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Background <p>This study characterizes the molecular interplay between respiratory syncytial virus (RSV) glycoproteins (G/F) and <i>Streptococcus pneumoniae</i> (<i>S.pn</i>) penicillin-binding proteins (PBPs), while evaluating RSV’s potential role in modulating <i>S.pn</i> β-lactam resistance.</p> Methods <p>Protein docking and pull-down assays assessed G/F-PBP interactions. In vitro RSV-<i>S.pn</i> co-culture experiments evaluated β-lactam susceptibility (MIC determination). We retrospectively analyzed 2012–2021 antimicrobial resistance data from 1-59-month-old community-acquired pneumonia patients at Chongqing Medical University Children’s Hospital with confirmed <i>S.pn</i> and/or RSV nasopharyngeal carriage.</p> Results <p>Computational modeling revealed low G/F-PBP binding affinity (iPTM &lt; 0.6), corroborated by absent PBP1a interaction in pull-down assays. RSV exposure did not alter <i>S.pn</i> β-lactam MICs (penicillin/amoxicillin ≤ 2&#xa0;µg/mL; cefepime/cefotaxime ≤ 1&#xa0;µg/mL; meropenem ≤ 0.25&#xa0;µg/mL). Retrospective data showed elevated penicillin resistance in RSV + <i>S.pn</i> co-detections vs. <i>S.pn</i> alone during 2012 (2.8% vs. 40.9%), 2017 (2.8% vs. 30.4%), and 2018 (6.2% vs. 38.6%) (all <i>p</i> &lt; 0.001). No RSV-associated resistance increases occurred for amoxicillin, cephalosporins, or meropenem.</p> Conclusions <p>RSV demonstrates negligible impact on <i>S.pn</i> β-lactam resistance mechanisms, elevated resistance rates to amoxicillin and cephalosporins necessitate enhanced antimicrobial stewardship through diagnostic-guided prescribing and resistance surveillance to optimize β-lactam efficacy in pediatric care.</p>

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Impact of respiratory syncytial virus on Streptococcus pneumoniae resistance to β-lactam antibiotics: an investigative study in children

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月9日

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  • Lu Li,
  • Yushun Wan,
  • Yuncheng Wang,
  • Ye Tao,
  • Xiao Long,
  • Enmei Liu,
  • Yu Deng

摘要

Background

This study characterizes the molecular interplay between respiratory syncytial virus (RSV) glycoproteins (G/F) and Streptococcus pneumoniae (S.pn) penicillin-binding proteins (PBPs), while evaluating RSV’s potential role in modulating S.pn β-lactam resistance.

Methods

Protein docking and pull-down assays assessed G/F-PBP interactions. In vitro RSV-S.pn co-culture experiments evaluated β-lactam susceptibility (MIC determination). We retrospectively analyzed 2012–2021 antimicrobial resistance data from 1-59-month-old community-acquired pneumonia patients at Chongqing Medical University Children’s Hospital with confirmed S.pn and/or RSV nasopharyngeal carriage.

Results

Computational modeling revealed low G/F-PBP binding affinity (iPTM < 0.6), corroborated by absent PBP1a interaction in pull-down assays. RSV exposure did not alter S.pn β-lactam MICs (penicillin/amoxicillin ≤ 2 µg/mL; cefepime/cefotaxime ≤ 1 µg/mL; meropenem ≤ 0.25 µg/mL). Retrospective data showed elevated penicillin resistance in RSV + S.pn co-detections vs. S.pn alone during 2012 (2.8% vs. 40.9%), 2017 (2.8% vs. 30.4%), and 2018 (6.2% vs. 38.6%) (all p < 0.001). No RSV-associated resistance increases occurred for amoxicillin, cephalosporins, or meropenem.

Conclusions

RSV demonstrates negligible impact on S.pn β-lactam resistance mechanisms, elevated resistance rates to amoxicillin and cephalosporins necessitate enhanced antimicrobial stewardship through diagnostic-guided prescribing and resistance surveillance to optimize β-lactam efficacy in pediatric care.