ArticleInfection and immunity2015
The majority of 9,729 group A streptococcus strains causing disease secrete SpeB cysteine protease: pathogenesis implications.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 40 citations in OpenAlex.
- Dynamic tethering of M protein drives pathological inflammation during group A Streptococcus infections.PLoS pathogens · 2026Article
- Performance of the Xpert Xpress Strep A for detection ofMicrobiology spectrum · 2026Article
- Comparison of pharyngeal and invasive isolates ofMicrobiology spectrum · 2025Article
- The intricate pathogenicity of Group AVirulence · 2024Review
- Clinical Snapshot of Group A Streptococcal Isolates from an Australian Tertiary Hospital.Pathogens (Basel, Switzerland) · 2024Article
- Immunomodulating Enzymes fromMicroorganisms · 2024Review
- Characterization of group A streptococci causing invasive diseases in Sri Lanka.Access microbiology · 2024Article
- Article
- Streptococcus pyogenes infects human endometrium by limiting the innate immune response.The Journal of clinical investigation · 2021Article
- Playing With Fire: Proinflammatory Virulence Mechanisms of Group AFrontiers in cellular and infection microbiology · 2021Review
- Alternative approaches to treat bacterial infections: targeting quorum-sensing.Expert review of anti-infective therapy · 2020Review
- The Streptococcal Protease SpeB Antagonizes the Biofilms of the Human Pathogen Staphylococcus aureus USA300 through Cleavage of the Staphylococcal SdrC Protein.Journal of bacteriology · 2020Article
- Polymorphisms in Regulator of Cov Contribute to the Molecular Pathogenesis of Serotype M28 Group A Streptococcus.The American journal of pathology · 2019Article
- Tissue Tropism in Streptococcal Infection: Wild-Type M1T1 Group AInfection and immunity · 2019Article
- Environmental pH and peptide signaling control virulence of Streptococcus pyogenes via a quorum-sensing pathway.Nature communications · 2019Article
- Integrated analysis of population genomics, transcriptomics and virulence provides novel insights into Streptococcus pyogenes pathogenesis.Nature genetics · 2019Article
- Catch Me if You Can: Streptococcus pyogenes Complement Evasion Strategies.Journal of innate immunity · 2019Review
- RocA Has Serotype-Specific Gene Regulatory and Pathogenesis Activities in Serotype M28 Group A Streptococcus.Infection and immunity · 2018Article
- Phenotypic Variation in the Group AmSphere · 2018Article
- Signaling by a Conserved Quorum Sensing Pathway Contributes to GrowthInfection and immunity · 2018Article
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group A streptococcus (GAS), the causative agent of pharyngitis and necrotizing fasciitis, secretes the potent cysteine protease SpeB. Several lines of evidence suggest that SpeB is an important virulence factor. SpeB is expressed in human infections, protects mice from lethal challenge when used as a vaccine, and contributes significantly to tissue destruction and dissemination in animal models. However, recent descriptions of mutations in genes implicated in SpeB production have led to the idea that GAS may be under selective pressure to decrease secreted SpeB protease activity during infection. Thus, two divergent hypotheses have been proposed. One postulates that SpeB is a key contributor to pathogenesis; the other, that GAS is under selection to decrease SpeB during infection. In order to distinguish between these alternative hypotheses, we performed casein hydrolysis assays to measure the SpeB protease activity secreted by 6,775 GAS strains recovered from infected humans. The results demonstrated that 84.3% of the strains have a wild-type SpeB protease phenotype. The availability of whole-genome sequence data allowed us to determine the relative frequencies of mutations in genes implicated in SpeB production. The most abundantly mutated genes were direct transcription regulators. We also sequenced the genomes of 2,954 GAS isolates recovered from nonhuman primates with experimental necrotizing fasciitis. No mutations that would result in a SpeB-deficient phenotype were identified. Taken together, these data unambiguously demonstrate that the great majority of GAS strains recovered from infected humans secrete wild-type levels of SpeB protease activity. Our data confirm the important role of SpeB in GAS pathogenesis and help end a long-standing controversy.
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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.