ArticleThe Journal of infectious diseases2010
Genetic switch to hypervirulence reduces colonization phenotypes of the globally disseminated group A streptococcus M1T1 clone.
Article in The Journal of infectious diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 101 citations in OpenAlex.
- Tracing the recent evolution of Group AEmerging microbes & infections · 2026Review
- Impact of cathelicidin cleavage by SpeB onbioRxiv : the preprint server for biology · 2026Article
- Molecular characterization of covRS mutations in M1FEBS open bio · 2026Article
- Streptococcus pyogenes Surveillance Through Surface Swab Samples to Track the Emergence of Streptococcal Toxic Shock Syndrome in Rural Japan.The Journal of infectious diseases · 2025Article
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- Characterization of a novelmBio · 2025Article
- Reduced interleukin-18 secretion by human monocytic cells in response to infections with hyper-virulent Streptococcus pyogenes.Journal of biomedical science · 2024Article
- Group A Streptococcus strains causing meningitis without distinct invasive phenotype.MicrobiologyOpen · 2024Article
- StreptococcusVirulence · 2023Article
- Detoxification of reactive oxygen species by the hyaluronic acid capsule of group AInfection and immunity · 2023Article
- Identification of distinct impacts of CovS inactivation on the transcriptome of acapsular group A streptococci.mSystems · 2023Article
- A Novel CovS Variant Harbored by a Colonization Strain Reduces Streptococcus pyogenes Virulence.Journal of bacteriology · 2023Article
- Article
- Low-toxinEmerging microbes & infections · 2022Article
- The Streptococcus pyogenes hyaluronic acid capsule promotes experimental nasal and skin infection by preventing neutrophil-mediated clearance.PLoS pathogens · 2022Article
- Review
- Playing With Fire: Proinflammatory Virulence Mechanisms of Group AFrontiers in cellular and infection microbiology · 2021Review
- Group A Streptococcus Infection of the Nasopharynx Requires Proinflammatory Signaling through the Interleukin-1 Receptor.Infection and immunity · 2020Article
- Extracellular bacterial lymphatic metastasis drives Streptococcus pyogenes systemic infection.Nature communications · 2020Article
- Strain-Dependent Effect of Capsule on Transmission and Persistence in an Infant Mouse Model of Group A Streptococcus Infection.Infection and immunity · 2020Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe recent resurgence of invasive group A streptococcal disease has been paralleled by the emergence of the M1T1 clone. Recently, invasive disease initiation has been linked to mutations in the covR/S 2-component regulator. We investigated whether a fitness cost is associated with the covS mutation that counterbalances hypervirulence.
methodsWild-type M1T1 group A Streptococcus and an isogenic covS-mutant strain derived from animal passage were compared for adherence to human laryngeal epithelial cells, human keratinocytes, or fibronectin; biofilm formation; and binding to intact mouse skin. Targeted mutagenesis of capsule expression of both strains was performed for analysis of its unique contribution to the observed phenotypes.
resultsThe covS-mutant bacteria showed reduced capacity to bind to epithelial cell layers as a consequence of increased capsule expression. The covS-mutant strain also had reduced capacity to bind fibronectin and to form biofilms on plastic and epithelial cell layers. A defect in skin adherence of the covS-mutant strain was demonstrated in a murine model.
conclusionReduced colonization capacity provides a potential explanation for why the covS mutation, which confers hypervirulence, has not become fixed in the globally disseminated M1T1 group A Streptococcus clone, but rather may arise anew under innate immune selection in individual patients.
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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.