Biology subjects

Bruns, E. L.

Publications and source records attributed to Bruns, E. L..

3 recordsLinked to original sources

bioRxiv2025

Pathogens pull hardest in the coevolutionary arms-race to determine age-specific transmission biases

Juveniles across a wide range of species are more susceptible to pathogenic infection than their adult conspecifics, often driving epidemic spread. While high juvenile susceptibility can be related to developmental timing, recent theoretical studies have found that hosts often evolve high juvenile susceptibility given a trade-off with other host traits. However, most research on age-specific infection has focused solely on host evolutionary dynamics, and the effect of pathogen evolution or coevolution on juvenile infection rates remains unknown. Here, we developed a coevolutionary adaptive dynamics model to investigate age-specific infectivity and contrast the outcome of coevolution with host evolution and pathogen evolution alone. We found strong differences in the evolutionary dynamics of hosts and pathogens in the absence of coevolution. While host evolution often favoured genotypes with intermediate levels of juvenile and adult resistance, pathogen evolution selected for extreme specialists. When hosts and pathogens were allowed to coevolve, the dynamics more closely resembled the pathogen dynamics; pathogens rapidly evolved to specialize on infecting a specific age class and this drove reciprocal specialization in host resistance. Our results illustrate that coevolution has the potential to shape age-specific patterns of infection that impact disease spread.

evolutionary biology↗

bioRxiv2024

The Emergence of Non-Linear Evolutionary Trade-offs and the Maintenance of Genetic Polymorphisms

Evolutionary models of quantitative traits often assume trade-offs between beneficial and detrimental traits, requiring modelers to specify a function linking costs to benefits. The choice of trade-off function is often consequential; functions that assume diminishing returns (accelerating costs) typically lead to single equilibrium genotypes, while decelerating costs often lead to evolutionary branching. Despite their importance, we still lack a strong theoretical foundation to base the choice of trade-off function. To address this gap, we explore how trade-off functions can emerge from the genetic architecture of a quantitative trait. We developed a multi-locus model of disease resistance, assuming each locus had random antagonistic pleiotropic effects on resistance and fecundity. We used this model to generate genotype landscapes and explored how additive versus epistatic genetic architectures influenced the shape of the trade-off function. Regardless of epistasis, our model consistently led to accelerating costs. We then used our genotype landscapes to build an evolutionary model of disease resistance. Unlike other models with accelerating costs, our approach often led to genetic polymorphisms at equilibrium. Our results suggest that accelerating costs are a strong null model for evolutionary trade-offs and that the eco-evolutionary conditions required for polymorphism may be more nuanced than previously believed.

evolutionary biology↗

bioRxiv2022

The evolution of age-specific resistance to infectious disease

AO_SCPLOWBSTRACTC_SCPLOWInnate, infection-preventing resistance often varies between host life-stages. Juveniles are more resistant than adults in some species, whereas the opposite pattern is true in others. This variation cannot always be explained by prior exposure or physiological constraints and so it has been hypothesised that trade-offs with other life-history traits may be involved. However, little is known about how trade-offs between various life-history traits and resistance at different life-stages affect the evolution of age-specific resistance. Here, we use a mathematical model to explore how trade-offs with natural mortality, reproduction and maturation combine to affect the evolution of resistance at different life-stages. Our results show that certain combinations of trade-offs have substantial effects on whether adults or juveniles are more resistant, with trade-offs between juvenile resistance and adult reproduction inherently more costly than trade-offs involving maturation or mortality (all else being equal), resulting in consistent evolution of lower resistance at the juvenile stage even when infection causes a lifelong fecundity reduction. Our model demonstrates how the differences between patterns of age-structured resistance seen in nature may be explained by variation in the trade-offs involved and our results suggest conditions under which trade-offs tend to select for lower resistance in juveniles than adults.

evolutionary biology↗