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1. Superinfection and the evolution of an initial asymptomatic stage

   https://doi.org/10.1098/rsos.202212  

   Saad-Roy, Chadi M.; Grenfell, Bryan T.; Levin, Simon A.; Pellis, Lorenzo; Stage, Helena B.; van den Driessche, P.; Wingreen, Ned S. (January 2021, Royal Society Open Science)

   null (Ed.)

   Pathogens have evolved a variety of life-history strategies. An important strategy consists of successful transmission by an infected host before the appearance of symptoms, that is, while the host is still partially or fully asymptomatic. During this initial stage of infection, it is possible for another pathogen to superinfect an already infected host and replace the previously infecting pathogen. Here, we study the effect of superinfection during the first stage of an infection on the evolutionary dynamics of the degree to which the host is asymptomatic (host latency) in that same stage. We find that superinfection can lead to major differences in evolutionary behaviour. Most strikingly, the duration of immunity following infection can significantly influence pathogen evolutionary dynamics, whereas without superinfection the outcomes are independent of host immunity. For example, changes in host immunity can drive evolutionary transitions from a fully symptomatic to a fully asymptomatic first infection stage. Additionally, if superinfection relative to susceptible infection is strong enough, evolution can lead to a unique strategy of latency that corresponds to a local fitness minimum, and is therefore invasible by nearby mutants. Thus, this strategy is a branching point, and can lead to coexistence of pathogens with different latencies. Furthermore, in this new framework with superinfection, we also find that there can exist two interior singular strategies. Overall, new evolutionary outcomes can cascade from superinfection. 

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2. Dynamics in a simple evolutionary-epidemiological model for the evolution of an initial asymptomatic infection stage

   https://doi.org/10.1073/pnas.1920761117  

   Saad-Roy, Chadi_M; Wingreen, Ned_S; Levin, Simon_A; Grenfell, Bryan_T (May 2020, Proceedings of the National Academy of Sciences)

   Significance Numerous factors affect early transmission by a newly infected host. A less symptomatic initial infection can persist longer due to reduced immune response, but at the cost of reduced transmission. Assuming simple trade-offs for progression and transmission rates in the initial infectious stage, we couple epidemiological and evolutionary dynamics. We find that fully asymptomatic, less symptomatic, or fully symptomatic first stages are possible evolutionary outcomes, with possible surprising bistability between zero and maximal asymptomatic behavior. This bistability implies that small changes in parameter values followed by reversion to their original values could lead to an alternative stable state with a qualitative difference in degree of first-stage symptoms. Therefore, disease control strategies can have dramatic evolutionary outcomes, cascading to epidemiological consequences. 

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3. Environmental Persistence of the World's Most Burdensome Infectious and Parasitic Diseases

   https://doi.org/10.3389/fpubh.2022.892366  

   Hopkins, Skylar R.; Jones, Isabel J.; Buck, Julia C.; LeBoa, Christopher; Kwong, Laura H.; Jacobsen, Kim; Rickards, Chloe; Lund, Andrea J.; Nova, Nicole; MacDonald, Andrew J.; et al (July 2022, Frontiers in Public Health)

   Humans live in complex socio-ecological systems where we interact with parasites and pathogens that spend time in abiotic and biotic environmental reservoirs (e.g., water, air, soil, other vertebrate hosts, vectors, intermediate hosts). Through a synthesis of published literature, we reviewed the life cycles and environmental persistence of 150 parasites and pathogens tracked by the World Health Organization's Global Burden of Disease study. We used those data to derive the time spent in each component of a pathogen's life cycle, including total time spent in humans versus all environmental stages. We found that nearly all infectious organisms were “environmentally mediated” to some degree, meaning that they spend time in reservoirs and can be transmitted from those reservoirs to human hosts. Correspondingly, many infectious diseases were primarily controlled through environmental interventions (e.g., vector control, water sanitation), whereas few (14%) were primarily controlled by integrated methods (i.e., combining medical and environmental interventions). Data on critical life history attributes for most of the 150 parasites and pathogens were difficult to find and often uncertain, potentially hampering efforts to predict disease dynamics and model interactions between life cycle time scales and infection control strategies. We hope that this synthetic review and associated database serve as a resource for understanding both common patterns among parasites and pathogens and important variability and uncertainty regarding particular infectious diseases. These insights can be used to improve systems-based approaches for controlling environmentally mediated diseases of humans in an era where the environment is rapidly changing. 

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4. Pathogens stabilize or destabilize depending on host stage structure

   https://doi.org/10.3934/mbe.2023901  

   Hite, Jessica L; de_Roos, André M (November 2023, Mathematical Biosciences and Engineering)

   A common assumption is that pathogens more readily destabilize their host populations, leading to an elevated risk of driving both the host and pathogen to extinction. This logic underlies many strategies in conservation biology and pest and disease management. Yet, the interplay between pathogens and population stability likely varies across contexts, depending on the environment and traits of both the hosts and pathogens. This context-dependence may be particularly important in natural consumer-host populations where size- and stage-structured competition for resources strongly modulates population stability. Few studies, however, have examined how the interplay between size and stage structure and infectious disease shapes the stability of host populations. Here, we extend previously developed size-dependent theory for consumer-resource interactions to examine how pathogens influence the stability of host populations across a range of contexts. Specifically, we integrate a size- and stage-structured consumer-resource model and a standard epidemiological model of a directly transmitted pathogen. The model reveals surprisingly rich dynamics, including sustained oscillations, multiple steady states, biomass overcompensation, and hydra effects. Moreover, these results highlight how the stage structure and density of host populations interact to either enhance or constrain disease outbreaks. Our results suggest that accounting for these cross-scale and bidirectional feedbacks can provide key insight into the structuring role of pathogens in natural ecosystems while also improving our ability to understand how interventions targeting one may impact the other. 

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5. Epidemic evolutionarily stable strategies within an age-structured host population

   https://doi.org/10.1073/pnas.2418170122  

   Eilersen, Andreas; Bjørnstad, Ottar N; Li, Ruiyun; Schreiber, Sebastian J; Pei, Zeyuan; Stenseth, Nils Chr (March 2025, Proceedings of the National Academy of Sciences)

   To understand infectious disease dynamics, we need to understand the inextricably intertwined nature of the ecology and evolution of pathogens and hosts. Epidemiological dynamics of many infectious diseases have highlighted the importance of considering the demographics of the societies in which they spread, particularly with respect to age structure. In addition, the waves of the recent COVID-19 pandemic driven by variant replacements at an unprecedented speed show that it is vital to consider the evolutionary aspects. The classic trade-off theory of virulence addresses aspects of pathogen evolution, but here we explore in more detail the possibility of society-specific evolutionarily stable strategies (ESS) during an unfolding pandemic. Theory posits the existence under some conditions of an ESS representing the evolutionary endpoint of change. By using a demographically realistic model incorporating infection rates that vary with age, we outline which evolutionary scenarios are plausible. Focusing on the rate of infection and duration of infectivity, we ask whether an ESS exists, what characterizes it, and as a result which long-term public-health consequences may be expected. We demonstrate that the ESS of an evolving pathogen depends upon the background age-dependent frailty and mortality rates. Our findings shed important light on the plausible long-term trajectories of highly evolvable novel pathogens. 

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