American Society of Naturalists

Jessica Clark, Luke McNally, and Tom J. Little (Feb 2021)

Host ageing can modulate epidemiological dynamics

Read the Article (Just Accepted)

Populations are often made up of individuals of different ages. These individuals of different ages often have different reproductive capabilities, risks of dying and susceptibilities to infection. Reproduction, mortality and susceptibility are also important aspects of infectious disease dynamics. Despite these parallels, and how common it is for populations to be age-structured, little research has explored how characteristics of population age structure, and specifically individual ageing can impact disease spread. Researchers at the University of Edinburgh took an interdisciplinary approach in addressing these questions. First, using the freshwater crustacean Daphnia magna, they carried out two experiments. The results show that the process of ageing within a single organism is not unidirectional. For example, whilst old mothers produce fewer offspring with an increase in their age, those offspring from old mothers performed equally or indeed better than offspring from young mothers, across a suite of traits including susceptibility to infection. Drawing on these experimental observations, they then developed a deterministic age-structured mathematical model that showed that age-specific susceptibility, maternal effects on offspring susceptibility, age-specific rates of reproduction and age-specific rates of mortality, can all affect infectious disease dynamics in direct and indirect ways. Using this model, they also showed that these dynamics are dependent on the ecological conditions experienced by the population, most noticeably the pressure of extrinsic mortality (for example, harvesting or rapid environmental change). In light of the rapid rate of human population age seen globally, the model was finally used to ask how slowing the process of ageing in humans (or those showing a similar ageing profile) could affect infectious disease dynamics, showing that an increase in lifespan without an increase in healthspan could increase disease transmission.

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Abstract

Reproduction, mortality and immune function often change with age, but do not invariably deteriorate. Across the tree of life, there is extensive variation in age-specific performance and changes to key life-history traits. These changes occur on a spectrum from classic senescence, where performance declines with age, to juvenescence, where performance improves with age. Reproduction, mortality and immune function are also important factors influencing the spread of infectious disease, yet there exists no comprehensive investigation into how the ageing spectrum of these traits impacts epidemics. We used a model laboratory infection system to compile an ageing profile of a single organism, including traits directly linked to pathogen susceptibility, and those that should indirectly alter pathogen transmission by influencing demography. We then developed generalizable epidemiological models demonstrating that different patterns of ageing produce dramatically different transmission landscapes: in many cases ageing can reduce the probability of epidemics, but it can also promote severity. This work provides context and tools for use across taxa by empiricists, demographers and epidemiologists, advancing our ability to accurately predict factors contributing to epidemics, or the potential repercussions of senescence manipulation.