Genetic switch to hypervirulence reduces colonization phenotypes of the globally disseminated group A streptococcus M1T1 clone.
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Microevolution of group A streptococci in vivo: capturing regulatory networks engaged in sociomicrobiology, niche adaptation, and hypervirulenceEmergence of a New Highly Successful Acapsular Group A Streptococcus Clade of Genotype emm89 in the United KingdomStreptococcus pyogenes biofilms-formation, biology, and clinical relevanceUnique Footprint in the scl1.3 Locus Affects Adhesion and Biofilm Formation of the Invasive M3-Type Group A StreptococcusMolecular and genomic characterization of pathogenic traits of group A Streptococcus pyogenesGlobal Analysis and Comparison of the Transcriptomes and Proteomes of Group A Streptococcus BiofilmsEvolutionary Constraints Shaping Streptococcus pyogenes-Host Interactions.Complete Genome Sequence of emm1 Streptococcus pyogenes A20, a Strain with an Intact Two-Component System, CovRS, Isolated from a Patient with Necrotizing Fasciitis.Screening of in vivo activated genes in Enterococcus faecalis during insect and mouse infections and growth in urineStreptococcal collagen-like protein A and general stress protein 24 are immunomodulating virulence factors of group A Streptococcus.Allelic replacement of the streptococcal cysteine protease SpeB in a Δsrv mutant background restores biofilm formation.The classical lancefield antigen of group a Streptococcus is a virulence determinant with implications for vaccine design.Importance of whole genome sequencing for the assessment of outbreaks in diagnostic laboratories: analysis of a case series of invasive Streptococcus pyogenes infections.The IL-8 protease SpyCEP is detrimental for Group A Streptococcus host-cells interaction and biofilm formation.Molecular characterization of the 2011 Hong Kong scarlet fever outbreak.Essential Genes in the Core Genome of the Human Pathogen Streptococcus pyogenes.M protein and hyaluronic acid capsule are essential for in vivo selection of covRS mutations characteristic of invasive serotype M1T1 group A Streptococcus.Intracellular Streptococcus pyogenes in human macrophages display an altered gene expression profile.Hyaluronan breakdown contributes to immune defense against group A StreptococcusRNA-mediated regulation in Gram-positive pathogens: an overview punctuated with examples from the group A Streptococcus.Disease manifestations and pathogenic mechanisms of Group A Streptococcus.Mutual exclusivity of hyaluronan and hyaluronidase in invasive group A Streptococcus.Inactivation of the CovR/S virulence regulator impairs infection in an improved murine model of Streptococcus pyogenes naso-pharyngeal infectionThe AgI/II family adhesin AspA is required for respiratory infection by Streptococcus pyogenes.RocA truncation underpins hyper-encapsulation, carriage longevity and transmissibility of serotype M18 group A streptococci.Characterization of the effect of the histidine kinase CovS on response regulator phosphorylation in group A Streptococcus.Niche-specific contribution to streptococcal virulence of a MalR-regulated carbohydrate binding protein.Serine/threonine protein kinase Stk is required for virulence, stress response, and penicillin tolerance in Streptococcus pyogenes.A group A Streptococcus ADP-ribosyltransferase toxin stimulates a protective interleukin 1β-dependent macrophage immune responseCationic antimicrobial peptide resistance mechanisms of streptococcal pathogens.CovRS-Regulated Transcriptome Analysis of a Hypervirulent M23 Strain of Group A Streptococcus pyogenes Provides New Insights into Virulence Determinants.Regulatory rewiring confers serotype-specific hyper-virulence in the human pathogen group A StreptococcusA conserved UDP-glucose dehydrogenase encoded outside the hasABC operon contributes to capsule biogenesis in group A StreptococcusRivR is a negative regulator of virulence factor expression in group A Streptococcus.Application of Whole-Genome Sequencing to an Unusual Outbreak of Invasive Group A Streptococcal Disease.Molecular analysis of an outbreak of lethal postpartum sepsis caused by Streptococcus pyogenes.Biofilm in group A streptococcal necrotizing soft tissue infections.The fibrinogen-binding M1 protein reduces pharyngeal cell adherence and colonization phenotypes of M1T1 group A Streptococcus.Natural disruption of two regulatory networks in serotype M3 group A Streptococcus isolates contributes to the virulence factor profile of this hypervirulent serotype.Molecular characterization of an invasive phenotype of group A Streptococcus arising during human infection using whole genome sequencing of multiple isolates from the same patient.
P2860
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P2860
Genetic switch to hypervirulence reduces colonization phenotypes of the globally disseminated group A streptococcus M1T1 clone.
description
2010 nî lūn-bûn
@nan
2010 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Genetic switch to hypervirulen ...... up A streptococcus M1T1 clone.
@ast
Genetic switch to hypervirulen ...... up A streptococcus M1T1 clone.
@en
type
label
Genetic switch to hypervirulen ...... up A streptococcus M1T1 clone.
@ast
Genetic switch to hypervirulen ...... up A streptococcus M1T1 clone.
@en
prefLabel
Genetic switch to hypervirulen ...... up A streptococcus M1T1 clone.
@ast
Genetic switch to hypervirulen ...... up A streptococcus M1T1 clone.
@en
P2093
P2860
P50
P356
P1476
Genetic switch to hypervirulen ...... up A streptococcus M1T1 clone.
@en
P2093
Andrew Hollands
Anjuli M Timmer
Sarah R Osvath
P2860
P356
10.1086/653124
P407
P577
2010-07-01T00:00:00Z