Streptococcus pyogenes
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ABSTRACT:
PROVIDER: PRJNA1137869 | ENA |
REPOSITORIES: ENA
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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 | GSE212238 | GEO
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
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 | GSE212241 | GEO
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 | GSE212239 | GEO
Project description:Group A Streptococcus (GAS) is a human-adapted pathogen responsible for a variety of diseases. The GAS M1UK lineage has contributed significantly to the recently reported increases in scarlet fever and invasive infections, however the basis for its evolutionary success is not yet fully understood. During the transition to systemic disease, the M1 serotype is known to give rise to spontaneous mutations in the CovRS two-component transcriptional regulation system that confer a fitness advantage during invasive infections. Mutations that inactivate CovS function result in the de-repression of key GAS virulence factors such as Streptolysin O (SLO), a pore-forming toxin and major trigger of inflammasome/interleukin-1-dependent inflammation. Conversely, expression of the streptococcal cysteine protease SpeB, which is required during initial stages of colonisation and onset of invasive disease, is typically lost in such mutants. In this study, we identified and characterised a novel covS mutation detected in three separate invasive M1UK isolates. The resulting CovSAla318Val mutation caused a significant upregulation of SLO resulting in increased inflammasome activation in human THP-1 macrophages, indicating an enhanced inflammatory potential. Surprisingly, SpeB production was unaffected. Site-directed mutagenesis was performed to assess the impact of this mutation on virulence and global gene expression. We found that the CovSAla318Val mutation led to subtle, virulence-specific changes of the CovRS regulon compared to previously characterised covS mutations, highlighting an unappreciated level of complexity in CovRS-dependent gene regulation. Continued longitudinal surveillance is warranted to determine whether this novel covS mutation will expand in the M1UK lineage.
2024-10-28 | GSE280498 | GEO
Project description:Dominance of M1UK clade among invasive M1 Streptococcus pyogenes isolates in the Netherlands in 2019
| PRJEB38751 | ENA
Project description:Expression of the extensive arsenal of virulence factors by Streptococcus pyogenes are controlled by many regulators, of which covR/S is one of the best characterized and can influence ~15% of the genome. Animal models have established that mutants of CovR/S arise spontaneously in vivo resulting in highly invasive organisms. We analyzed a pharyngeal and a blood isolate of S. pyogenes recovered from the same individual 13 days apart. The two isolates varied in many phenotypic properties including speB production, which were reflected in transcriptome analyses. Pulsed field gel electrophoresis, multilocus sequence typing, and partial sequencing of some key genes failed to show any differences except for an 11-base insert in the covS gene in the blood isolate. These results showing that pharyngeal and blood isolates from a single individual which differ by a simple insertion, provide evidence for the model that regulatory gene mutations allow S. pyogenes to invade different niches in the body. A chip study using total RNA recovered from two separate wild-type cultures of group A Streptococcus, Streptococcus pyogenes UH322 and UH328. Each chip measures the expression level of 1865 genes replicated twice from 7 fully sequenced strains of Streptococcus pyogenes (M1_GAS NC_002737; MGAS10394 NC_006086; MGAS315 NC_004070; MGAS5005 NC_007297; MGAS6180 NC_007296; MGAS8232 NC_003485; SSI-1 NC_004606 with fourteen 24-mer probe pairs (PM/MM) per gene, with three-fold technical redundancy.
2010-05-01 | E-GEOD-21316 | biostudies-arrayexpress
Project description:Streptococcus pyogenes emm1 causing invasive disease in Belgium (2020-2023)
| PRJNA1003449 | ENA