Speaker
Description
Commensal bacteria are also often major opportunistic pathogens with important public health consequences. For example, Escherichia coli colonises the gut of all humans and occasionally causes intestinal and extra-intestinal infections responsible for ~1M deaths worldwide each year. The colonization of hosts by E. coli is a highly dynamical process with strain turnover in the gut over timescales of weeks to months. Coexistence of multiple strains is seen at multiple levels from intra-host to the inter-host (epidemiological) level. Intriguingly, we do not know much about the bacterial genetic factors involved in colonisation and how they evolve. Several virulence genes (genes increasing the propensity of the bacteria to cause infection, that are present or absent) are associated with longer persistence in the host. This rises several questions: what explains the intermediate frequency of these genes in spite of their apparent fitness advantage? Are there other benefits or costs associated with virulence genes? Here we develop an epidemiological and evolutionary model describing the colonisation dynamics of commensal bacteria such as E. coli, including events of colonization, strain replacement and strain loss. We first delineate the conditions in which strains with and without virulence genes can coexist thanks to different colonization strategies. Second, we re-analyse a large dataset with longitudinal follow-up of healthy children to infer the colonization strategies associated with several virulence genes and quantify their fitness advantage. This work sheds light on the epidemiological and evolutionary factors shaping the diversity of bacterial virulence genes.
