ArticleNature communications2020
Prophage exotoxins enhance colonization fitness in epidemic scarlet fever-causing Streptococcus pyogenes.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 71 citations in OpenAlex.
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- Group A Streptococcal Virulence Factors and Vaccine Development-An Update.Microorganisms · 2026Review
- Horizontal transfer of ΦHKU.vir and its role in the evolution of acapsular emm89 group A Streptococcus in Taiwan.Infection · 2026Article
- T cells in Group AFrontiers in cellular and infection microbiology · 2026Review
- Exo-Tox: Identifying Exotoxins from secreted bacterial proteins.BioData mining · 2025Article
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- Proinflammatory synergy between protease and superantigen streptococcal pyogenic exotoxins.Infection and immunity · 2025Article
- Insights into diversity, host-range, and temporal stability of Bacteroides and Phocaeicola prophages.BMC microbiology · 2025Article
- A Rapid Molecular Detection Tool for Toxigenic M1UK Streptococcus pyogenes.The Journal of infectious diseases · 2025Article
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Corrections and comments
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Authors and funding
19 authors at 8 institutions in 6 countries.
Funding
Abstract
The re-emergence of scarlet fever poses a new global public health threat. The capacity of North-East Asian serotype M12 (emm12) Streptococcus pyogenes (group A Streptococcus, GAS) to cause scarlet fever has been linked epidemiologically to the presence of novel prophages, including prophage ΦHKU.vir encoding the secreted superantigens SSA and SpeC and the DNase Spd1. Here, we report the molecular characterization of ΦHKU.vir-encoded exotoxins. We demonstrate that streptolysin O (SLO)-induced glutathione efflux from host cellular stores is a previously unappreciated GAS virulence mechanism that promotes SSA release and activity, representing the first description of a thiol-activated bacterial superantigen. Spd1 is required for resistance to neutrophil killing. Investigating single, double and triple isogenic knockout mutants of the ΦHKU.vir-encoded exotoxins, we find that SpeC and Spd1 act synergistically to facilitate nasopharyngeal colonization in a mouse model. These results offer insight into the pathogenesis of scarlet fever-causing GAS mediated by prophage ΦHKU.vir exotoxins.
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What OpenQuestion holds
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.