ArticleJournal of bacteriology2010
Variation in Streptococcus pyogenes NAD+ glycohydrolase is associated with tissue tropism.
Article in Journal of bacteriology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Presence of Group A streptococcus frequently assayed virulence genes in invasive disease: a systematic review and meta-analysis.Frontiers in cellular and infection microbiology · 2024Pooled it
- Nosocomial Transmission of Necrotizing Fasciitis: A Molecular Characterization of Group A Streptococcal DNases in Clinical Virulence.Microorganisms · 2024Article
- Molecular characterization ofMicrobial genomics · 2024Article
- Streptolysin S is required for Streptococcus pyogenes nasopharyngeal and skin infection in HLA-transgenic mice.PLoS pathogens · 2024Article
- Interplay between human STING genotype and bacterial NADase activity regulates inter-individual disease variability.Nature communications · 2023Article
- Structural basis underlying the synergism of NADase and SLO during group A Streptococcus infection.Communications biology · 2023Article
- Article
- Streptococcus pyogenes can support or inhibit growth of Haemophilus influenzae by supplying or restricting extracellular NAD.PloS one · 2022Article
- TheJournal of bacteriology · 2021Article
- Group AFrontiers in cellular and infection microbiology · 2019Article
- Molecular Epidemiology, Ecology, and Evolution of Group A Streptococci.Microbiology spectrum · 2018Review
- Binding of NADmBio · 2017Article
- Tissue tropisms in group A Streptococcus: what virulence factors distinguish pharyngitis from impetigo strains?Current opinion in infectious diseases · 2016Review
- NAD+-Glycohydrolase Promotes Intracellular Survival of Group A Streptococcus.PLoS pathogens · 2016Article
- Article
- Article
- The Streptococcus pyogenes NAD(+) glycohydrolase modulates epithelial cell PARylation and HMGB1 release.Cellular microbiology · 2015Article
- Consequences of the variability of the CovRS and RopB regulators among Streptococcus pyogenes causing human infections.Scientific reports · 2015Article
- Article
- Molecular epidemiology and genomics of group A Streptococcus.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Streptococcus pyogenes is an important pathogen that causes a variety of diseases. The most common infections involve the throat (pharyngitis) or skin (impetigo); however, the factors that determine tissue tropism and severity are incompletely understood. The S. pyogenes NAD(+) glycohydrolase (SPN) is a virulence factor that has been implicated in contributing to the pathogenesis of severe infections. However, the role of SPN in determining the bacterium's tissue tropism has not been evaluated. In this report, we examine the sequences of spn and its endogenous inhibitor ifs from a worldwide collection of S. pyogenes strains. Analysis of average pairwise nucleotide diversity, average number of nucleotide differences, and ratio of nonsynonymous to synonymous substitutions revealed significant diversity in spn and ifs. Application of established models of molecular evolution shows that SPN is evolving under positive selection and diverging into NAD(+) glycohydrolase (NADase)-active and -inactive subtypes. Additionally, the NADase-inactive SPN subtypes maintain the characteristics of a functional gene while ifs becomes a pseudogene. Thus, NADase-inactive SPN continues to evolve under functional constraint. Furthermore, NADase activity did not correlate with invasive disease in our collection but was associated with tissue tropism. The ability to cause infection at both the pharynx and the skin ("generalist" strains) is correlated with NADase-active SPN, while the preference for causing infection at either the throat or the skin ("specialist" strains) is associated with NADase-inactive SPN. These findings suggest that SPN has a NADase-independent function and prompt a reevaluation of the role of SPN in streptococcal pathogenesis.
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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.