Broad-host-range Kayvirus phages preferentially infect Staphylocococcus aureus cells with β-glycosylated WTA, the

Andrea Jurado1, Carlos C Gómez-Cambronero2, Ana Rodríguez1

  • 1Instituto de Productos Lácteos de Asturias (IPLA-CSIC), Oviedo, Spain; DairySafe Group. Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Oviedo, Spain.

Abstract

Insights

Staphylococcus aureus phage infection efficiency is influenced by wall teichoic acid (WTA) glycosylation. Phages show varied interactions with TarS and TarM modifications, with SigB also regulating infectivity.

Area of Science:

  • Microbiology
  • Virology
  • Molecular Biology

Background:

  • Wall teichoic acid (WTA) glycosylation in Staphylococcus aureus impacts host immune interactions and bacteriophage (phage) adsorption.
  • Specific glycosylation patterns, like β-glycosylation (TarS) and α-glycosylation (TarM), differentially affect phage infectivity.

Purpose of the Study:

  • To investigate the influence of WTA glycosylation, specifically TarS and TarM modifications, on the infectivity of broad-host-range phages phiIPLA-RODI and phage K.
  • To identify additional regulatory factors involved in S. aureus phage infectivity.

Main Methods:

  • Spot tests were used to assess phage infectivity on S. aureus strains with varying WTA glycosylation statuses.
  • Genetic analysis was performed to identify regulatory elements controlling tarS and tarM expression.
  • The role of quorum-sensing system Agr and alternative sigma factor SigB in phage infectivity was examined.

Main Results:

  • Broad-host-range phages phiIPLA-RODI and phage K demonstrated enhanced infectivity on strains with TarS-mediated modifications, despite not requiring WTA glycosylation.
  • TarM presence correlated with decreased susceptibility to phiIPLA-RODI, particularly in non-encapsulated strains.
  • Mutations in the Agr system reduced phage susceptibility, and SigB was identified as a novel regulator of TarS expression, impacting phage infectivity.

Conclusions:

  • S. aureus phages have evolved to optimize infection in mammalian hosts, with WTA glycosylation playing a complex role.
  • The findings highlight the intricate interplay between phage, host genetics (Agr, SigB), and WTA modification in determining infection outcomes.
  • While promising for phage therapy, the ecological impact of high-dose phage application warrants further investigation.

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