ArticleInfection and immunity2009
CovS simultaneously activates and inhibits the CovR-mediated repression of distinct subsets of group A Streptococcus virulence factor-encoding genes.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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.
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.
Who cites it
91 citing papers in PubMed, 122 citations in OpenAlex.
- Complement-mediated opsonization of invasive group A Streptococcus pyogenes strain AP53 is regulated by the bacterial two-component cluster of virulence responder/sensor (CovRS) system.The Journal of biological chemistry · 2013Trial
- Group A Streptococcus secreted esterase hydrolyzes platelet-activating factor to impede neutrophil recruitment and facilitate innate immune evasion.PLoS pathogens · 2012Trial
- Impact of cathelicidin cleavage by SpeB onbioRxiv : the preprint server for biology · 2026Article
- The diabetic wound microenvironment drives emergence and maintenance of CovRS variants in group BInfection and immunity · 2026Article
- Molecular characterization of covRS mutations in M1FEBS open bio · 2026Article
- Acquisition of toxin-encoding lysogenic bacteriophage elements enhances the virulence of pandemicInfection and immunity · 2026Article
- Molecular Characterization of the Group A Streptococcus Virulence-Regulatory System FasBCAX.Molecular microbiology · 2025Article
- The group AInfection and immunity · 2025Article
- The invasive GAS puzzle in Italy: genomic insights from a hospital cohort in a fragmented surveillance landscape.Frontiers in cellular and infection microbiology · 2025Article
- Article
- Identification of distinct impacts of CovS inactivation on the transcriptome of acapsular group A streptococci.mSystems · 2023Article
- Hyperphosphorylation of the Group A Streptococcal Control of Virulence Regulator Increases Promoter Occupancy Specifically at Virulence Factor-Encoding Genes.Journal of bacteriology · 2023Article
- RopB represses the transcription ofLife science alliance · 2023Article
- A Novel CovS Variant Harbored by a Colonization Strain Reduces Streptococcus pyogenes Virulence.Journal of bacteriology · 2023Article
- Article
- Slipped-strand mispairing within a polycytidine tract in transcriptional regulatorFrontiers in microbiology · 2023Article
- The Bacterial Markers of Identification of Invasive CovR/CovS-Inactivated Group AMicrobiology spectrum · 2022Article
- CovS inactivation reduces CovR promoter binding at diverse virulence factor encoding genes in group A Streptococcus.PLoS pathogens · 2022Article
- Article
- Incidence and Effects of Acquisition of the Phage-EncodedFrontiers in microbiology · 2021Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To colonize and cause disease at distinct anatomical sites, bacterial pathogens must tailor gene expression in a microenvironment-specific manner. The molecular mechanisms that control the ability of the human bacterial pathogen group A Streptococcus (GAS) to transition between infection sites have yet to be fully elucidated. A key regulator of GAS virulence gene expression is the CovR-CovS two-component regulatory system (also known as CsrR-CsrS). covR and covS mutant strains arise spontaneously during invasive infections and, in in vivo models of infection, rapidly become dominant. Here, we compared wild-type GAS with covR, covS, and covRS isogenic mutant strains to investigate the heterogeneity in the types of natural mutations that occur in covR and covS and the phenotypic consequences of covR or covS mutation. We found that the response regulator CovR retains some regulatory function in the absence of CovS and that CovS modulates CovR to significantly enhance repression of one group of genes (e.g., the speA, hasA, and ska genes) while it reduces repression of a second group of genes (e.g., the speB, grab, and spd3 genes). We also found that different in vivo-induced covR mutations can lead to strikingly different transcriptomes. While covS mutant strains show increased virulence in several invasive models of infection, we determined that these mutants are significantly outcompeted by wild-type GAS during growth in human saliva, an ex vivo model of upper respiratory tract infection. We propose that CovS-mediated regulation of CovR activity plays an important role in the ability of GAS to cycle between pharyngeal and invasive infections.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.