Phages and the Evolution of Bacterial Pathogens: from Genomic Rearrangements to Lysogenic Conversion

Abstract

Comparative genomics demonstrated that the chromosomes from bacteria and their viruses (bacteriophages) are coevolving. This process is most evident for bacterial pathogens where the majority contain prophages or phage remnants integrated into the bacterial DNA. Many prophages from bacterial pathogens encode virulence factors. Two situations can be distinguished: Vibrio cholerae, Shiga toxin-producing Escherichia coli, Corynebacterium diphtheriae, and Clostridium botulinum depend on a specific prophage-encoded toxin for causing a specific disease, whereas Staphylococcus aureus, Streptococcus pyogenes, and Salmonella enterica serovar Typhimurium harbor a multitude of prophages and each phage-encoded virulence or fitness factor makes an incremental contribution to the fitness of the lysogen. These prophages behave like “swarms” of related prophages. Prophage diversification seems to be fueled by the frequent transfer of phage material by recombination with superinfecting phages, resident prophages, or occasional acquisition of other mobile DNA elements or bacterial chromosomal genes. Prophages also contribute to the diversification of the bacterial genome architecture. In many cases, they actually represent a large fraction of the strain-specific DNA sequences. In addition, they can serve as anchoring points for genome inversions. The current review presents the available genomics and biological data on prophages from bacterial pathogens in an evolutionary framework

Ecological and Evolutionary Benefits of Temperate Phage: What Does or Doesn't Kill You Makes You Stronger

“…Prophage-encoded genes are responsible for virulence of a number of well-known human diseases (e.g., cholera, [2] scarlet fever, [23] shigella, [24] diphtheria, [25] and botulism [26] ) where prophage encode toxins or proteins that modulate host-pathogen interaction, such as antigens and effector proteins. [27] Often the production of toxins -botulism and shiga toxin for example -requires lysis of the cell to release the toxin, such that benefits accrue to related bacterial cells within the infection rather than the producing cells themselves. [28] Carriage of multiple prophages -polylysogeny -is common among pathogens, allowing acquisition of multiple traits and contributing to diversity in disease pathology.…”

Role of phages in the pathogenesis of Burkholderia, or ‘Where are the toxin genes in Burkholderia phages?’

“…Phage-encoded toxin and effector genes are frequently arranged in a transcriptionally self-contained cluster termed a "moron" [9]. Morons are frequently transcribed in the opposite orientation as the surrounding phage genes and are often located near the end of the prophage, as in lambda bor, where as others are embedded in an otherwise typical phage operon, as in lambda lom [32,33].…”

“…In many pathogens, phages have been instrumental in the acquisition of virulence traits [8,9]. Moreover, in many bacteria, prophages are largely responsible for strain-specific differences in toxin and effector gene content [10][11][12][13][14].…”

Gene transfer agents: phage-like elements of genetic exchange

“…Transduction may affect virulence in bacteria [100][101][102] . For example, in Vibrio cholerae the cholera toxin, a key virulence determinant, is encoded in the genome of the temperate phage ΦCTX 103 .…”