Mutant fixation in the presence of a natural enemy

Abstract

In the extensive literature about mutant invasion and fixation, populations are typically assumed to exist in isolation from their ecosystem. Yet, populations are part of ecological communities, and enemy-victim (e.g. predator-prey or pathogen-host) dynamics are particularly common. We use computational models to re-visit the established theory about mutant fixation in the presence of a natural enemy, which equally attacks both wild-type and mutant populations. We consider advantageous and disadvantageous mutants, whose fitness is unrelated to the infection. Using spatially structured agent-based as well as patch models of a population that is subject to infection, we investigate the fixation probability of a mutant that is introduced into the population at quasi-equilibrium. We find that infection significantly weakens selection. Thus, the presence of infection increases the fixation probability of disadvantageous mutants and decreases the fixation probability of advantageous mutants, with the magnitude of the effect rising with the infection rate. We show that this occurs because infection induces spatial structures, in which mutant and wild-type individuals are mostly spatially separated. Thus, instead of mutant and wild-type individuals competing with each other, it is mutant and wild-type 'patches' that compete, resulting in smaller fitness differences and hence weakened selection. Because natural enemies such as infections are ubiquitous, this has broad applicability to natural systems. Our results imply that the burden of deleterious mutants in natural populations might be significantly higher than expected from mutant invasion theory developed in the absence of natural enemies.

Compartmental structure in the secondary lymphoid tissue can slow downin vivoHIV-1 evolution in the presence of strong CTL responses

“…Mutant fixation probabilities are well-understood in constant population models [45], such as the Moran or Fisher Wright processes, and a subdivision of the population into equally sized demes has not been found to alter mutant fixation probabilities under assumptions that are applicable here [35–37]. Subdivision of populations into demes of unequal sizes, however, has been found to weaken selection [45], and predator-prey type population fluctuations have been shown to also weaken selection [46]. Since both aspects apply to our current scenario, we investigated the fixation probability of an advantageous mutant in our model.…”

“…Two forces apply to our system that can in principle account for the weakened selection observed in our simulations (compared to standard Moran process predictions). These are population fluctuations brought about by the CTL response (predator-prey dynamics, [46]), and the population structure involving two demes with unequal population sizes [47]. In the one-compartment control model, CTL-induced fluctuations in the infected cell population appears to drive the reduced mutant fixation probabilities for stronger CTL responses (Figure 1).…”