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Parallel Evolution of Group B Streptococcus Hypervirulent Clonal Complex 17 Unveils New Pathoadaptive Mutations.
Alexandre Almeida1,2,3, Isabelle Rosinski-Chupin1,2, Céline Plainvert4,5,6,7,8
1Institut Pasteur, Unité Ecologie et Evolution de la Résistance aux Antibiotiques, Paris, France.
Msystems
|September 15, 2017
Summary
Group B Streptococcus (GBS) clonal complex 17 (CC17) causes significant neonatal disease. Genomic analysis reveals distinct evolutionary paths and genetic adaptations in CC17, particularly mutations in virulence regulators like CovRS, differentiating carriage from disease strains.
Area of Science:
- Microbiology
- Genomics
- Infectious Diseases
Background:
- Group B Streptococcus (GBS) is a major cause of neonatal infections globally.
- Clonal complex 17 (CC17) is disproportionately represented in neonatal GBS cases, but its specific adaptations remain unclear.
Purpose of the Study:
- To conduct a comprehensive genomic analysis of 626 GBS CC17 isolates to identify genetic traits enabling human adaptation.
- To differentiate between genetic factors associated with GBS carriage versus clinical disease in CC17 strains.
- To compare CC17 evolution with other human-adapted GBS lineages (CC1, CC19, CC23).
Main Methods:
- Whole-genome sequencing of 626 GBS CC17 isolates.
- Comparative genomic analysis with 923 GBS genomes from CC1, CC19, and CC23.
- Identification of genetic mutations and evolutionary patterns.
- Analysis of genes involved in metabolism, adhesion, regulation, and immune evasion.
Main Results:
- CC17 exhibits a distinct evolutionary trajectory compared to other human-adapted GBS lineages, with recurrently targeted functions in nucleotide/amino acid metabolism, cell adhesion, regulation, and immune evasion.
- Disease-specific CC17 isolates frequently showed mutations in the CovS and Stk1 kinases, highlighting the CovRS pathway's role in GBS pathogenicity.
- Convergent evolution was observed in cell envelope components (capsule, pilus, Rib), suggesting adaptation to host immune pressures.
- Novel targets of evolution not previously linked to virulence were identified, potentially revealing new GBS pathogenesis mechanisms.
Conclusions:
- The study elucidates the genetic underpinnings of GBS CC17's adaptation to humans and its increased pathogenicity in neonates.
- The CovRS regulatory pathway is crucial for distinguishing between GBS carriage and disease isolates.
- Findings have significant implications for GBS vaccine development and the discovery of novel virulence factors.
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