ArticlePloS one2015
Genomic analysis reveals the molecular basis for capsule loss in the group B Streptococcus population.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Genomic characterization of group BMicrobial genomics · 2025Article
- Maternal Streptococcus agalactiae colonization in Europe: data from the multi-center DEVANI study.Infection · 2025Article
- Performance Evaluation of NovaplexMicroorganisms · 2024Article
- CRISPR/Cas9 Landscape: Current State and Future Perspectives.International journal of molecular sciences · 2023Review
- Population genomics of Group B Streptococcus reveals the genetics of neonatal disease onset and meningeal invasion.Nature communications · 2022Article
- Optimizing the Parametrization of Homologue Classification in the Pan-Genome Computation for a Bacterial Species: Case Study Streptococcus pyogenes.Methods in molecular biology (Clifton, N.J.) · 2022Review
- Epidemiological Characterization of Group B Streptococcus Infections in Alberta, Canada: An Update from 2014 to 2020.Microbiology spectrum · 2021Article
- GBS-SBG - GBS Serotyping by Genome Sequencing.Microbial genomics · 2021Article
- Group BACS infectious diseases · 2021Article
- Molecular Identification of Invasive Non-typeable Group BFrontiers in cellular and infection microbiology · 2021Article
- Increasing incidence of group B streptococcus neonatal infections in the Netherlands is associated with clonal expansion of CC17 and CC23.Scientific reports · 2020Article
- Prevalence of group B streptococcus among pregnant women and newborns at Hawassa University comprehensive specialized hospital, Hawassa, Ethiopia.BMC infectious diseases · 2019Article
- Perinatal Streptococcus agalactiae Epidemiology and Surveillance Targets.Clinical microbiology reviews · 2018Review
- Diminished Capsule Exacerbates Virulence, Blood-Brain Barrier Penetration, Intracellular Persistence, and Antibiotic Evasion of Hyperhemolytic Group B Streptococci.The Journal of infectious diseases · 2018Article
- Final follicular maturation by administration of GnRH agonist plus HCG versus HCG in normal responders in ART cycles: An RCT.International journal of reproductive biomedicine · 2017Article
- Comparison of molecular serotyping approaches of Streptococcus agalactiae from genomic sequences.BMC genomics · 2017Article
- Serotype Distribution, Population Structure, and Antimicrobial Resistance of Group B Streptococcus Strains Recovered from Colonized Pregnant Women.Journal of clinical microbiology · 2017Article
- Real-time PCR-based serotyping of Streptococcus agalactiae.Scientific reports · 2016Article
- Immune Responses to Invasive Group B Streptococcal Disease in Adults.Emerging infectious diseases · 2016Article
- Serotype IV Streptococcus agalactiae ST-452 has arisen from large genomic recombination events between CC23 and the hypervirulent CC17 lineages.Scientific reports · 2016Article
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Authors and funding
16 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human and bovine bacterial pathogen Streptococcus agalactiae (Group B Streptococcus, GBS) expresses a thick polysaccharide capsule that constitutes a major virulence factor and vaccine target. GBS can be classified into ten distinct serotypes differing in the chemical composition of their capsular polysaccharide. However, non-typeable strains that do not react with anti-capsular sera are frequently isolated from colonized and infected humans and cattle. To gain a comprehensive insight into the molecular basis for the loss of capsule expression in GBS, a collection of well-characterized non-typeable strains was investigated by genome sequencing. Genome based phylogenetic analysis extended to a wide population of sequenced strains confirmed the recently observed high clonality among GBS lineages mainly containing human strains, and revealed a much higher degree of diversity in the bovine population. Remarkably, non-typeable strains were equally distributed in all lineages. A number of distinct mutations in the cps operon were identified that were apparently responsible for inactivation of capsule synthesis. The most frequent genetic alterations were point mutations leading to stop codons in the cps genes, and the main target was found to be cpsE encoding the portal glycosyl transferase of capsule biosynthesis. Complementation of strains carrying missense mutations in cpsE with a wild-type gene restored capsule expression allowing the identification of amino acid residues essential for enzyme activity.
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