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Research into EPEC is intense and provides a good virulence model of other<jats:italic>E. coli<\/jats:italic>infections as well as other pathogenic bacteria. Although the virulence mechanisms are now better understood, they are extremely complex and much remains to be learnt. The pathogenesis of EPEC depends on the formation of an ultrastructural lesion in which the bacteria make intimate contact with the host apical enterocyte membrane. The formation of this lesion is a consequence of the ability of EPEC to adhere in a localized manner to the host cell, aided by bundle-forming pili. Tyrosine phosphorylation and signal transduction events occur within the host cell at the lesion site, leading to a disruption of the host cell mechanisms and, consequently, to diarrhea. These result from the action of highly regulated EPEC secreted proteins which are released via a type III secretion system, many genes of which are located within a pathogenicity island known as the locus of enterocyte effacement. Over the last few years, dramatic increases in our knowledge of EPEC virulence have taken place. This review therefore aims to provide a broad overview of and update to the virulence aspects of EPEC.<\/jats:p><\/jats:sec>","DOI":"10.1128\/cmr.16.3.365-378.2003","type":"journal-article","created":{"date-parts":[[2003,7,12]],"date-time":"2003-07-12T13:05:17Z","timestamp":1058015117000},"page":"365-378","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":184,"title":["Virulence of Enteropathogenic<i>Escherichia coli<\/i>, a Global Pathogen"],"prefix":"10.1128","volume":"16","author":[{"given":"S. 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