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While the conditions that favour the maintenance of cooperation have been extensively investigated, the significance of non-social selection pressures on social behaviours has received little attention. In the absence of non-social selection pressures, patches of cooperators are vulnerable to invasion by cheats. However, we show both theoretically, and experimentally with the bacterium Pseudomonas fluorescens, that cheats may be unable to invade patches of cooperators under strong non-social selection (both a novel abiotic environment and to a lesser extent, the presence of a virulent parasite). This is because beneficial mutations are most likely to arise in the numerically dominant cooperator population. Given the ubiquity of novel selection pressures on microbes, these results may help to explain why cooperation is the norm in natural populations of microbes. [ABSTRACT FROM AUTHOR]

To many pathogenic bacteria, human hosts are an evolutionary dead end. This begs the question what evolutionary forces have shaped their virulence traits. Why are these bacteria so virulent? The coincidental evolution hypothesis suggests that such virulence factors result from adaptation to other ecological niches. In particular, virulence traits in bacteria might result from selective pressure exerted by protozoan predator. Thus, grazing resistance may be an evolutionarily exaptation for bacterial pathogenicity. This hypothesis was tested by subjecting a well characterized collection of 31 Escherichia coli strains (human commensal or extra-intestinal pathogenic) to grazing by the social haploid amoeba Dictyostelium discoideum. We then assessed how resistance to grazing correlates with some bacterial traits, such as the presence of virulence genes. Whatever the relative population size (bacteria/amoeba) for a non-pathogenic bacteria strain, D. discoideum was able to phagocytise, digest and grow. In contrast, a pathogenic bacterium strain killed D. discoideum above a certain bacteria/ amoeba population size. A plating assay was then carried out using the E. coli collection faced to the grazing of D. discoideum. E. coli strains carrying virulence genes such as iroN, irp2, fyuA involved in iron uptake, belonging to the B2 phylogenetic group and being virulent in a mouse model of septicaemia were resistant to the grazing from D. discoideum. Experimental proof of the key role of the irp gene in the grazing resistance was evidenced with a mutant strain lacking this gene. Such determinant of virulence may well be originally selected and (or) further maintained for their role in natural habitat: resistance to digestion by free-living protozoa, rather than for virulence per se. [ABSTRACT FROM AUTHOR]

Understanding the effect of multiple infections is essential for the prediction (and eventual control) of virulence evolution. Some theoretical studies have considered the possibility that several strains coexist in the same host (coinfection), but few have taken their within-host dynamics explicitly into account. Here, we develop a nested approach based on a simple model for the interaction of parasite strains with their host's immune system. We study virulence evolution by linking the within-host dynamics to an epidemiological framework that incorporates multiple infections. Our model suggests that antigenically similar parasite strains cannot coexist in the long term inside a host. We also find that the optimal level of virulence increases with the efficiency of multiple infections. Finally, we notice that coinfections create heterogeneity in the host population (with susceptible hosts and infected hosts), which can lead to evolutionary branching in the parasite population and the emergence of a hypervirulent parasite strategy. We interpret this result as a parasite specialization to the infectious state of the hosts. Our study has experimental and theoretical implications in a virulence management perspective. [ABSTRACT FROM AUTHOR]

Spatial self-structuring has been a focus of recent interest among evolutionary ecologists. We review recent developments in the study of the interplay between spatial self-structuring and evolution. We first discuss the relative merits of the various theoretical approaches to spatial modelling in ecology. Second, we synthesize the main theoretical studies of the evolution of cooperation in spatially structured populations. We show that population viscosity is generally beneficial to cooperation, because cooperators can reap additional benefits from being clustered. A similar mechanism can explain the evolution of honest communication and of reduced virulence in host–parasite interactions. We also discuss some recent innovative empirical results that test these theories. Third, we show the relevance of these results to the general field of evolutionary ecology. An important conclusion is that kin selection is the main process that drives evolution of cooperation in viscous populations. Many results of kin selection theory can be recovered as emergent properties of spatial ecological dynamics. We discuss the implications of these results for the study of multilevel selection and evolutionary transitions. We conclude by sketching some perspectives for future research, with a particular emphasis on the topics of evolutionary branching, criticality, spatial fluctuations and experimental tests of theoretical predictions. Space is the place – Sun Ra [ABSTRACT FROM AUTHOR]

Most models of virulence evolution assume that a parasite cannot raise its transmission rate without causing more harm to its host. However, the existence of such trade-off relationships has recently been challenged. Here, we study how a trade-off can emerge from a model that explicitly incorporates within-host dynamics. We find that the existence and the convexity of the trade-off are robust, which implies a definite level of evolutionarily stable virulence (ESV) for the parasite. However, we also show that the dependence of the ESV on parameter values may be very strong. One possible consequence of this sensitivity is that relationships between transmission and virulence observed across populations need not conform to the patterns expected on the basis of a common (fixed) trade-off. We discuss possible experiments and implications of our results for the development of virulence management strategies. [ABSTRACT FROM AUTHOR]

We analyze the evolutionary consequences of host resistance (the ability to decrease the probability of being infected by parasites) for the evolution of parasite virulence (the deleterious effect of a parasite on its host). When only single infections occur, host resistance does not affect the evolution of parasite virulence. However, when superinfections occur, resistance tends to decrease the evolutionarily stable (ES) level of parasite virulence. We first study a simple model in which the host does not coevolve with the parasite (i.e., the frequency of resistant hosts is independent of the parasite). We show that a higher proportion of resistant host decreases the ES level of parasite virulence. Higher levels of the efficiency of host resistance, however, do not always decrease the ES parasite virulence. The implications of these results for virulence management (evolutionary consequences of public health policies) are discussed. Second, we analyze the case where host resistance is allowed to coevolve with parasite virulence using the classical gene-for-gene (GFG) model of host-parasite interaction. It is shown that GFG coevolution leads to lower parasite virulence (in comparison with a fully susceptible host population). The model clarifies and relates the different components of the cost of parasitism: infectivity (ability to infect the host) and virulence (deleterious effect) in an evolutionary perspective. [ABSTRACT FROM AUTHOR]

Examines the dynamics of multiple infection and the evolution of virulence. Conflict of interest among clones sharing a host; Force of infection when double infections are frequent; Dependence of stable strategy virulence on the interaction within hosts.