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1.
Bull Math Biol ; 86(6): 62, 2024 Apr 25.
Article in English | MEDLINE | ID: mdl-38662120

ABSTRACT

Hosts 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.


Subject(s)
Biological Evolution , Host-Pathogen Interactions , Mathematical Concepts , Virulence , Animals , Age Factors , Models, Biological , Host-Parasite Interactions/immunology , Biological Coevolution , Humans , Longevity
2.
J Theor Biol ; 579: 111688, 2024 02 21.
Article in English | MEDLINE | ID: mdl-38096978

ABSTRACT

Many 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.


Subject(s)
Biological Evolution , Parasites , Animals , Mutation , Phenotype , Host-Parasite Interactions/genetics
3.
Evolution ; 77(12): 2631-2641, 2023 Dec 02.
Article in English | MEDLINE | ID: mdl-37778003

ABSTRACT

Hyperparasites (species which parasitize other parasites) are common in natural populations, affecting many parasitic taxa, including: eukaryotic parasites; bacterial and fungal pathogens. Hyperparasitism is therefore likely to shape the ecology and evolution of many host-parasite systems, representing a promising method for biocontrol (e.g., treating antimicrobial resistant infections). However, the eco-evolutionary consequences of hyperparasitism have received little attention. We use a host-parasite-hyperparasite model to explore how introducing a hyperparasite drives the evolution of parasite virulence, and what impact this has on the host population. We show when the introduction of a hyperparasite selects for higher or lower parasite virulence, and the changes in virulence experienced by the host population. Crucially, we show that variation in the direct effects of hyperparasites on virulence and transmission, and the probability of cotransmission, can lead to a previously unseen hysteresis effect, whereby small shifts in hyperparasite characteristics can lead to sudden shifts in parasite virulence. We also show that hyperparasites can induce diversification in parasite virulence, leading to the coexistence of high and low virulence strains. Our results show hyperparasites can have dramatic effects on the evolution of parasite virulence, and that the use of hyperparasites in biocontrol should be approached with caution.


Subject(s)
Parasites , Animals , Virulence , Ecology , Biological Evolution , Host-Parasite Interactions
4.
Evol Lett ; 7(4): 262-272, 2023 Aug.
Article in English | MEDLINE | ID: mdl-37475754

ABSTRACT

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.

6.
Bull Math Biol ; 85(5): 42, 2023 04 15.
Article in English | MEDLINE | ID: mdl-37060428

ABSTRACT

Many 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 host's 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.


Subject(s)
Communicable Diseases , Disease Resistance , Humans , Disease Resistance/genetics , Age of Onset , Biological Evolution , Models, Biological , Mathematical Concepts , Communicable Diseases/epidemiology
7.
Evol Med Public Health ; 11(1): 80-89, 2023.
Article in English | MEDLINE | ID: mdl-37007165

ABSTRACT

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.

8.
Evol Med Public Health ; 11(1): 90-100, 2023.
Article in English | MEDLINE | ID: mdl-37007166

ABSTRACT

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.

9.
Proc Biol Sci ; 290(1991): 20222000, 2023 01 25.
Article in English | MEDLINE | ID: mdl-36695037

ABSTRACT

Innate, 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 hypothesized 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.


Subject(s)
Communicable Diseases , Life History Traits , Humans , Reproduction/physiology , Fertility , Age Factors , Biological Evolution
10.
Nat Commun ; 13(1): 6018, 2022 10 13.
Article in English | MEDLINE | ID: mdl-36229442

ABSTRACT

While the negative effects that pathogens have on their hosts are well-documented in humans and agricultural systems, direct evidence of pathogen-driven impacts in wild host populations is scarce and mixed. Here, to determine how the strength of pathogen-imposed selection depends on spatial structure, we analyze growth rates across approximately 4000 host populations of a perennial plant through time coupled with data on pathogen presence-absence. We find that infection decreases growth more in the isolated than well-connected host populations. Our inoculation study reveals isolated populations to be highly susceptible to disease while connected host populations support the highest levels of resistance diversity, regardless of their disease history. A spatial eco-evolutionary model predicts that non-linearity in the costs to resistance may be critical in determining this pattern. Overall, evolutionary feedbacks define the ecological impacts of disease in spatially structured systems with host gene flow being more important than disease history in determining the outcome.


Subject(s)
Biological Evolution , Host-Pathogen Interactions , Host-Pathogen Interactions/genetics , Humans , Population Dynamics
11.
Evolution ; 76(6): 1153-1169, 2022 06.
Article in English | MEDLINE | ID: mdl-35420704

ABSTRACT

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.


Subject(s)
Biological Evolution , Parasites , Animals , Host-Parasite Interactions , Models, Theoretical , Social Behavior , Virulence
12.
Epidemics ; 38: 100546, 2022 03.
Article in English | MEDLINE | ID: mdl-35183834

ABSTRACT

Mathematical modelling and statistical inference provide a framework to evaluate different non-pharmaceutical and pharmaceutical interventions for the control of epidemics that has been widely used during the COVID-19 pandemic. In this paper, lessons learned from this and previous epidemics are used to highlight the challenges for future pandemic control. We consider the availability and use of data, as well as the need for correct parameterisation and calibration for different model frameworks. We discuss challenges that arise in describing and distinguishing between different interventions, within different modelling structures, and allowing both within and between host dynamics. We also highlight challenges in modelling the health economic and political aspects of interventions. Given the diversity of these challenges, a broad variety of interdisciplinary expertise is needed to address them, combining mathematical knowledge with biological and social insights, and including health economics and communication skills. Addressing these challenges for the future requires strong cross-disciplinary collaboration together with close communication between scientists and policy makers.


Subject(s)
COVID-19 , Pandemics , COVID-19/epidemiology , Humans , SARS-CoV-2
13.
J Evol Biol ; 35(2): 205-224, 2022 02.
Article in English | MEDLINE | ID: mdl-35030276

ABSTRACT

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.


Subject(s)
Parasites , Adaptation, Physiological/genetics , Animals , Biological Evolution , Host-Parasite Interactions/genetics , Parasites/genetics , Population Dynamics
14.
PLOS Glob Public Health ; 2(4): e0000298, 2022.
Article in English | MEDLINE | ID: mdl-36962415

ABSTRACT

The COVID-19 pandemic, caused by the coronavirus SARS-CoV-2, has led to a wide range of non-pharmaceutical interventions being implemented around the world to curb transmission. However, the economic and social costs of some of these measures, especially lockdowns, has been high. An alternative and widely discussed public health strategy for the COVID-19 pandemic would have been to 'shield' those most vulnerable to COVID-19 (minimising their contacts with others), while allowing infection to spread among lower risk individuals with the aim of reaching herd immunity. Here we retrospectively explore the effectiveness of this strategy using a stochastic SEIR framework, showing that even under the unrealistic assumption of perfect shielding, hospitals would have been rapidly overwhelmed with many avoidable deaths among lower risk individuals. Crucially, even a small (20%) reduction in the effectiveness of shielding would have likely led to a large increase (>150%) in the number of deaths compared to perfect shielding. Our findings demonstrate that shielding the vulnerable while allowing infections to spread among the wider population would not have been a viable public health strategy for COVID-19 and is unlikely to be effective for future pandemics.

15.
Evolution ; 75(12): 3175-3180, 2021 12.
Article in English | MEDLINE | ID: mdl-34633080

ABSTRACT

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.


Subject(s)
Parturition , Sex Ratio , Female , Humans , Male , Population Dynamics , Pregnancy
16.
J Theor Biol ; 527: 110832, 2021 10 21.
Article in English | MEDLINE | ID: mdl-34252402

ABSTRACT

The epidemiology of sexually transmitted infections (STIs) is inherently linked to host mating dynamics. Studies across many taxa show that adult sex ratio, a major determinant of host mating dynamics, is often skewed - sometimes strongly - toward males or females. However, few predictions exist for the effects of skewed sex ratio on STI epidemiology, and none when coupled with sex biased disease characteristics. Here we use mathematical modelling to examine how interactions between sex ratio and disease characteristics affect STI prevalence in males and females. Notably, we find that while overall disease prevalence peaks at equal sex ratios, prevalence per sex peaks at skewed sex ratios. Furthermore, disease characteristics, sex-biased or not, drive predictable differences in male and female STI prevalence as sex ratio varies, with higher transmission and lower virulence generally increasing differences between the sexes for a given sex ratio. Our work reveals new insights into how STI prevalence in males and females depends on a complex interaction between host population sex ratio and disease characteristics.


Subject(s)
HIV Infections , Sexually Transmitted Diseases , Adult , Bias , Female , Humans , Male , Prevalence , Sex Ratio , Sexual Behavior , Sexually Transmitted Diseases/epidemiology
18.
Curr Biol ; 31(4): R174-R177, 2021 02 22.
Article in English | MEDLINE | ID: mdl-33621500

ABSTRACT

Herd immunity is an important yet often misunderstood concept in epidemiology. As immunity accumulates in a population - naturally during the course of an epidemic or through vaccination - the spread of an infectious disease is limited by the depletion of susceptible hosts. If a sufficient proportion of the population is immune - above the 'herd immunity threshold' - then transmission generally cannot be sustained. Maintaining herd immunity is therefore critical to long-term disease control. In this primer, we discuss the concept of herd immunity from first principles, clarify common misconceptions, and consider the implications for disease control.


Subject(s)
Communicable Disease Control , Immunity, Herd , Animals , Epidemics/prevention & control , Epidemics/statistics & numerical data , Humans , Mice , Vaccination
19.
Lancet Planet Health ; 5(2): e84-e92, 2021 02.
Article in English | MEDLINE | ID: mdl-33581070

ABSTRACT

BACKGROUND: Climate change threatens to undermine the past 50 years of gains in public health. In response, the National Health Service (NHS) in England has been working since 2008 to quantify and reduce its carbon footprint. This Article presents the latest update to its greenhouse gas accounting, identifying interventions for mitigation efforts and describing an approach applicable to other health systems across the world. METHODS: A hybrid model was used to quantify emissions within Scopes 1, 2, and 3 of the Greenhouse Gas Protocol, as well as patient and visitor travel emissions, from 1990 to 2019. This approach complements the broad coverage of top-down economic modelling with the high accuracy of bottom-up data wherever available. Available data were backcasted or forecasted to cover all years. To enable the identification of measures to reduce carbon emissions, results were disaggregated by organisation type. FINDINGS: In 2019, the health service's emissions totalled 25 megatonnes of carbon dioxide equivalent, a reduction of 26% since 1990, and a decrease of 64% in the emissions per inpatient finished admission episode. Of the 2019 footprint, 62% came from the supply chain, 24% from the direct delivery of care, 10% from staff commute and patient and visitor travel, and 4% from private health and care services commissioned by the NHS. INTERPRETATION: This work represents the longest and most comprehensive accounting of national health-care emissions globally, and underscores the importance of incorporating bottom-up data to improve the accuracy of top-down modelling and enabling detailed monitoring of progress as health systems act to reduce emissions. FUNDING: Wellcome Trust.


Subject(s)
Carbon Footprint/statistics & numerical data , Climate Change , State Medicine/statistics & numerical data , Carbon Dioxide/analysis , Delivery of Health Care , England , Greenhouse Gases/analysis , Health Care Sector , Humans , Transportation
20.
J Evol Biol ; 33(12): 1795-1805, 2020 12.
Article in English | MEDLINE | ID: mdl-33073411

ABSTRACT

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.


Subject(s)
Biological Evolution , Host-Parasite Interactions , Models, Genetic , Sex , Animals , Female , Heterozygote , Male , Reproduction, Asexual
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