PLoS Pathogens (Apr 2010)

A genomic survey of positive selection in Burkholderia pseudomallei provides insights into the evolution of accidental virulence.

  • Tannistha Nandi,
  • Catherine Ong,
  • Arvind Pratap Singh,
  • Justin Boddey,
  • Timothy Atkins,
  • Mitali Sarkar-Tyson,
  • Angela E Essex-Lopresti,
  • Hui Hoon Chua,
  • Talima Pearson,
  • Jason F Kreisberg,
  • Christina Nilsson,
  • Pramila Ariyaratne,
  • Catherine Ronning,
  • Liliana Losada,
  • Yijun Ruan,
  • Wing-Kin Sung,
  • Donald Woods,
  • Richard W Titball,
  • Ifor Beacham,
  • Ian Peak,
  • Paul Keim,
  • William C Nierman,
  • Patrick Tan

DOI
https://doi.org/10.1371/journal.ppat.1000845
Journal volume & issue
Vol. 6, no. 4
p. e1000845

Abstract

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Certain environmental microorganisms can cause severe human infections, even in the absence of an obvious requirement for transition through an animal host for replication ("accidental virulence"). To understand this process, we compared eleven isolate genomes of Burkholderia pseudomallei (Bp), a tropical soil microbe and causative agent of the human and animal disease melioidosis. We found evidence for the existence of several new genes in the Bp reference genome, identifying 282 novel genes supported by at least two independent lines of supporting evidence (mRNA transcripts, database homologs, and presence of ribosomal binding sites) and 81 novel genes supported by all three lines. Within the Bp core genome, 211 genes exhibited significant levels of positive selection (4.5%), distributed across many cellular pathways including carbohydrate and secondary metabolism. Functional experiments revealed that certain positively selected genes might enhance mammalian virulence by interacting with host cellular pathways or utilizing host nutrients. Evolutionary modifications improving Bp environmental fitness may thus have indirectly facilitated the ability of Bp to colonize and survive in mammalian hosts. These findings improve our understanding of the pathogenesis of melioidosis, and establish Bp as a model system for studying the genetics of accidental virulence.