A Tale about Shigella: Evolution, Plasmid, and Virulence

Shigella spp. cause hundreds of millions of intestinal infections each year. They target the mucosa of the human colon and are an important model of intracellular bacterial pathogenesis. Shigella is a pathovar of Escherichia coli that is characterized by the presence of a large invasion plasmid, pINV, which encodes the characteristic type III secretion system and icsA used for cytosol invasion and cell-to-cell spread, respectively. First, we review recent advances in the genetic aspects of Shigella, shedding light on its evolutionary history within the E. coli lineage and its relationship to the acquisition of pINV. We then discuss recent insights into the processes that allow for the maintenance of pINV. Finally, we describe the role of the transcription activators VirF, VirB, and MxiE in the major virulence gene regulatory cascades that control the expression of the type III secretion system and icsA. This provides an opportunity to examine the interplay between these pINV-encoded transcriptional activators and numerous chromosome-encoded factors that modulate their activity. Finally, we discuss novel chromosomal genes icaR, icaT, and yccE that are regulated by MxiE. This review emphasizes the notion that Shigella and E. coli have walked the fine line between commensalism and pathogenesis for much of their history.

Automated summary

Shigella spp. cause a large number of intestinal infections each year, targeting the mucosa of the human colon. They are an important model for studying intracellular bacterial pathogenesis. Shigella is a pathovar of Escherichia coli and is characterized by the presence of a plasmid, pINV, which encodes the type III secretion system and icsA for cytosol invasion and cell-to-cell spread, respectively. Recent research has focused on the genetic aspects, maintenance of pINV, and the role of transcription activators in virulence gene regulation. The interplay between pINV-encoded activators and chromosome-encoded factors is also explored, along with novel chromosomal genes regulated by MxiE.