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In kin selection theory in the evolution of social behaviours, the relatedness between interacting individuals is influenced by the spatial structure of the population. It is generally considered that in the 'viscous' population competition among individuals tends to suppress the evolution of altruism. We consider that more complex interactions produce specific spatial patterns in the presence of competitive interaction, which could alter the process of kin selection in a given space. Here, we theoretically studied the joint evolution of altruism and resource exploitation in a spatially structured population. The simulations indicated that joint evolution can result in self-organisation of regularly arranged cluster structures, which creates a new 'level of selection', and significantly promotes the evolution of altruism through a promotion of kin selection. The analysis also suggested synergetic effects of the joint evolution of two traits, including an evolutionary suicide of the population.

International audience; Information is a crucial currency for living organisms as it allows them to adjust their behaviour to environmental fluctuations. Thus, natural selection should have favoured the capacity of collecting information from different sources, including social interactions whereby individuals could quickly gain reliable information. However, such conditions may also favour the gathering of potentially detrimental information, such as false or misinterpreted accounts of environmental and social phenomena such as rumours, which may spread via informational cascades. We applied ecological and evolutionary principles to investigate how the propagation of social information at a populational level affects the propensity to assimilate it, here defined as the gullibilty. Our results show that the evolution of an individual's susceptibility to assimilate information strongly depends on eco-evolutionary feedbacks, in particular when both useful and detrimental information circulate. We discuss our results regarding the different information transmission mechanisms involved with particular attention to specific cases of social learning.

Solving the markov chain presented in Section 3; Finding the optimum gullibility in Section 3

Information plays an important role not only in evolution—genetics can be seen as a mechanism to transfer information from one generation to the next—but also in ecology: virtually all organisms use information about their environment to adjust their behavior and life histories. Indeed, being adapted to something can be defined as having the right information to solve the life-history problems that this creates. It then becomes irrelevant precisely where this information came from (genetics, experience, culture, etc.) but rather becomes an issue of how to assess the fitness value of this information. Here I will explore in some detail the conceptual consequences of the information-based view of evolution. In particular, I will focus on how individuals are actually associations of smaller units that depend on each other’s genetic information and on information from multiple external sources. An important and fundamental problem arises when these different sources of information do not suggest the same adaptations. Conflicting information may thus give new insight into the causes of stress.

Bacteria produce a great diversity of siderophores to scavenge for iron in their environment. We suggest that this diversity results from the interplay between siderophore producers (cooperators) and non-producers (cheaters): when there are many cheaters exploiting a siderophore type it is beneficial for a mutant to produce a siderophore unusable by the dominant population. We formulated and analysed a mathematical model for tagged public goods to investigate the potential for the emergence of diversity. We found that, although they are rare most of the time, cheaters play a key role in maintaining diversity by regulating the different populations of cooperators. This threshold-triggered feedback prevents any stain of cooperators from dominating the others. Our study provides a novel general mechanism for the evolution of diversity that may apply to many forms of social behaviour.

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.

Offspring quality and quantity are subject to a trade-off. Depending on species, ant colonies can produce either numerous winged queens that start new colonies alone (independent colony foundation [ICF]) or one propagule consisting of reproductives helped by workers (fission). Some species do both. In the Rhytidoponera impressa group, colonies with winged queens use ICF, whereas colonies with mated workers use fission. We assessed the effect of latitude and environment on colonial reproduction by collecting 79 colonies along the Australian east coast. A population dynamical model predicted that from tropical north to temperate south, seasonal fluctuations and harsher conditions should lead to a decrease in ICF success (-48%), making fission a suitable alternative. Yet, our empirical data showed that ICF persists at a higher rate than expected, presumably because it allows aerial dispersal, unlike fission. Investigation of colony demography and measurement of lean and fat weights in virgin winged queens and workers showed that, from north to south, colonies increase quality of queens relative to workers (+50%) at the cost of quantity (-86%). This modification limits the decrease in ICF success (-34%). A tremendous range of offspring phenotypes associated with quality-quantity trade-offs make ants competitive in diverse habitats.

Like many other bacteria, Pseudomonas aeruginosa sequesters iron from the environment through the secretion, and subsequent uptake, of iron-binding molecules. As these molecules can be taken up by other bacteria in the population than those who secreted them, this is a form of cooperation through a public good. Traditionally, this problem has been studied by comparing the relative fitnesses of siderophore-producing and non-producing strains, but this gives no information about the fate of strains that do produce intermediate amounts of siderophores. Here, we investigate theoretically how the amount invested in this form of cooperation evolves. We use a mechanistic description of the laboratory protocols used in experimental evolution studies to describe the competition and cooperation of the bacteria. From this dynamical model we derive the fitness following the adaptive dynamics method. The results show how selection is driven by local siderophore production and local competition. Because siderophore production reduces the growth rate, local competition decreases with the degree of relatedness (which is a dynamical variable in our model). Our model is not restricted to the analysis of small phenotypic differences and allows for theoretical exploration of the effects of large phenotypic differences between cooperators and cheats. We predict that an intermediate ESS level of cooperation (molecule production) should exist. The adaptive dynamics approach allows us to assess evolutionary stability, which is often not possible in other kin-selection models. We found that selection can lead to an intermediate strategy which in our model is always evolutionarily stable, yet can allow invasion of strategies that are much more cooperative. Our model describes the evolution of a public good in the context of the ecology of the microorganism, which allows us to relate the extent of production of the public good to the details of the interactions.

We present a general epidemiological model of host-parasite interactions that includes various forms of superinfection. We use this model to study the effects of different host life-history traits on the evolution of parasite virulence. In particular, we analyze the effects of natural host death rate on the evolutionarily stable parasite virulence. We show that, contrary to classical predictions, an increase in the natural host death rate may select for lower parasite virulence if some form of superinfection occurs. This result is in agreement with the experimental results and the verbal argument presented by Ebert and Mangin (1997). This experiment is discussed in the light of the present model. We also point out the importance of superinfections for the effect of nonspecific immunity on the evolution of virulence. In a broader perspective, this model demonstrates that the occurrence of multiple infections may qualitatively alter classical predictions concerning the effects of various host life-history traits on the evolution of parasite virulence.

The occurrence of polygyny and polyandry in social insects has long puzzled evolutionary biologists. If cooperation requires genetic relatedness, how do we explain the occurrence and maintenance of mechanisms that reduce the degree of relatedness among colony members? A much‐discussed hypothesis states that genetically diverse colonies are more resistant to parasitism than homogenous colonies because genetic diversity reduces the spread of a disease within a colony. However, as we will argue in this note, a necessary condition for the parasite hypothesis is that genetically heterogeneous colonies have a larger suite of parasites that are capable of infecting them. This implicit relationship is important because it implies that even if the cost per infection is reduced, this may not be sufficient to offset the increased rate of acquiring infections. The advantages of genetic heterogeneity as a defense against parasites thus may not be as big as commonly thought.

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.

Recent studies indicate that the time required for virus-infected cells to become vulnerable for the activity of CTL is of significance for the capacity of CTL to control ongoing viral reproduction. To investigate whether this applies to the effectiveness of HIV-1-specific CTL, we measured virus production in cultures containing CD4(+) T cells inoculated with HIV at low multiplicity of infection, and CTL directed against an early protein, Rev, or a late protein, RT. The Rev-specific CTL prevented at least 2 log(10) more HIV-1 production, in 10 days, than similar numbers of RT-specific CTL. To study how CTL effectiveness depends on variations in the potency of effector functions and kinetics of HIV protein expression, we developed a mathematical model describing CTL-target cell interactions during successive infection cycles. The results show that substantially higher CTL-mediated target cell elimination rates are required to achieve control as there is less time for CTL to act before infected cells release progeny virions. Furthermore, in vitro experiments with HIV recombinant viruses showed that the RT-specific CTL were at least as effective as the Rev-specific CTL, but only if the RT epitope was expressed as part of the early protein Nef. Together these results indicate that CTL control ongoing HIV reproduction more effectively if they are able to recognize infected cells earlier during individual viral replication cycles. This provides rationale for immunization strategies that aim at inducing, boosting or skewing CTL responses to early regulatory proteins in AIDS vaccine development.

It is well known that most organisms are composed of smaller subunits, including not only cells and semi-independent organelles but often also a whole suite of parasites, commensal organisms, and other symbionts (Buss 1987; Margulis 1970; Bouchard and Huneman 2013). The process of association of these subunits has been recognized as contributing to many of the major transitions that have occurred in the course of evolution (Maynard Smith and Szathmary 1995; Michod 1999). As a result, the selective forces that have led to the subunits foregoing their evolutionary sovereignty are being better appreciated (van Baalen and Jansen 2001), but little is known yet about the mechanisms that maintain the dynamic coherence of the associations. In this respect there are many parallels with classical ecological questions. In spite of the fact that the processes that dynamically generate and maintain biodiversity in ecosystems (competition, herbivory, predation, parasitism, and so forth) are quite well known, we still have difficulty in understanding and predicting the outcome. This parallel is obvious if one considers the history of the disciplines. Biologists and philosophers of biology have long been concerned with the status of associations of entities that are not stricto sensu organisms, but look like organisms at least as much as they look like collectives: ant colonies, wasp colonies (Seeley 1995; Holldobler and Wilson 2008), termite mounds (Turner 2000), Portuguese men-of-war, slime molds (Bonner 1959), etc. The insight that organisms can be composed of other organisms is quite old, and dates back to the concept of ‘‘superorganism’’ already developed by the geologist Hutton in the 18th century. Since then, the idea has resurfaced multiple times, for instance, from the ecologist Clements (1916), following Forbes (1887) who suggested that lakes are microcosms, and more recently in Lovelock’s Gaia hypothesis. Sober and Wilson (1998) reinitiated a discussion on precisely what superorganisms are (Bouchard 2010). This includes questions such as whether they are really targets of selection just like organisms (Gardner and Grafen 2009), and how they come into being (Reeve and Holldobler 2007). Some evolutionary biologists argue, however, that the very concept of superorganism is unnecessary and can be replaced by a more general understanding of organism (Queller and Strassmann 2009). Ecologists such as Clements were concerned by the fact that ecosystems (or at least some of them) seem to behave in a functionally unified and coherent way, with feedback loops, division of labor, regulations, and other features supposed to be characteristic of metazoan organisms. The notion of a ‘‘superorganism’’ thus carries at least implicitly a link with ecology. However, history proved to be on the other side–with those who, with Gleason (1926) and against Clements, argued that nothing special makes an ecosystem cohesive, and that the assemblage of species in a community does not reflect any kind of organicity. Ecological theory as it further unfolded in the 1950s and ’60s (e.g., Hutchinson, MacArthur and Wilson, etc.) was built upon the notions of population, community, and ecosystem without using the concept of superorganism. M. van Baalen (&) Eco-Evolutionary Mathematics, Institut Biologie de l’Ecole Normale Superieure (UMR 8197), CNRS, Paris, France e-mail: minus.van.baalen@ens.fr

The social amoebaDictyostelium discoideumis widely studied for its multicellular development program as a response to starvation and constitutes a model of choice in microbial cooperation studies. Aggregates of up to 106cells form fruiting bodies containing two cell types: (i) dormant spores (~80%) that can persist for months in the absence of nutrients, and (ii) dead stalk cells (~20%) that promote the dispersion of the spores towards nutrient-rich areas.It is often overlooked that not all cells aggregate upon starvation. Using a new quantitative approach based on time-lapse fluorescence microscopy and a low ratio of reporting cells, we have quantified this fraction of non-aggregating cells. In realistic starvation conditions, up to 15% of cells do not aggregate, which makes this third cell fate a significant component of the population-level response of social amoebae to starvation. Non-aggregating cells have an advantage over cells in aggregates since they resume growth earlier upon arrival of new nutrients, but have a shorter lifespan under prolonged starvation. We find that phenotypic heterogeneities linked to cell nutritional state bias the representation of cells in the aggregating vs. non-aggregating fractions, and thus regulate population partitioning. Next, we report that the fraction of non-aggregating cells depends on genetic factors that regulate the timing of starvation, signal sensing efficiency and aggregation efficiency. In addition, interactions between clones in mixtures of non-isogenic cells affect the partitioning of each clone into both fractions. We further test the evolutionary significance of the non-aggregating cell fraction. The partitioning of cells into aggregating and non-aggregating fractions is optimal in fluctuating environments with an unpredictable duration of starvation periods.D. discoideumthus constitutes a model system lying at the intersection of microbial cooperation and bet hedging, defining a new frontier in microbiology and evolution studies

Many ecological interactions that are called mutualistic are in fact mixtures of antagonistic and mutualistic aspects. For example, plasmids exploit their bacterial hosts but also protect them against external threats. In this study, we analyse the conditions for the evolution of what we call ‘dangerous liaisons’: interactions combining mutualistic and antagonistic aspects. Starting point of our analysis is a model that was proposed as early as 1934. In this model, partners have to form a complex (either temporary or long lasting) in order to interact. Using this model framework we then set out to define and tease apart private interests of the interacting partners from their common good. This dichotomy provides a unifying perspective to classify ecological interactions. We discuss some examples to illustrate how the outcome of the interaction may depend on densities or on other contextual variables. Finally, we note that having a common good is not a necessary condition for partners to have aligned interests. In a dangerous liaison partners may have interest to cooperate even when this does not bolster the common good.

Bacteria produce a great diversity of siderophores to scavenge for iron in their environment. We suggest that this diversity results from the interplay between siderophore producers (cooperators) and non-producers (cheaters): when there are many cheaters exploiting a siderophore type it is beneficial for a mutant to produce a siderophore unusable by the dominant population. We formulated and analysed a mathematical model for tagged public goods to investigate the potential for the emergence of diversity. We found that, although they are rare most of the time, cheaters play a key role in maintaining diversity by regulating the different populations of cooperators. This threshold-triggered feedback prevents any stain of cooperators from dominating the others. Our study provides a novel general mechanism for the evolution of diversity that may apply to many forms of social behaviour.

International audience; Arising from M. A. Nowak, C. E. Tarnita & E. O. Wilson 466, 1057-1062 (2010); Nowak et al. reply. Nowak et al. argue that inclusive fitness theory has been of little value in explaining the natural world, and that it has led to negligible progress in explaining the evolution of eusociality. However, we believe that their arguments are based upon a misunderstanding of evolutionary theory and a misrepresentation of the empirical literature. We will focus our comments on three general issues.

International audience; 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.

International audience; We study the evolution of a spatially structured population with two age classes using spatial moment equations. In the model, adults can either help juveniles by increasing their survival, or adopt a cannibalistic behaviour and consume juveniles. While cannibalism is the sole evolutionary outcome when the population is well-mixed, both cannibalism and parental care can be evolutionarily stable if the population is viscous. Our analysis allows us to make two main technical points. First, we present a method to define invasion fitness in class-structured viscous populations, which allows us to apply adaptive dynamics methodology. Second, we show that ordinary pair approximation introduces an important quantitative bias in the evolutionary model, even on random networks. We propose a correction to the ordinary pair approximation that yields quantitative accuracy, and discuss how the bias associated with this approach is precisely what allows us to identify subtle aspects associated with the evolutionary dynamics of spatially structured populations.

This study addresses the question of how spatial heterogeneity in prey productivity and migration act to determine geographic patterns in antagonistic coevolution with a predator. We develop and analyze a quantitative coevolutionary model for a predator-prey interaction. If the model is modified appropriately, the results could broadly apply to multispecies communities and to herbivore-plant, parasite-host, and parasitoid-host associations. Model populations are distributed over a gradient in prey birth rate (as a measure of productivity). Each population, in each patch, is made up of a suite of strains. Each strain of the predator has a certain ability to successfully attack each strain of the prey. We consider scenarios of isolated patches, global migration, and stepping-stone (i.e., local) migration over a linear string of patches. The most pervasive patterns are the following: investments in predator offense and prey defense are both maximal in the patches of highest prey productivity; when there are no constraints on maximal investment, mean predation evolves to highest levels in the most productive patches; similarly, the predator has a greater impact (measured as the percentage reduction in prey density) on the prey population in high productivity patches as compared with low productivity ones-in spite (even after evolution) of prey abundance being highest in the most productive patches; and migration has the net effect of shunting relatively offensive and defensive strains from productive patches to nonproductive ones, potentially resulting in the elimination of otherwise rare, low-investment clones. A modification of the model to gene-for-gene type interactions predicts that generalist strains (in terms of the range of strains the predator can exploit or the prey can fend off) dominate in productive areas of the prey, whereas specialists prevail in marginal habitats. Assuming a wide range of productivities over the prey's geographical distribution, the greatest strain diversity should be found in habitats of intermediate productivity. We discuss the implications of our study for adaptation and conservation. Empirical studies are in broad accord with our findings.

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.

In harsh environments, sessile organisms can make their habitat more hospitable by buffering environmental stress or increasing resource availability. Although the ecological significance of such local facilitation is widely established, the evolutionary aspects have been seldom investigated. Yet addressing the evolutionary aspects of local facilitation is important because theoretical studies show that systems with such positive interactions can exhibit alternative stable states and that such systems may suddenly become extinct when they evolve (evolutionary suicide). Arid ecosystems currently experience strong changes in climate and human pressures, but little is known about the effects of these changes on the selective pressures exerted on the vegetation. Here, we focus on the evolution of local facilitation in arid ecosystems, using a lattice-structured model explicitly considering local interactions among plants. We found that the evolution of local facilitation depends on the seed dispersal strategy. In systems characterized by short-distance seed dispersal, adaptation to a more stressful environment leads to high local facilitation, allowing the population to escape extinction. In contrast, systems characterized by long-distance seed dispersal become extinct under increased stress even when allowed to adapt. In this case, adaptation in response to climate change and human pressures could give the final push to the desertification of arid ecosystems.

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.

There is ample theoretical and experimental evidence that virulence evolution depends on the immune response of the host. In this article, we review a number of recent studies that attempt to explicitly incorporate the dynamics of the immune system (instead of merely representing it by a single black box parameter) in models for the evolution of parasite virulence. A striking observation is that the type of infection (acute or chronic) is invariably considered to be a constraint that model assumptions have to satisfy rather than as a potential outcome of the interaction of the parasite with its host's immune system. We argue that avoiding making assumptions about the type of infection will lead to a better understanding of infectious diseases, even though a number of fundamental and technical problems remain. Dynamical modeling of the immune system opens a wide range of perspectives: for understanding how the immune system eradicates a parasite (which it does for most pathogens but not for all, HIV being a notorious example of a virus that is not completely eliminated), for studying multiple infections through concomitant immunity, for understanding the emergence and evolution of the immune system in animals, and for evolutionary epidemiology in general (e.g., predicting evolutionary consequences of new therapies and public health policies). We conclude by discussing new approaches based on embedded (or nested) models and identify future perspectives for the modeling of infectious diseases.

Though it is commonly supposed that there is a trade-off between virulence and transmission, there is little data and little insight into what it should look like. Here, we consider the specific case of vector-borne parasites (inspired by human malaria) and analyse an embedded model to understand how specific life-cycle aspects may affect this trade-off. First, we find that, for such parasites, the transmission function may have an S-shape. Second, we find that the trade-off obtained for vector-borne parasites is less sensitive to parameter variations than the trade-off obtained for directly transmitted parasites. Third, we find that other parasite traits, such as the conversion from replicative to infective stages, could have important epidemiological implications. Finally, we compare the effect of treatments targeting either the asexual or the sexual parasite life-stage.

Arid ecosystems are liable to undergo sudden discontinuous transitions from a vegetated to a desert state as a result of human pressure and climate change. A predictive framework about the conditions under which such transitions occur is lacking. Here, we derive and analyze a general model describing the spatial dynamics of vegetation in arid ecosystems considering local facilitation as an essential process. We investigate the conditions under which continuous or discontinuous transitions from a vegetated to a desert state are likely to occur. We focus on arid ecosystems but our approach is sufficiently general to be applied to other ecosystems with severe environmental conditions. The model exhibits bistability and vegetation patchiness. High local facilitation decreases the risk of discontinuous transitions. Moreover, for arid ecosystems where local facilitation is a driving process, vegetation patchiness indicates proximity to a transition point, but does not allow distinguishing between continuous and discontinuous transitions.

Though predation, productivity (nutrient richness), spatial heterogeneity, and disturbance regimes are known to influence species diversity, interactions between these factors remain largely unknown. Predation has been shown to interact with productivity and with spatial heterogeneity, but few experimental studies have focused on how predation and disturbance interact to influence prey diversity. We used theory and experiments to investigate how these factors influence diversification of Pseudomonas fluorescens by manipulating both predation (presence or absence of Bdellovibrio bacteriovorus) and disturbance (frequency and intensity of disturbance). Our results show that in a homogeneous environment, predation is essential to promote prey species diversity. However, in most but not all treatments, elevated diversity was transitory, implying that the effect of predation on diversity was strongly influenced by disturbance. Both our experimental and theoretical results suggest that disturbance interacts with predation by modifying the interplay of resource and apparent competition among prey.

We investigate the evolution of manipulation of host dispersal behaviour by parasites using spatially explicit individual-based simulations. We find that when dispersal is local, parasites always gain from increasing their hosts' dispersal rate, although the evolutionary outcome is determined by the costs-to-benefits ratio. However, when dispersal can be non-local, we show that parasites investing in an intermediate dispersal distance of their hosts are favoured even when the manipulation is not costly, due to the intrinsic spatial dynamics of the host–parasite interaction. Our analysis highlights the crucial importance of ecological spatial dynamics in evolutionary processes and reveals the theoretical possibility that parasites could manipulate their hosts' dispersal.

The evolution of altruism, especially as directed to non-kin, is an enigma of evolutionary biology. Explanations would come easier, however, if altruists were readily recognized. Arguably the simplest recognition system is a conspicuous, heritable tag. A green beard would do it. A few examples of the ‘green beard effect’ have been reported in human interactions, though beards per se and greenness tend not to feature. A problem with this explanation is the improbability of one gene encoding all three functions (altruism, tag and recognition). Based on modelling, Jansen and van Baalen identify a further problem with this theory: even if green beard genes can be selectively advantageous, altruism is unstable under previous assumptions. But, they add, the evolution of cooperation using a recognition mechanism may be more likely if many beard colours coexist. Resolving the enigma of the evolution of altruism is helped along by models showing that the coexistence of many tags makes the evolution of cooperation using a recognition mechanism more likely. The evolution of altruism, a behaviour that benefits others at one's own fitness expense, poses a darwinian paradox. The paradox is resolved if many interactions are with related individuals so that the benefits of altruism are reaped by copies of the altruistic gene in other individuals1, a mechanism called kin selection2. However, recognition of altruists could provide an alternative route towards the evolution of altruism1,3,4,5. Arguably the simplest recognition system is a conspicuous, heritable tag, such as a green beard1,3. Despite the fact that such genes have been reported6,7,8, the ‘green beard effect’3 has often been dismissed because it is unlikely that a single gene can code for altruism and a recognizable tag1,3,9. Here we model the green beard effect and find that if recognition and altruism are always inherited together, the dynamics are highly unstable, leading to the loss of altruism. In contrast, if the effect is caused by loosely coupled separate genes, altruism is facilitated through beard chromodynamics in which many beard colours co-occur. This allows altruism to persist even in weakly structured populations and implies that the green beard effect, in the form of a fluid association of altruistic traits with a recognition tag, can be much more prevalent than hitherto assumed.

We investigate how the evolution of communication strategies affects signal credibility when there is common interest as well as a conflict between communicating individuals. Taking alarm calls as an example, we show that if the temptation to cheat is low, a single signal is used in the population. If the temptation increases cheaters will erode the credibility of a signal, and an honest mutant using a different signal ('a private code') will be very successful until this, in turn, is cracked by cheaters. In such a system, signal use fluctuates in time and space and hence the meaning of a given signal is not constant. When the temptation to cheat is too large, no honest communication can maintain itself in a Tower of Babel of many signals. We discuss our analysis in the light of the Green Beard mechanism for the evolution of altruism.

Recent studies indicate that the time required for virus-infected cells to become vulnerable for the activity of CTL is of significance for the capacity of CTL to control ongoing viral reproduction. To investigate whether this applies to the effectiveness of HIV-1-specific CTL, we measured virus production in cultures containing CD4(+) T cells inoculated with HIV at low multiplicity of infection, and CTL directed against an early protein, Rev, or a late protein, RT. The Rev-specific CTL prevented at least 2 log(10) more HIV-1 production, in 10 days, than similar numbers of RT-specific CTL. To study how CTL effectiveness depends on variations in the potency of effector functions and kinetics of HIV protein expression, we developed a mathematical model describing CTL-target cell interactions during successive infection cycles. The results show that substantially higher CTL-mediated target cell elimination rates are required to achieve control as there is less time for CTL to act before infected cells release progeny virions. Furthermore, in vitro experiments with HIV recombinant viruses showed that the RT-specific CTL were at least as effective as the Rev-specific CTL, but only if the RT epitope was expressed as part of the early protein Nef. Together these results indicate that CTL control ongoing HIV reproduction more effectively if they are able to recognize infected cells earlier during individual viral replication cycles. This provides rationale for immunization strategies that aim at inducing, boosting or skewing CTL responses to early regulatory proteins in AIDS vaccine development.

Introduction Why do plants cover the earth and give the world a green appearance? This question is not as trivial as it might seem at first sight. Hairston et al . (1960) hypothesized that herbivores cannot ransack the earth of its green blanket because they are kept low in number by predators. They tacitly ignored the possibility that plants defend themselves directly against a suite of herbivores and together exhibit such great diversity in defense mechanisms that “super” herbivores able to master all plant defenses did not evolve and those that overcome the defenses of some plants are limited by the availability of these plants. Strong et al . (1984) recognized both possibilities in their review on the impact of herbivorous arthropods on plants, but they also favored the view that predators suppress the densities of herbivores, and thereby reduce the threat of plants being eaten. The two explanatory mechanisms (plant defense versus predator impact), however, may well act in concert. Ever since the seminal review paper by Price et al . (1980) ecologists have become increasingly aware that plant defenses include more than just trickery to reduce the herbivore's capacity for (population) growth. For example, the plant may provide facilities to promote the foraging success of the herbivore's enemies. This form of defense is termed indirect as opposed to direct defense against herbivores.

Both the patient who is infected with a communicable disease and the doctor treating the patient share a common interest: the eradication of the infection. That the treatment chosen by the doctor may have detrimental consequences for the population at large is not the primary concern of the doctor or the patient. Such matters are the concern of the larger-scale medical and political organizations that deal with the development of public health policies such as vaccination programs and possibly, as investigated in this book, “virulence management” strategies. Development of such policies is not only a complicated issue because of the intricacies of host–parasite interactions themselves, but also because the common aims of the public health authority and the population do not always overlap very well (Anderson et al. 1997). Of course, the community benefits when an individual ceases to be infective. However, parasites are not inert players in the game, and will adapt to any measures that are taken on a sufficiently large scale. Therefore, the development of some public health policies may not be beneficial to the community as a whole. The global resurgence of tuberculosis (TB) and the fact that many malaria parasites have become resistant against most preventive treatments are just two examples of the detrimental consequences of the large-scale application of individually beneficial medical treatment. The insight that strategies to fight parasites should be based not only on shortterm effects, but also on evolutionary considerations, is gaining ground (Ewald 1993, 1994a). For example, measures could be taken to counteract the development of resistance to antibiotics or other chemotherapeutic treatments (Baquero and Blazquez 1997; Bonhoeffer et al. 1997; Levy 1998; see Chapter 23). But other parasite traits evolve too. By working out how virulence may change in response to changes in the parasite’s transmission cycle (Ewald 1994a; Van Baalen and Sabelis 1995b; see Chapter 2) one obtains an insight into the scope for such virulence management. It has already been pointed out that measures taken to reduce the impact of a particular disease may involve ethical dilemmas. For instance, Anderson and May (1991) note that when a population is vaccinated against the poliomyelitis virus, the force of infection of this virus decreases. This means that fewer people will become infected, which is the desired beneficial effect. However, it also means that those who do become infected are likely to become so at a later age (polio was more commonly a childhood disease before vaccination); in the case of polio

Virulence management can be defined as that set of policies that not only aims to minimize the short-term impact of parasites on their host population (e.g., incidence, mortality, and morbidity), but also to account for the longer-term consequences of the evolutionary responses of these parasites, for example by adopting measures that select for less virulent strains. An important question pertaining to the scope of virulence management concerns the effect of contact structures in the host population. For successful transmission many parasites require close contact between the host they are infecting and new susceptible hosts. Consequently, the network of social contact in their host population is of paramount importance. It has already become clear that differently structured networks lead to different types of epidemiology (Keeling 1999). For example, a sparsely connected host population is more difficult to invade than a densely connected host population. But to what extent will the contact structure of their host population affect the evolution of the parasites, in particular of their virulence? Can we change the selective pressures on the parasites by modifying these contact structures? Claessen and de Roos (1995) and Rand et al. (1995) carried out computer simulations of evolving parasites in spatially structured host populations and concluded that less virulent (hypovirulent) parasites are favored with respect to well-mixed systems. Clearly, parasite evolution does depend on host population structure. Qualitative insight into the pertinent aspects of population structure, in the form of social networks, is still lacking, however (Wallinga et al. 1999). Networks of social contacts may vary in a number of ways. First, the number of social contacts per host may vary (across the host population and in time). The relevance of whether a parasite’s host interacts with a large or small number of other hosts is not immediately obvious, as explained below. Second, the overall structure of the social network may vary. Consider the contact structures depicted in Figures 7.1a and 7.1b. In both networks every host is connected to three other hosts, but in one the overall structure is laid out in a regular fashion (Figure 7.1a) whereas in the other it is completely random (Figure 7.1b). Watts and Strogatz (1998) and Keeling (1999) showed that such variations in network structure may have far-reaching consequences for, among other things, epidemiology. For example, a parasite can expand more rapidly in a random contact network than in a regular network, as suggested by the shaded nodes in Figures 7.1a and 7.1b. But

The standard assumption underlying the formulation of models for population dynamics (such as the logistic growth equation, the Lotka–Volterra predator–prey model, and the Kermack and McKendrick epidemiological equations, to name a few) is that populations spread homogeneously through space and that individuals mix rapidly. It is not a new insight that spatial structure is often an essential component of the ecological (and evolutionary) dynamics of populations, and there have been many approaches to understanding the various consequences of spatial structure. In this chapter I address one of the more recently developed techniques for modeling spatial population dynamics. The oldest approach is to assume that populations are subdivided into different discrete subpopulations that are linked through migration (the “metapopulation” approach). This may be a reasonable assumption for certain systems (groups of parasites living in different hosts, for example), but space often has a more a continuous aspect. For example, a forest may be highly structured without having clear boundaries between subpopulations. Such situations are often modeled using a diffusion formalism, but this approach has its shortcomings as well. In particular, when one considers spatial spread of a population (or gene), individuality (discreteness) and its associated stochasticity may be important (Durrett and Levin 1994b). In a diffusion model, the rate of population growth is determined by the spread of “nano-individuals” at the wave front, whereas in reality it is often determined by the more erratic process of dispersal and subsequent successful settlement of individuals. Not only might this give quantitatively wrong estimates [e.g., the conditions under which an epidemic can arise; see Chapter 6 and Jeltsch et al. (1997)], it can also yield qualitatively wrong

Aggregated spatial distributions of prey and predators promote stability of the otherwise unstable Nicholson-Bailey model. Nevertheless, when both predators and prey choose patches in an ideal free way, sufficiently aggregated distributions will only arise if patch quality (e.g., reflected in prey fecundity) is very heterogeneous. This requirement profoundly limits the possibilities for simultaneous population dynamical and evolutionary stability. However, stability is not necessary for coexistence. Under cyclic or chaotic dynamics, the rate at which species change their distributions becomes important. Here we consider two endpoints of a continuum of rates. The first is "rigid" selection of patch types based on the expected long-term distribution of conditions. The second is "flexible" selection based on current conditions. We carried out systematic surveys of the population-level consequences of coevolutionarily stable patch-selection strategies for different combinations of rigid and flexible strategies of predator and prey. First, if both prey and predators have rigid strategies, the evolutionary end result is either a stable population dynamical equilibrium or diverging cycles eventually leading to extinction. Second, for the case with rigid prey and flexible predators, the persistence boundary in parameter space is shifted from the boundaries obtained for rigid predators. The mechanism underlying persistence is different in that the flexible strategies of the predators destabilize the equilibrium, while the evolutionary response of the rigid prey leads to reduced cycles. Third, if both prey and predators are flexible, simulations lead either to chaotic fluctuations or to extinction (but not to stable equilibria, nor to limit cycles), and the conditions for coexistence are much wider than those under rigid patch selection. These simulations suggest that information constraints on adaptive patch choice have a major impact on predator-prey persistence under nonequilibrium conditions. We discuss how these predictions can be tested by field observations on expansions and contractions in dietary range (or habitat range) in relation to population fluctuations.

Group selection can overcome individual selection for selfishness and favour altruism if there is variation among the founders of the spatially distinct groups, and groups with many altruists become substantially larger (or exist longer) than groups with few. Whether altruism can evolve in populations that do not have an alternation of local population growth and global dispersal ("viscous populations") has been disputed for some time. Limited dispersal protects the altruists from the non-altruists, but also hinders the export of altruism. In this article, we used the Pair Approximation technique (tracking the dynamics of pairs of neighbours instead of single individuals) to derive explicit invasion conditions for rare mutants in populations with limited dispersal. In such viscous populations, invading mutants form clusters, and ultimately, invasion conditions depend on the properties of such clusters. Thus there is selection on a higher level than that of the individual; in fact, invasion conditions define the unit of selection in viscous populations. We treat the evolution of altruism as a specific example, but the method is of more general interest. In particular, an important advantage is that the spatial aspects can be incorporated into game theory in a straightforward fashion; we will specify the ESS for a more general model. The invasion condition can be interpreted in terms of inclusive fitness. In contrast with Hamilton's model, the coefficient of relatedness is not merely a given genetical constant but depends on local population dynamical processes (birth, dispersal and death of individuals). With a simple birth rate function, Hamilton's rule is recovered: the cost to the donor should be less than the benefit to the recipient weighted with the coefficient of relatedness. As the coefficient of relatedness is roughly proportional to an individual's number of neighbours, benefits to the recipient must be substantial to outweigh the costs, confirming earlier studies. We discuss the consequences for the evolution of dispersal and outline how the method may be extended to study evolution in interacting populations.Copyright 1998 Academic Press

Most models for coevolution of hosts and parasites are based on the assumption that resistance of hosts to parasites is an all–or–nothing effect. In many cases, for example where parasites require an appropriate receptor on host cells, this is a reasonable assumption. However, in many other cases, for example where hosts mount an immune response, this picture may be too simple. An immune system is expensive to maintain, which poses a question as to how much of its resources a host should allocate to resist parasites: if the risk of infection is low, natural selection may favour hosts with less effective immune systems. As optimal allocation to defence will depend on the force of infection, and the force of infection, in turn, depends on the level of defence in the rest of the host population, a game–theoretic approach is necessary. Here I analyse a simple model for the evolution of the ability to recover from infection. If parasites are not allowed to coevolve, the outcome is a single evolutionarily stable strategy (ESS). If the parasites coevolve, multiple evolutionary outcomes are possible, one in which the parasites are relatively avirulent and common and the hosts invest little in recovery ability, and another (the escalated arms race) where parasites are rare but virulent and the hosts invest heavily in defence.