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Characterisation of the genetic mutation driving enhanced superantigen SpeA expression in Streptococcus pyogenes M1UK (initial)

ABSTRACT: A new variant of group A Streptococcus (GAS) serotype M1 (designated ‘M1UK’) has been reported in the United Kingdom, linked with seasonal scarlet fever surges, marked increase in invasive infections, and exhibiting enhanced expression of the superantigen SpeA. The progenitor GAS ‘M1global’ and M1UK clones can be differentiated by 27 SNPs and 4 indels, yet the mechanism for speA upregulation is unknown. Here we investigate the previously unappreciated expansion of M1UK in Australia, now isolated from the majority of serious infections caused by serotype M1 GAS. M1UK sub-lineages circulating in Australia also contain a novel toxin repertoire associated with epidemic scarlet fever causing GAS in Asia. A single SNP in the M1UK tmRNA gene ssrA drives enhanced SpeA superantigen expression as a result of ssrA terminator readthrough in the M1UK lineage. This represents a new paradigm of toxin expression and urges enhanced international surveillance.

ORGANISM(S): Streptococcus pyogenes

PROVIDER: GSE212238 | GEO | 2023/01/30

REPOSITORIES: GEO

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Characterisation of the genetic mutation driving enhanced superantigen SpeA expression in Streptococcus pyogenes M1UK (second SP1448)

Project description:A new variant of group A Streptococcus (GAS) serotype M1 (designated ‘M1UK’) has been reported in the United Kingdom, linked with seasonal scarlet fever surges, marked increase in invasive infections, and exhibiting enhanced expression of the superantigen SpeA. The progenitor GAS ‘M1global’ and M1UK clones can be differentiated by 27 SNPs and 4 indels, yet the mechanism for speA upregulation is unknown. Here we investigate the previously unappreciated expansion of M1UK in Australia, now isolated from the majority of serious infections caused by serotype M1 GAS. M1UK sub-lineages circulating in Australia also contain a novel toxin repertoire associated with epidemic scarlet fever causing GAS in Asia. A single SNP in the M1UK tmRNA gene ssrA drives enhanced SpeA superantigen expression as a result of ssrA terminator readthrough in the M1UK lineage. This represents a new paradigm of toxin expression and urges enhanced international surveillance.

2023-01-30 | GSE212242 | GEO

Characterisation of the genetic mutation driving enhanced superantigen SpeA expression in Streptococcus pyogenes M1UK (second SP1380)

2023-01-30 | GSE212241 | GEO

Characterisation of the genetic mutation driving enhanced superantigen SpeA expression in Streptococcus pyogenes M1UK (second 5448)

2023-01-30 | GSE212239 | GEO

Microarray analysis of genes involved in Streptolysin S immunity

Project description:Group A Streptococcus (GAS) is one of the world’s most successful pathogens, causing a multitude of common infections such as pharyngitis, cellulitis, and impetigo. It is also responsible for more severe diseases such as rheumatic fever, necrotizing fasciitis, and toxic shock syndrome. Group A Streptococcus produces a powerful peptide toxin known as streptolysin S (SLS). Although recent advances have begun to uncover the structure of SLS, many questions remain as to its route of synthesis, export and function. A fundamental yet unanswered question about SLS is the mechanism employed by GAS to resist the effects of its own toxin. To address this question, we developed a unique microarray-based approach aimed at identifying bacterial genes involved in SLS immunity. We measured changes in gene expression in a non-SLS producing GAS strain (∆SLS) after exposure to active SLS, as well as to an inactive SLS isoform. Initial exposure of a non-SLS producing GAS to the native SLS toxin resulted in significant upregulation of several gene candidates. Proteins encoded by these gene candidates were produced and tested for their ability to neutralize SLS toxin activity in vitro. The protein encoded by the gene Spy_0787 decreased the cytolytic activity of wt SLS by 50%. Bacterial immunity is still a relatively unknown and unexplained phenomena. Insights into how toxin-producing microorganisms achieve resistance against the effects of their own toxin could uncover important therapeutic targets to neutralize virulence factors such as SLS, as well as other related peptide toxins. The microarray technique described here can be leveraged to other microbial systems to understand how microorganisms in general react to antibacterial and cytotoxic compounds for which the mechanism of action is unknown.

2013-09-01 | GSE48775 | GEO

Transcriptome comparison of M1T1 WT, AP and delta CovS strains

Project description:Group A streptococci (GAS) may engage different sets of virulence strategies, depending on the site of infection and host context. We previously isolated 2 phenotypic variants of a globally disseminated M1T1 GAS clone: a virulent wild-type (WT) strain, characterized by a SpeB(+)/SpeA(-)/Sda1(low) phenotype, and a hypervirulent animal-passaged (AP) strain, better adapted to survive in vivo, with a SpeB(-)/SpeA(+)/Sda1(high) phenotype. This AP strain arises in vivo due to the selection of bacteria with mutations in covS, the sensor part of a key 2-component regulatory system, CovR/S. To determine whether covS mutations explain the hypervirulence of the AP strain, we deleted covS from WT bacteria (DeltaCovS) and were able to simulate the hypervirulence and gene expression phenotype of naturally selected AP bacteria. Correction of the covS mutation in AP bacteria reverted them back to the WT phenotype. Our data confirm that covS plays a direct role in regulating GAS virulence.

2010-09-22 | GSE24246 | GEO

Increase of emm1 isolates among group A Streptococcus strains causing scarlet fever during 2011-2015 in Shanghai, China

Project description:emm1 increases in scarlet fever outbreaks

| PRJEB35406 | ENA

M1 and M6 serotypes, Wild-type vs. Mga- GAS

Project description:JRS4 is our wild-type M6 serotype GAS and JRS519 is our Mga- M6 serotype GAS. SF370 is our wild-type M1 serotype GAS and KSM165L is our Mga- M1 serotype GAS. Table 1: Genomic Normalization Description: Step by Step instructions for the removal of outlier background data and any ORF data that did not meet threshold of 2SD above background average, using original data from gpr file provided in each of the sample files. Table 2: M1 Mga+ vs Mga- Description: Step by Step instructions for the removal of outlier data as compared across all possible data points for each ORF. Data points after genomic normalization are used with resultant averages and standard deviations for each ORF computed. Table 3: M6 Mga+ vs Mga- Description: Step by Step instructions for the removal of outlier data as compared across all possible data points for each ORF. Data points after genomic normalization are used with resultant averages and standard deviations for each ORF computed. Keywords: repeat sample

2005-04-06 | GSE1895 | GEO

Influence of RD2 on gene expression in serotype M1 and M49 GAS isolates

Project description:We used RNA-Seq to assess how the presence/absence of the RD2 pathogenicity island influences global gene expression in the parental serotype M1 GAS isolate MGAS2221 and the parental serotype M49 isolate NZ131

2021-03-12 | GSE167343 | GEO

Transcriptome comparison of M1T1 WT, AP and delta CovS strains

2010-09-22 | E-GEOD-24246 | biostudies-arrayexpress

Kawasaki Disease and Other Febrile Illnesses

Project description:ABSTRACT Background. Acute Kawasaki disease (KD) is difficult to distinguish from other acute rash/fever illnesses, in part because the etiologic agent(s) and pathophysiology remain poorly characterized. As a result, diagnosis and critical therapies may be delayed. Methods. We used DNA microarrays to identify possible diagnostic features of KD. We compared gene expression patterns in the blood of 23 children with acute KD and 18 age-matched febrile children with three illnesses that resemble KD. Results. Genes associated with platelet and neutrophil activation were expressed at higher levels in KD patients than in patients with acute adenovirus infections or systemic adverse drug reactions but not in patients with scarlet fever; genes associated with B cell activation were also expressed at higher levels in KD patients than in controls. A striking absence of interferon-stimulated gene expression in the KD patients was confirmed in an independent cohort of KD subjects. We successfully predicted the diagnosis in 21 of 23 KD patients and 7 of 8 adenovirus patients using a set of 38 gene transcripts. Conclusions. These findings provide insight into the molecular features that distinguish KD from other febrile illnesses, and support the feasibility of developing novel diagnostic reagents for KD based on the host response. A disease state experiment design type is where the state of some disease such as infection, pathology, syndrome, etc is studied. Disease State: One of Kawasaki Disease (KD) or control (C) of Scarlet fever (C-sf), adenovirus infection (C-ai) or drug reaction (C-dr) disease_state_design

2010-06-24 | E-GEOD-15297 | biostudies-arrayexpress

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