ArticleCell reports2022
Interspecies recombination, not de novo mutation, maintains virulence after β-lactam resistance acquisition in Streptococcus pneumoniae.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- Clinically relevant genomic and phenotypic differences in virulence, antimicrobial resistance, and biofilm-associated tolerance between Streptococcus suis lineages ST1 and ST123.Veterinary research · 2026Article
- Crotonylation driving Streptococcus pneumoniae adaption and virulence.Journal of advanced research · 2026Article
- Antibacterial Benzimidazole-2-Methanamines as Allosteric Modulators ofJournal of medicinal chemistry · 2026Article
- A mini review of genome-predicted β-lactam susceptibility inFrontiers in cellular and infection microbiology · 2026Review
- Penicillin-Binding Proteins inAntibiotics (Basel, Switzerland) · 2026Review
- Lipoteichoic acid mediates binding ofmSphere · 2025Article
- Review
- Amoxicillin-non-susceptibleAntimicrobial agents and chemotherapy · 2025Observational
- Triggering Toll-Like Receptor 5 Signaling During Pneumococcal Superinfection Prevents the Selection of Antibiotic Resistance.The Journal of infectious diseases · 2024Article
- Biological puzzles solved by usingJournal of bacteriology · 2024Review
- The Effect of the Stringent Response and Oxidative Stress Response on Fitness Costs of De Novo Acquisition of Antibiotic Resistance.International journal of molecular sciences · 2024Article
- Convergent impact of vaccination and antibiotic pressures on pneumococcal populations.Cell chemical biology · 2024Review
- Coordinated regulation of osmotic imbalance by c-di-AMP shapes ß-lactam tolerance in Group BmicroLife · 2024Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
As opposed to de novo mutation, β-lactam resistance in S. pneumoniae is often conferred via homologous recombination during horizontal gene transfer. We hypothesize that β-lactam resistance in pathogenic streptococci is restricted to naturally competent species via intra-/interspecies recombination due to in vivo fitness trade-offs of de novo penicillin-binding protein (PBP) mutations. We show that de novo mutant populations have abrogated invasive disease capacity and are difficult to evolve in vivo. Conversely, serially transformed recombinant strains efficiently integrate resistant oral streptococcal DNA, gain penicillin resistance and tolerance, and retain virulence in mice. Large-scale changes in pbp2X, pbp2B, and non-PBP-related genes occur in recombinant isolates. Our results indicate that horizontal transfer of β-lactam resistance engenders initially favorable or minimal cost changes in vivo compared with de novo mutation(s), underscoring the importance of recombination in the emergence of β-lactam resistance and suggesting why some pathogenic streptococci lacking innate competence remain universally susceptible.
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