ArticlePLoS pathogens2010
Highly frequent mutations in negative regulators of multiple virulence genes in group A streptococcal toxic shock syndrome isolates.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
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106 citing papers in PubMed.
- 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
- A protease-sensing circuit links neutrophil inflammation to virulence regulation inbioRxiv : the preprint server for biology · 2026Article
- Pathoadaptive evolution and clonal dissemination of community- associated methicillin-resistant Staphylococcus aureus in Egypt.BMC infectious diseases · 2026Article
- Identifying genetic variations ineLife · 2025Article
- An Autopsy Case of Rapidly Fulminant Group A Streptococcus Infection in a Previously Healthy 67-Year-Old Woman.Cureus · 2024Article
- Characteristics of Streptococcal Toxic Shock Syndrome Caused by Different Beta-hemolytic Streptococci Species: A Single-center Retrospective Study.Open forum infectious diseases · 2024Article
- Reduced interleukin-18 secretion by human monocytic cells in response to infections with hyper-virulent Streptococcus pyogenes.Journal of biomedical science · 2024Article
- RopB-regulated SpeB cysteine protease degrades extracellular vesicles-associated streptolysin O and bacterial proteins from group AVirulence · 2023Article
- Elucidation of independently modulated genes inmSystems · 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
- The Bacterial Markers of Identification of Invasive CovR/CovS-Inactivated Group AMicrobiology spectrum · 2022Article
- Genomic Characterization of Group A Streptococci Causing Pharyngitis and Invasive Disease in Colorado, USA, June 2016- April 2017.The Journal of infectious diseases · 2022Article
- CovS inactivation reduces CovR promoter binding at diverse virulence factor encoding genes in group A Streptococcus.PLoS pathogens · 2022Article
- Streptococcal Toxic Shock Syndrome Induced by Group A Streptococcus with the emm28 Genotype That Developed after a Uterine Cancer Test.Internal medicine (Tokyo, Japan) · 2021Article
- The CovR regulatory network drives the evolution of Group B Streptococcus virulence.PLoS genetics · 2021Article
- Article
46 more citing papers are in PubMed but not listed here.
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7 authors.
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Abstract
Streptococcal toxic shock syndrome (STSS) is a severe invasive infection characterized by the sudden onset of shock and multiorgan failure; it has a high mortality rate. Although a number of studies have attempted to determine the crucial factors behind the onset of STSS, the responsible genes in group A Streptococcus have not been clarified. We previously reported that mutations of csrS/csrR genes, a two-component negative regulator system for multiple virulence genes of Streptococcus pyogenes, are found among the isolates from STSS patients. In the present study, mutations of another negative regulator, rgg, were also found in clinical isolates of STSS patients. The rgg mutants from STSS clinical isolates enhanced lethality and impaired various organs in the mouse models, similar to the csrS mutants, and precluded their being killed by human neutrophils, mainly due to an overproduction of SLO. When we assessed the mutation frequency of csrS, csrR, and rgg genes among S. pyogenes isolates from STSS (164 isolates) and non-invasive infections (59 isolates), 57.3% of the STSS isolates had mutations of one or more genes among three genes, while isolates from patients with non-invasive disease had significantly fewer mutations in these genes (1.7%). The results of the present study suggest that mutations in the negative regulators csrS/csrR and rgg of S. pyogenes are crucial factors in the pathogenesis of STSS, as they lead to the overproduction of multiple virulence factors.
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