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Defensive symbionts in the host microbiome can confer protection from infection or reduce the harms of being infected by a parasite. Defensive symbionts are therefore promising agents of biocontrol that could be used to control or ameliorate the impact of infectious diseases. Previous theory has shown how symbionts can evolve along the parasitism–mutualism continuum to confer greater or lesser protection to their hosts and in turn how hosts may coevolve with their symbionts to potentially form a mutualistic relationship. However, the consequences of introducing a defensive symbiont for parasite evolution and how the symbiont may coevolve with the parasite have received relatively little theoretical attention. Here, we investigate the ecological and evolutionary implications of introducing a tolerance-conferring defensive symbiont into an established host–parasite system. We show that while the defensive symbiont may initially have a positive impact on the host population, parasite and symbiont evolution tend to have a net negative effect on the host population in the long term. This is because the introduction of the defensive symbiont always selects for an increase in parasite virulence and may cause diversification into high- and low-virulence strains. Even if the symbiont experiences selection for greater host protection, this simply increases selection for virulence in the parasite, resulting in a net negative effect on the host population. Our results therefore suggest that tolerance-conferring defensive symbionts may be poor biocontrol agents for population-level infectious disease control. [ABSTRACT FROM AUTHOR]

Non-pharmaceutical interventions (NPIs), such as social distancing and contact tracing, are important public health measures that can reduce pathogen transmission. In addition to playing a crucial role in suppressing transmission, NPIs influence pathogen evolution by mediating mutation supply, restricting the availability of susceptible hosts, and altering the strength of selection for novel variants. Yet it is unclear how NPIs might affect the emergence of novel variants that are able to escape pre-existing immunity (partially or fully), are more transmissible or cause greater mortality. We analyse a stochastic two-strain epidemiological model to determine how the strength and timing of NPIs affect the emergence of variants with similar or contrasting life-history characteristics to the wild type. We show that, while stronger and timelier NPIs generally reduce the likelihood of variant emergence, it is possible for more transmissible variants with high cross-immunity to have a greater probability of emerging at intermediate levels of NPIs. This is because intermediate levels of NPIs allow an epidemic of the wild type that is neither too small (facilitating high mutation supply), nor too large (leaving a large pool of susceptible hosts), to prevent a novel variant from becoming established in the host population. However, since one cannot predict the characteristics of a variant, the best strategy to prevent emergence is likely to be an implementation of strong, timely NPIs. [ABSTRACT FROM AUTHOR]

Objectives/aims: Prolonged infections of immunocompromised individuals have been proposed as a crucial source of new variants of SARS-CoV-2 during the COVID-19 pandemic. In principle, sustained within-host antigenic evolution in immunocompromised hosts could allow novel immune escape variants to emerge more rapidly, but little is known about how and when immunocompromised hosts play a critical role in pathogen evolution. Materials and methods: Here, we use a simple mathematical model to understand the effects of immunocompromised hosts on the emergence of immune escape variants in the presence and absence of epistasis. Conclusions: We show that when the pathogen does not have to cross a fitness valley for immune escape to occur (no epistasis), immunocompromised individuals have no qualitative effect on antigenic evolution (although they may accelerate immune escape if within-host evolutionary dynamics are faster in immunocompromised individuals). But if a fitness valley exists between immune escape variants at the between-host level (epistasis), then persistent infections of immunocompromised individuals allow mutations to accumulate, therefore, facilitating rather than simply speeding up antigenic evolution. Our results suggest that better genomic surveillance of infected immunocompromised individuals and better global health equality, including improving access to vaccines and treatments for individuals who are immunocompromised (especially in lower- and middle-income countries), may be crucial to preventing the emergence of future immune escape variants of SARS-CoV-2. [ABSTRACT FROM AUTHOR]

Social contacts can facilitate the spread of both survival‐related information and infectious diseases, but little is known about how these processes combine to shape host and parasite evolution. Here, we use a theoretical model that captures both infection and information transmission processes to investigate how host sociality (contact effort) and parasite virulence (disease‐associated mortality rate) (co)evolve. We show that selection for sociality (and in turn, virulence) depends on both the intrinsic costs and benefits of social information and infection as well as their relative prevalence in the population. Specifically, greater sociality and lower virulence evolve when the risk of infection is either low or high and social information is neither very common nor too rare. Lower sociality and higher virulence evolve when the prevalence patterns are reversed. When infection and social information are both at moderate levels in the population, the direction of selection depends on the relative costs and benefits of being infected or informed. We also show that sociality varies inversely with virulence, and that parasites may be unable to prevent runaway selection for higher contact efforts. Together, these findings provide new insights for our understanding of group living and how apparently opposing ecological processes can influence the evolution of sociality and virulence in a range of ways. [ABSTRACT FROM AUTHOR]

Host and parasite evolution are closely intertwined, with selection for adaptations and counter‐adaptations forming a coevolutionary feedback loop. Coevolutionary dynamics are often difficult to intuit due to these feedbacks and are hard to demonstrate empirically in most systems. Theoretical models have therefore played a crucial role in shaping our understanding of host–parasite coevolution. Theoretical models vary widely in their assumptions, approaches and aims, and such variety makes it difficult, especially for non‐theoreticians and those new to the field, to: (1) understand how model approaches relate to one another; (2) identify key modelling assumptions; (3) determine how model assumptions relate to biological systems; and (4) reconcile the results of different models with contrasting assumptions. In this review, we identify important model features, highlight key results and predictions and describe how these pertain to model assumptions. We carry out a literature survey of theoretical studies published since the 1950s (n = 219 papers) to support our analysis. We identify two particularly important features of models that tend to have a significant qualitative impact on the outcome of host–parasite coevolution: population dynamics and the genetic basis of infection. We also highlight the importance of other modelling features, such as stochasticity and whether time proceeds continuously or in discrete steps, that have received less attention but can drastically alter coevolutionary dynamics. We finish by summarizing recent developments in the field, specifically the trend towards greater model complexity, and discuss likely future directions for research. [ABSTRACT FROM AUTHOR]

The classical view of sex ratio evolution, popularized by R. A. Fisher, is that the sex ratio at birth should be equal when males and females require the same level of parental investment. Thus, although differences in mortality between the sexes during parental investment will cause deviations from an equal sex ratio at birth, differential mortality after parental investment should have no effect. However, a recent theoretical model appears to contradict this view, suggesting that differential mortality after the period of parental investment does cause deviations from an equal sex ratio at birth. Moreover, the life stage at which mortality differs (juvenile vs. adult) is predicted to cause contrasting effects on sex ratio evolution. These results are in stark contrast with Fisher's hypothesis. Here, we resolve this disparity by analyzing a stage‐ and sex‐ structured model of population dynamics. We find that selection always drives the population to an equal sex ratio at birth regardless of differential mortality effects after parental investment, thus confirming Fisher's hypothesis. The disparity appears to be due to incorrect accounting of mutant‐resident unions, which we avoid by considering separate union classes for different types of mutant‐resident unions. [ABSTRACT FROM AUTHOR]

Parasites can select for sexual reproduction in host populations, preventing replacement by faster‐growing asexual genotypes. This is usually attributed to so‐called 'Red Queen dynamics' (RQD), where antagonistic coevolution causes fluctuating selection in allele frequencies, which provides sex with an advantage over asex. However, parasitism may also maintain sex in the absence of RQD when sexual populations are more genetically diverse—and hence more resistant, on average—than clonal populations, allowing sex and asex to coexist at a stable equilibrium. Although the maintenance of sex due to RQD has been studied extensively, the conditions that allow sex and asex to stably coexist have yet to be explored in detail. In particular, we lack an understanding of how host demography and parasite epidemiology affect the maintenance of sex in the absence of RQD. Here, I use an eco‐evolutionary model to show that both population density and the type and strength of virulence are important for maintaining sex, which can be understood in terms of their effects on disease prevalence and severity. In addition, I show that even in the absence of heterozygote advantage, asexual heterozygosity affects coexistence with sex due to variation in niche overlap. These results reveal which host and parasite characteristics are most important for the maintenance of sex in the absence of RQD, and provide empirically testable predictions for how demography and epidemiology mediate competition between sex and asex. [ABSTRACT FROM AUTHOR]

Sexually transmitted infections (STIs) are predicted to play an important role in the evolution of host mating strategies, and vice versa, yet our understanding of host‐STI coevolution is limited. Previous theoretical work has shown mate choice can evolve to prevent runaway STI virulence evolution in chronic, sterilizing infections. Here, I generalize this theory to examine how a broader range of life‐history traits influence coevolution; specifically, how host preferences for healthy mates and STI virulence coevolve when infections are acute and can cause mortality or sterility, and hosts do not form long‐term sexual partnerships. I show that mate choice reduces both mortality and sterility virulence, with qualitatively different outcomes depending on the mode of virulence, costs associated with mate choice, recovery rates, and host lifespan. For example, fluctuating selection—a key finding in previous work—is most likely when hosts have moderate lifespans, STIs cause sterility and long infections, and costs of mate choice are low. The results reveal new insights into the coevolution of mate choice and STI virulence as different life‐history traits vary, providing increased support for parasite‐mediated sexual selection as a potential driver of host mate choice, and mate choice as a constraint on the evolution of virulence. [ABSTRACT FROM AUTHOR]

Understanding how parasites adapt to changes in host resistance is crucial to evolutionary epidemiology. Experimental studies have demonstrated that parasites are more capable of adapting to gradual, rather than sudden changes in host phenotype, as the latter may require multiple mutations that are unlikely to arise simultaneously. A key, but as yet unexplored factor is precisely how interactions between mutations (epistasis) affect parasite evolution. Here, we investigate this phenomenon in the context of infectivity range, where parasites may experience selection to infect broader sets of genotypes. When epistasis is strongly positive, we find that parasites are unlikely to evolve broader infectivity ranges if hosts exhibit sudden, rather than gradual changes in phenotype, in close agreement with empirical observations. This is due to a low probability of fixing multiple mutations that individually confer no immediate advantage. When epistasis is weaker, parasites are more likely to evolve broader infectivity ranges if hosts make sudden changes in phenotype, which can be explained by a balance between mutation supply and selection. Thus, we demonstrate that both the rate of phenotypic change in hosts and the form of epistasis between mutations in parasites are crucial in shaping the evolution of infectivity range. [ABSTRACT FROM AUTHOR]

Antagonistic coevolution between hosts and parasites is thought to drive a range of biological phenomena including the maintenance of sexual reproduction. Of particular interest are conditions that produce persistent fluctuations in the frequencies of genes governing host-parasite specificity (coevolutionary cycling), as sex may be more beneficial than asexual reproduction in a constantly changing environment. Although many studies have shown that coevolutionary cycling can lead to the maintenance of sex, the effects of ecological feedbacks on the persistence of these fluctuations in gene frequencies are not well understood. Here, we use a simple deterministic model that incorporates ecological feedbacks to explore how parasitic reductions in host fecundity affect the maintenance of coevolutionary cycling. We demonstrate that parasitic castration is inherently destabilizing and may be necessary for coevolutionary cycling to persist indefinitely, but also reduces the likelihood that sexually reproducing individuals will find a fertile partner, which may select against sex. These findings suggest that castrators can play an important role in shaping host evolution and are likely to be good targets for observing fluctuations in gene frequencies that govern specificity in host-parasite interactions. [ABSTRACT FROM AUTHOR]