ArticleThe American journal of pathology2015
A naturally occurring single amino acid replacement in multiple gene regulator of group A Streptococcus significantly increases virulence.
Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Carbon metabolism and niche adaptation inmSphere · 2026Review
- Functional divergence of the gut microbiome associated with lifestyle and helminth infection in Indigenous Peninsular Malaysian.Research square · 2026Article
- Detectable effects of bacterial phylogeny on virulence but not phage efficacy in anISME communications · 2026Article
- Genomic epidemiology ofFrontiers in microbiology · 2023Article
- In silico characterisation of stand-alone response regulators of Streptococcus pyogenes.PloS one · 2020Article
- Polymorphisms in Regulator of Cov Contribute to the Molecular Pathogenesis of Serotype M28 Group A Streptococcus.The American journal of pathology · 2019Article
- Metal sensing and regulation of adaptive responses to manganese limitation by MtsR is critical for group A streptococcus virulence.Nucleic acids research · 2019Article
- RocA Has Serotype-Specific Gene Regulatory and Pathogenesis Activities in Serotype M28 Group A Streptococcus.Infection and immunity · 2018Article
- Molecular Epidemiology, Ecology, and Evolution of Group A Streptococci.Microbiology spectrum · 2018Review
- Unravelling pathogenetic mechanisms of epidemic lineages.Virulence · 2017Article
- The Regulatory Small RNA MarS Supports Virulence of Streptococcus pyogenes.Scientific reports · 2017Article
- Emergence of a Streptococcus dysgalactiae subspecies equisimilis stG62647-lineage associated with severe clinical manifestations.Scientific reports · 2017Article
- Contribution of Secreted NADase and Streptolysin O to the Pathogenesis of Epidemic Serotype M1 Streptococcus pyogenes Infections.The American journal of pathology · 2017Article
- Regulatory gene mutation: a driving force behind group a Streptococcus strain- and serotype-specific variation.Molecular microbiology · 2017Review
- Genomic Landscape of Intrahost Variation in Group A Streptococcus: Repeated and Abundant Mutational Inactivation of the fabT Gene Encoding a Regulator of Fatty Acid Synthesis.Infection and immunity · 2016Article
- Point mutations in the major outer membrane protein drive hypervirulence of a rapidly expanding clone of Campylobacter jejuni.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Hypervirulent emm59 Clone in Invasive Group A Streptococcus Outbreak, Southwestern United States.Emerging infectious diseases · 2016Article
- Unique Footprint in the scl1.3 Locus Affects Adhesion and Biofilm Formation of the Invasive M3-Type Group A Streptococcus.Frontiers in cellular and infection microbiology · 2016Article
- Phosphorylation events in the multiple gene regulator of group A Streptococcus significantly influence global gene expression and virulence.Infection and immunity · 2015Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Single-nucleotide polymorphisms (SNPs) are the most common source of genetic variation within a species; however, few investigations demonstrate how naturally occurring SNPs may increase strain virulence. We recently used group A Streptococcus as a model pathogen to study bacteria strain genotype-patient disease phenotype relationships. Whole-genome sequencing of approximately 800 serotype M59 group A Streptococcus strains, recovered during an outbreak of severe invasive infections across North America, identified a disproportionate number of SNPs in the gene encoding multiple gene regulator of group A Streptococcus (mga). Herein, we report results of studies designed to test the hypothesis that the most commonly occurring SNP, encoding a replacement of arginine for histidine at codon 201 of Mga (H201R), significantly increases virulence. Whole transcriptome analysis revealed that the H201R replacement significantly increased expression of mga and 54 other genes, including many proven virulence factors. Compared to the wild-type strain, a H201R isogenic mutant strain caused significantly larger skin lesions in mice. Serial quantitative bacterial culture and noninvasive magnetic resonance imaging also demonstrated that the isogenic H201R strain was significantly more virulent in a nonhuman primate model of joint infection. These findings show that the H201R replacement in Mga increases the virulence of M59 group A Streptococcus and provide new insight to how a naturally occurring SNP in bacteria contributes to human disease phenotypes.
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Registered trials
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.