Escherichia coli expresses type-I fimbriae; these are protrusions from the outer cell wall and have been identified as a virulence factor. They are also expressed by commensal strains of E. coli although (at any one time) only by a small proportion of the population. The orthodox interpretation of this is that fimbriation is regulated so as (i) to trigger a host-based release of nutrients in the form of inflammation signals by slightly activating host defenses and (ii) while avoiding a full scale inflammatory response. This article presents a number of computer simulations of the evolution of fimbriae to scrutinize the evolutionary plausibility of this orthodox view. It turns out that these simulations suggest a revised interpretation of the fimbriae mediated parasitehost interaction. Rather than being a passive victim the host is actively providing a niche that evolutionary favors less virulent parasites. The article closes with a number of testable predictions of this model
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