive propensity of differing M types is proposed. The vast majority of GAS infection is benign. Nonetheless, many divergent M types possess limited capacity to cause invasive infection. M1T1 GAS readily switch to a covRS mutant form that is neutrophil resistant and frequently associated with systemic infection. Whilst non-M1 GAS are shown in this study to less frequently accumulate covRS mutations in vivo, such mutants are isolated from invasive infections and exhibit neutrophil resistance and enhanced virulence. The reduced capacity of non-M1 GAS to switch to the hypervirulent covRS mutant form provides an explanation for the comparatively less frequent isolation of non-M1 serotypes from invasive human infections.

Indexed as

AnimalsCells, CulturedDisease ProgressionDNA, BacterialDNA Mutational AnalysisGenetic Complementation TestHistidine KinaseHumansImmune EvasionIntracellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMicroarray AnalysisMutationNeutrophilsStreptococcal InfectionsCovS protein, Streptococcus pyogenesDNA, BacterialHistidine KinaseIntracellular Signaling Peptides and Proteins

Identifiers

PMID20814186
PMCPMC3219504
OpenAlexW2093356046

What OpenQuestion holds

Textmetadata
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.