Enterococcus faecalis prophage dynamics and contributions to pathogenic traits

PLoS Genet. 2013 Jun;9(6):e1003539. doi: 10.1371/journal.pgen.1003539. Epub 2013 Jun 6.


Polylysogeny is frequently considered to be the result of an adaptive evolutionary process in which prophages confer fitness and/or virulence factors, thus making them important for evolution of both bacterial populations and infectious diseases. The Enterococcus faecalis V583 isolate belongs to the high-risk clonal complex 2 that is particularly well adapted to the hospital environment. Its genome carries 7 prophage-like elements (V583-pp1 to -pp7), one of which is ubiquitous in the species. In this study, we investigated the activity of the V583 prophages and their contribution to E. faecalis biological traits. We systematically analyzed the ability of each prophage to excise from the bacterial chromosome, to replicate and to package its DNA. We also created a set of E. faecalis isogenic strains that lack from one to all six non-ubiquitous prophages by mimicking natural excision. Our work reveals that prophages of E. faecalis V583 excise from the bacterial chromosome in the presence of a fluoroquinolone, and are able to produce active phage progeny. Intricate interactions between V583 prophages were also unveiled: i) pp7, coined EfCIV583 for E. faecalis chromosomal island of V583, hijacks capsids from helper phage 1, leading to the formation of distinct virions, and ii) pp1, pp3 and pp5 inhibit excision of pp4 and pp6. The hijacking exerted by EfCIV583 on helper phage 1 capsids is the first example of molecular piracy in Gram positive bacteria other than staphylococci. Furthermore, prophages encoding platelet-binding-like proteins were found to be involved in adhesion to human platelets, considered as a first step towards the development of infective endocarditis. Our findings reveal not only a role of E. faecalis V583 prophages in pathogenicity, but also provide an explanation for the correlation between antibiotic usage and E. faecalis success as a nosocomial pathogen, as fluoriquinolone may provoke release of prophages and promote gene dissemination among isolates.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chromosomes, Bacterial / genetics
  • Cross Infection / genetics
  • Enterococcus faecalis / genetics*
  • Enterococcus faecalis / pathogenicity
  • Genome, Bacterial
  • Host-Pathogen Interactions / genetics*
  • Humans
  • Prophages / genetics*
  • Prophages / metabolism
  • Prophages / pathogenicity
  • Virulence Factors / genetics*
  • Virulence Factors / metabolism
  • Virus Activation / genetics*


  • Virulence Factors

Grant support

RCM is grateful to Fundação para a Ciência e Tecnologia for financial support through PhD scholarship SFRH/BD/43461/2008. This work was supported by INRA funds, the French Agence Nationale de la Recherche grant ANR-06-PATHO-008, and FCT through bench fees associated with the studentship SFRH/BD/43461/2008. The authors acknowledge Fundação para a Ciência e Tecnologia for grant PEst-OE/EQB/LA0004/2011. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.