A number of ecologically and economically important pathogens exhibit a complex transmission dynamics that involves distinct transmission modes. In this paper, we study the evolutionary dynamics of pathogens for which transmission includes direct host-to-host as well as indirect environmental transmission. Different routes of infection spread require specific adaptations of the parasite, which may result in conflicting selection pressures. Using the framework of Adaptive dynamics, we investigate how these conflicting selection pressures are resolved in the course of evolution and determine the conditions for evolutionary diversification of pathogen strains. We show that evolutionary branching and subsequent evolution of specialist strains occurs in wide parameter regions but evolutionary bi-stability and evolution of generalist pathogens are possible as well. Our analysis reveals that the relative contributions of direct and environmental transmission, as well as the underlying ecological dynamics, play a crucial role in shaping the course of pathogen evolution. Our findings may explain the coexistence of high and low virulence strains observed in several pathogenic organisms using different transmission modes (e.g., influenza viruses) and highlight the importance of considering ecological dynamics in virulence management.
COBISS.SI-ID: 1024420948
A virus infecting a host faces a heterogeneous and a spatially structured environment. Using a mathematical model that incorporates two types of target cells and spatial structuring, we investigate conditions for viral within-host diversification. We show that branching occurs for a wide range of parameters but that it always requires some spatial structure. Applying our model to the case of HIV, we show that it captures three main properties of the co-receptor switch observed in many HIV infections: the initial dominance of virus strains that infect CCR5+ cells, the late switch in some (but, importantly, not all) HIV infections and the associated drop in the number of uninfected T-cells. This suggests that the co-receptor switch could result from gradual adaptation of the virus population to target cell heterogeneity. More generally, we argue that evolutionary ecology can help us better understand the course of some infections.
COBISS.SI-ID: 1024287316
We study the adaptive dynamics of virulence of a pathogen transmitted both via direct contacts between hosts and via free pathogens that survive in the environment. The model is very flexible with a number of trade-off functions linking virulence to other pathogen-related parameters and with two incidence functions that describe the contact rates between hosts and between a host and free pathogens. Instead of making a priori particular assumptions about the shapes of these functions, we introduce a construction method to create specific pairs of incidence functions such that the model becomes an optimization model. Unfolding the optimization model leads to coexistence of pathogen strains and evolutionary branching of virulence. The construction method is applicable to a wide range of eco-evolutionary models.
COBISS.SI-ID: 1024441940
The existing classification of evolutionarily singular strategies in Adaptive Dynamics assumes an invasion exponent that is differentiable twice as a function of both the resident and the invading trait. Motivated by nested models for studying the evolution of infectious diseases, we consider an extended framework in which the selection gradient exists (so the definition of evolutionary singularities extends verbatim), but where the invasion fitness may lack the smoothness necessary for the classification `a la Geritz et al. We derive the classification of singular strategies with respect to their convergence stability and invasibility and determine the condition for the existence of nearby dimorphisms. In addition to evolutionarily stable strategies (ESSs) and invadable strategies, we observe what we call one-sided ESSs: singular strategies that are invadable from one side of the singularity but uninvadable from the other. Studying the regions of mutual invasibility in the vicinity of a one-sided ESS, we discover that two isoclines spring in a tangent manner from the singular point at the diagonal of the Mutual Invasibility Plot. The curvature of the two isoclines (i.e. the way in which they unfold) determines whether these onesided ESSs act as ESSs or as branching points. Since the curvature is not uniquely determined by the monomorphic invasion exponent we conclude that, contrary to the standard setting of Adaptive Dynamics, the fate of dimorphisms nearby a singular strategy can, in general, not be deduced from the monomorphic invasion exponent. We demonstrate our findings on a specific example from evolutionary epidemiology.
We investigate eco-evolutionary cycles in the joint dynamics of pathogen virulence and predator population density when hosts carrying virulent infections are exposed to increased risk of predation. We introduce a new technique to find trade-off functions under which the model exhibits limit cycles; this technique provides a constructive proof that the system is able to generate limit cycles, and can be applied to other eco-evolutionary models as well. We also study a concrete example in detail to confirm that eco-evolutionary cycles occur in a significant part of the parameter space and to briefly explore other evolutionary outcomes in the same model.