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Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
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Gp05, a Prophage-Encoded Virulence Factor, Contributes to Persistent Methicillin-Resistant Staphylococcus aureus

Yi Li1, Fengli Zhu1, Adhar C Manna2

  • 1The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, California, USA.

Microbiology Spectrum
|June 26, 2023
PubMed
Summary
This summary is machine-generated.

A novel prophage gene, gp05, drives persistent methicillin-resistant Staphylococcus aureus (MRSA) endovascular infections by impacting metabolism and immune response. This discovery offers a new target for treating challenging MRSA infections resistant to vancomycin.

Keywords:
MRSAendovascular infectionphage-encoded virulence factorvancomycin persistence

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Area of Science:

  • Microbiology and Infectious Diseases
  • Molecular Biology
  • Pharmacology

Background:

  • Persistent endovascular infections caused by methicillin-resistant Staphylococcus aureus (MRSA) pose a significant public health challenge.
  • These infections often exhibit susceptibility to antibiotics like vancomycin (VAN) *in vitro*, yet persist *in vivo*, indicating unique resistance mechanisms.
  • Prophages, mobile genetic elements in MRSA, contribute to bacterial virulence and resistance, but their specific roles in persistent infections are not fully understood.

Purpose of the Study:

  • To investigate the role of a specific prophage gene, ϕ80α_gp05 (gp05), in vancomycin (VAN) treatment failure and persistent outcomes in MRSA endovascular infections.
  • To elucidate the mechanisms by which gp05 influences MRSA virulence, host immune responses, and antibiotic efficacy.

Main Methods:

  • Utilized isogenic MRSA strain sets with gp05 overexpression and chromosomal deletion mutants.
  • Assessed the impact of gp05 on metabolic pathways (tricarboxylic acid cycle), pigment production, and stringent response activation (p)ppGpp.
  • Evaluated VAN treatment efficacy in an experimental MRSA infective endocarditis model.

Main Results:

  • The prophage gene gp05 significantly influences MRSA's tricarboxylic acid cycle activity and carotenoid pigment production.
  • Gp05 modulates (p)ppGpp production, affecting the stringent response, phenol-soluble modulins, and neutrophil bactericidal activity.
  • Gp05 expression is directly linked to persistence during vancomycin treatment in a murine endocarditis model.

Conclusions:

  • Gp05 acts as a significant virulence factor, contributing to persistent MRSA endovascular infections through multiple pathways.
  • The findings highlight the complex interplay between prophage-encoded factors, bacterial metabolism, host immunity, and antibiotic treatment failure.
  • Gp05 represents a potential novel therapeutic target for combating life-threatening persistent MRSA infections.