In the face of infectious disease, organisms evolved a range of defense mechanisms, with a clear distinction between those that are constitutive (always active) and those that are inducible (elicited by parasites). Both defense strategies have evolved from each other, but we lack an understanding of the conditions that favor one strategy over the other. While it is hard to generalize about their degree of protection, it is possible to make generalizations about their associated fitness costs, which are commonly detected. By definition, constitutive defenses are always "on," and are therefore associated with a fixed cost, independent of parasite exposure. Inducible defenses, on the other hand, may lack costs in the absence of parasites but become costly when defense is elicited through processes such as immunopathology. Bacteria can evolve constitutive defense against phage by modification/masking of surface receptors, which is often associated with reduced fitness in the absence of phage. Bacteria can also evolve inducible defense using the CRISPR-Cas (clustered regularly interspaced short palindromic repeat, CRISPR associated) immune system, which is typically elicited upon infection. CRISPR-Cas functions by integrating phage sequences into CRISPR loci on the host genome. Upon re-infection, CRISPR transcripts guide cleavage of phage genomes. In nature, both mechanisms are important. Using a general theoretical model and experimental evolution, we tease apart the mechanism that drives their evolution and show that infection risk determines the relative investment in the two arms of defense.
Hosts have evolved a diverse range of defence mechanisms in response to challenge by infectious organisms (parasites and pathogens). Whether defence is through avoidance of infection, control of the growth of the parasite once infected, clearance of the infection, tolerance to the disease caused by infection or innate and/or acquired immunity, it will have important implications for the population ecology (epidemiology) of the host-parasite interaction. As a consequence, it is important to understand the evolutionary dynamics of defence in the light of the ecological feedbacks that are intrinsic to the interaction. Here, we review the theoretical models that examine how these feedbacks influence the nature and extent of the defence that will evolve. We begin by briefly comparing different evolutionary modelling approaches and discuss in detail the modern game theoretical approach (adaptive dynamics) that allows ecological feedbacks to be taken into account. Next, we discuss a number of models of host defence in detail and, in particular, make a distinction between 'resistance' and 'tolerance'. Finally, we discuss coevolutionary models and the potential use of models that include genetic and game theoretical approaches. Our aim is to review theoretical approaches that investigate the evolution of defence and to explain how the type of defence and the costs associated with its acquisition are important in determining the level of defence that evolves.
There is an increasing recognition that evolutionary processes play a key role in determining the dynamics of range expansion. Recent work demonstrates that neutral mutations arising near the edge of a range expansion sometimes surf on the expanding front leading them rather than that leads to reach much greater spatial distribution and frequency than expected in stationary populations. Here, we extend this work and examine the surfing behavior of nonneutral mutations. Using an individual-based coupled-map lattice model, we confirm that, regardless of its fitness effects, the probability of survival of a new mutation depends strongly upon where it arises in relation to the expanding wave front. We demonstrate that the surfing effect can lead to deleterious mutations reaching high densities at an expanding front, even when they have substantial negative effects on fitness. Additionally, we highlight that this surfing phenomenon can occur for mutations that impact reproductive rate (i.e., number of offspring produced) as well as mutations that modify juvenile competitive ability. We suggest that these effects are likely to have important consequences for rates of spread and the evolution of spatially expanding populations.
Tolerance and resistance provide hosts with two distinct defense strategies against parasitism. In resistance the hosts ''fight'' the parasite directly, whereas in tolerance the hosts fight the disease by ameliorating the damage that infection causes. There is increasing recognition that the two mechanisms may exhibit very different evolutionary behaviors. Although empirical work has often noted considerable variance in tolerance within hosts, theory has predicted the fixation of tolerance due to positive frequency dependence through a feedback with disease prevalence. Here we reconcile these findings through a series of dynamic game theoretical models. We emphasize that there is a crucial distinction between tolerance to the effects of disease-induced mortality and tolerance to the effect of the disease-induced reductions in fecundity. Only mortality tolerance has a positive effect on parasite fitness, whereas sterility tolerance is neutral and may therefore result in polymorphisms. The nature of the costs to defense and their relationship to trade-offs between resistance and tolerance are crucial in determining the likelihood of variation, whereas the co-evolution of the parasite will not affect diversity. Our findings stress that it is important to measure the effects of different mechanisms on characteristics that affect the epidemiology of the parasite to completely understand the evolutionary dynamics of defense.tolerance ͉ resistance ͉ genetic variation ͉ evolutionary branching
Due to the importance of infectious disease, there is a large body of theory on the evolution of either hosts or, more commonly, parasites. Here we present a fully coevolutionary model of a host-parasite system that includes ecological dynamics that feed back into the coevolutionary outcome, and we show that highly virulent parasites may evolve due to the coevolutionary process. Parasite evolution is very sensitive to evolution in the host, and virulence fluctuates substantially when mutation rates vary between host and parasite. Evolutionary branching in the host leads to parasites increasing their virulence, and small changes in host resistance drive large changes in parasite virulence. Evolutionary branching in one species does not cause branching in the other. Our work emphasizes the importance of considering coevolutionary dynamics and shows that certain highly virulent parasites may result from responses to host evolution.
Understanding the coevolution of hosts and parasites is one of the key challenges for evolutionary biology. In particular, it is important to understand the processes that generate and maintain variation. Here, we examine a coevolutionary model of hosts and parasites where infection does not depend on absolute rates of transmission and defense but is approximately all-or-nothing, depending on the relative levels of defense and infectivity of the host and the parasite. We show that considerable diversity can be generated and maintained because of epidemiological feedbacks, with strains differing in the range of host and parasite types they can respectively infect or resist. Parasites with broad and narrow ranges therefore coexist, as do broadly and narrowly resistant hosts, but this diversity occurs without the assumption of highly specific gene interactions. In contrast to gene-for-gene models, cycling in strain types is found only under a restrictive set of circumstances. The generation of diversity in both hosts and parasites is dependent on the shape of the trade-off relationships but is more likely in long-lived hosts and chronic disease with long infectious periods. Overall, our model shows that significant diversity in infectivity and resistance range can evolve and be maintained from initially monomorphic populations.
Natural, agricultural and human populations are structured, with a proportion of interactions occurring locally or within social groups rather than at random. This within-population spatial and social structure is important to the evolution of parasites but little attention has been paid to how spatial structure affects the evolution of host resistance, and as a consequence the coevolutionary outcome. We examine the evolution of resistance across a range of mixing patterns using an approximate mathematical model and stochastic simulations. As reproduction becomes increasingly local, hosts are always selected to increase resistance. More localized transmission also selects for higher resistance, but only if reproduction is also predominantly local. If the hosts disperse, lower resistance evolves as transmission becomes more local. These effects can be understood as a combination of genetic (kin) and ecological structuring on individual fitness. When hosts and parasites coevolve, local interactions select for hosts with high defence and parasites with low transmissibility and virulence. Crucially, this means that more population mixing may lead to the evolution of both fast-transmitting highly virulent parasites and reduced resistance in the host.
Victims of infection are expected to suffer increasingly as parasite population growth increases. Yet, under some conditions, faster growing parasites do not appear to cause more damage and infections can be quite tolerable. We studied these conditions by assessing how the relationship between parasite population growth and host health is sensitive to environmental variation. In experimental infections of the crustacean Daphnia magna and its bacterial parasite Pasteuria ramosa we show how easily an interaction can shift from a severe interaction, i.e. when host fitness declines substantially with each unit of parasite growth, to a tolerable relationship by changing only simple environmental variables: temperature and food availability. We explored the evolutionary and epidemiological implications of such a shift by modelling pathogen evolution and disease spread under different levels of infection severity, and find that environmental shifts that promote tolerance ultimately result in populations harbouring more parasitized individuals. We also find that the opportunity for selection, as indicated by the variance around traits, varied considerably with the environmental treatment. Thus our results suggest two mechanisms that could underlie co-evolutionary hot-and coldspots: spatial variation in tolerance and spatial variation in the opportunity for selection.
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