FIG 3.

Model of the pathobiology of enteropathogenic E. coli (EPEC) infection, highlighting major virulence genes that were associated with the clinical outcomes in the present study. Ler is a negative autoregulator of the locus of enterocyte effacement (LEE), on which several EPEC virulence genes are located, including components of the type III secretion system (T3SS); thus, Ler can attenuate the virulence of EPEC strains; Map is a LEE-encoded effector protein that changes mitochondrial functions in the host; CesT is a major chaperone for T3SS effectors which facilitates EPEC intestinal colonization; EspB is a component of the T3SS apparatus and induces immune cell death; EspP is an autotransporter serine-protease which contributes to biofilm formation and host defense modulation.