Biology subjects

Buckingham, L. J.

Publications and source records attributed to Buckingham, L. J..

4 recordsLinked to original sources

bioRxiv2023

Coevolution of age-structured tolerance and virulence

AO_SCPLOWBSTRACTC_SCPLOWHosts can evolve a variety of defences against parasitism, including resistance (which prevents or reduces the spread of infection) and tolerance (which protects against virulence). Some organisms have evolved different levels of tolerance at different life-stages, which is likely to be the result of coevolution with pathogens, and yet it is currently unclear how coevolution drives patterns of age-specific tolerance. Here, we use a model of tolerance-virulence coevolution to investigate how age structure influences coevolutionary dynamics. Specifically, we explore how coevolution unfolds when tolerance and virulence (disease-induced mortality) are age-specific compared to when these traits are uniform across the host lifespan. We find that coevolutionary cycling is relatively common when host tolerance is age-specific, but cycling does not occur when tolerance is the same across all ages. We also find that age-structured tolerance can lead to selection for higher virulence in shorter-lived than in longer-lived hosts, whereas non-age-structured tolerance always leads virulence to increase with host lifespan. Our findings therefore suggest that age structure can have substantial qualitative impacts on host-pathogen coevolution.

evolutionary biology↗

bioRxiv2023

Separation of Evolutionary Timescales in Coevolving Species

AO_SCPLOWBSTRACTC_SCPLOWMany coevolutionary processes, including host-parasite and host-symbiont interactions, involve one species or trait which evolves much faster than the other. Whether or not a coevolutionary trajectory converges depends on the relative rates of evolutionary change in the two species, and so current adaptive dynamics approaches generally either determine convergence stability by considering arbitrary (often comparable) rates of evolutionary change or else rely on necessary or sufficient conditions for convergence stability. We propose a method for determining convergence stability in the case where one species is expected to evolve much faster than the other. This requires a second separation of timescales, which assumes that the faster evolving species will reach its evolutionary equilibrium (if one exists) before a new mutation arises in the more slowly evolving species. This method, which is likely to be a reasonable approximation for many coevolving species, both provides straightforward conditions for convergence stability and is less computationally expensive than traditional analysis of coevolution models, as it reduces the trait space from a two-dimensional plane to a one-dimensional manifold. In this paper, we present the theory underlying this new separation of timescales and provide examples of how it could be used to determine coevolutionary outcomes from models.

evolutionary biology↗

bioRxiv2022

The Evolution of the Age of Onset of Resistance to Infectious Disease

AO_SCPLOWBSTRACTC_SCPLOWMany organisms experience an increase in disease resistance as they age but the time of life at which this change occurs varies. Increases in resistance are partially due to prior exposure and physiological constraints but these cannot fully explain the observed patterns of age-related resistance. An alternative explanation is that developing resistance at an earlier age incurs costs to other life-history traits. Here, we explore how trade-offs with host reproduction or mortality affect the evolution of the onset of resistance, depending on when during the hosts life-cycle the costs are paid (only when resistance is developing, only when resistant or throughout the lifetime). We find that the timing of the costs is crucial to determining evolutionary outcomes, often making the difference between resistance developing at an early or late age. Accurate modelling of biological systems therefore relies on knowing not only the shape of trade-offs but also when they take effect. We also find that the evolution of the rate of onset of resistance can result in evolutionary branching. This provides an alternative, possible evolutionary history of populations which are dimorphic in disease resistance, where the rate of onset of resistance has diversified rather than the level of resistance.

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↗