Virulence evolution at the front line of spreading epidemics

Abstract

Understanding and predicting the spatial spread of emerging pathogens is a major challenge for the public health management of infectious diseases. Theoretical epidemiology shows that the speed of an epidemic is governed by the life-history characteristics of the pathogen and its ability to disperse. Rapid evolution of these traits during the invasion may thus affect the speed of epidemics. Here we study the influence of virulence evolution on the spatial spread of an epidemic. At the edge of the invasion front, we show that more virulent and transmissible genotypes are expected to win the competition with other pathogens. Behind the front line, however, more prudent exploitation strategies outcompete virulent pathogens. Crucially, even when the presence of the virulent mutant is limited to the edge of the front, the invasion speed can be dramatically altered by pathogen evolution. We support our analysis with individual-based simulations and we discuss the additional effects of demographic stochasticity taking place at the front line on virulence evolution. We confirm that an increase of virulence can occur at the front, but only if the carrying capacity of the invading pathogen is large enough. These results are discussed in the light of recent empirical studies examining virulence evolution at the edge of spreading epidemics.

Spatial evolutionary epidemiology of spreading epidemics

“…Because it allows us to shed light on the effect of genetic structure, our approach differs from previous works based on partial differential equations [18][19][20]39]. Indeed, models based on partial differential equations assume implicitly that local population sizes are very large.…”

“…By contrast, our framework considers finite local population sizes and, therefore, allows us to take into account genetic structure in the population through generalized coefficients of relatedness. On the other hand, a major advantage of reaction-diffusion models over our theoretical framework is that they allow the computation of the speed of the invasion wave [20]. Although attempts have been made to compute invasion speed using spatial moment equations (e.g.…”

“…Several experimental studies using microbial systems support this prediction [15][16][17]. Second, recent attempts have been made to model pathogen evolution in spatially spreading epidemics [18][19][20][21][22]. These studies show that selection at the frontline of the epidemics is very different than near an endemic equilibrium.…”

“…First, the build-up of differentiation is driven by the quantity fq S=SI À q S=I which is expected to be high in the early stage of a spreading epidemic. The abundance of SSI triplets at the frontline of epidemics generates differentiation because selection for transmission is particularly high at the tip of the front [20]. Second, relatedness between strains located one or two sites away can also affect differentiation in this model.…”

Short Rotations in Forest Plantations Accelerate Virulence Evolution in Root-Rot Pathogenic Fungi

“…Despite still imprecise experimental characterizations, mainly based on proxies, and a complex theory including the transmission-virulence trade-off hypothesis [14], the evolution at this trait is thought to be tightly related to the spread of diseases [11,15,16]. This evolutionary perspective, together with the large spatio-temporal scales considered in forestry and the often numerous uncertainties about the biology of the pathogens, make integrative experimental assessments of the effects of common forestry practices on fungal pathogen populations hardly feasible.…”