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1. Bidirectional interactions between host social behaviour and parasites arise through ecological and evolutionary processes

   https://doi.org/10.1017/S0031182020002048  

   Hawley, Dana M.; Gibson, Amanda K.; Townsend, Andrea K.; Craft, Meggan E.; Stephenson, Jessica F. (March 2021, Parasitology)

   null (Ed.)

   Abstract An animal's social behaviour both influences and changes in response to its parasites. Here we consider these bidirectional links between host social behaviours and parasite infection, both those that occur from ecological vs evolutionary processes. First, we review how social behaviours of individuals and groups influence ecological patterns of parasite transmission. We then discuss how parasite infection, in turn, can alter host social interactions by changing the behaviour of both infected and uninfected individuals. Together, these ecological feedbacks between social behaviour and parasite infection can result in important epidemiological consequences. Next, we consider the ways in which host social behaviours evolve in response to parasites, highlighting constraints that arise from the need for hosts to maintain benefits of sociality while minimizing fitness costs of parasites. Finally, we consider how host social behaviours shape the population genetic structure of parasites and the evolution of key parasite traits, such as virulence. Overall, these bidirectional relationships between host social behaviours and parasites are an important yet often underappreciated component of population-level disease dynamics and host–parasite coevolution. 

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2. Age‐prevalence curves in a multi‐species parasite community

   https://doi.org/10.1111/1365-2435.14701  

   Preston, Daniel L; Falke, Landon P; Novak, Mark (January 2025, Functional Ecology)

   Abstract The relationship between infection prevalence and host age is informative because it can reveal processes underlying disease dynamics. Most prior work has assumed that age‐prevalence curves are shaped by infection rates, host immunity and/or infection‐induced mortality. Interactions between parasites within a host have largely been overlooked as a source of variation in age‐prevalence curves.We used field survey data and models to examine the role of interspecific interactions between parasites in shaping age‐prevalence curves. The empirical dataset included quantification of parasite infection prevalence for eight co‐occurring trematodes in over 15,000 snail hosts. We characterized age‐prevalence curves for each taxon, examined how they changed over space in relation to co‐occurring trematodes and tested whether the shape of the curves aligned with expectations for the frequencies of coinfections by two taxa in the same host. The models explored scenarios that included negative interspecific interactions between parasites, variation in the force‐of‐infection (FOI) and infection‐induced mortality that varied with host age, which were mechanisms hypothesized to be important in the empirical dataset.In the empirical dataset, four trematode parasites had monotonic increasing age‐prevalence curves and four had unimodal age‐prevalence curves. Some of the curves remained consistent in shape in relation to the prevalence of other potentially interacting trematodes, while some shifted from unimodal to monotonic increasing, suggesting release from negative interspecific interactions. The most common taxa with monotonic increasing curves had lower co‐infection frequencies than expected, suggesting they were competitively dominant. Taxa with unimodal curves had coinfection frequencies that were closer to those expected by chance.The model showed that negative interspecific interactions between parasites can cause a unimodal age‐prevalence curve in the subordinate taxon. Increases in the FOI and/or infection‐induced mortality of the dominant taxon cause shifts in the peak prevalence of the subordinate taxon to a younger host age. Infection‐induced mortality that increased with host age was the only scenario that caused a unimodal curve in the dominant taxon.Results indicated that negative interspecific interactions between parasites contributed to variation in the shape of age‐prevalence curves across parasite taxa and support the growing importance of incorporating interactions between parasites in explaining population‐level patterns of host infection over space and time. Read the freePlain Language Summaryfor this article on the Journal blog. 

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3. Causation without correlation: parasite-mediated frequency-dependent selection and infection prevalence

   https://doi.org/10.1098/rsbl.2021.0321  

   Lively, Curtis M.; Xu, Julie; Ben-Ami, Frida (December 2021, Biology Letters)

   Parasite-mediated selection is thought to maintain host genetic diversity for resistance. We might thus expect to find a strong positive correlation between host genetic diversity and infection prevalence across natural populations. Here, we used computer simulations to examine host–parasite coevolution in 20 simi-isolated clonal populations across a broad range of values for both parasite virulence and parasite fecundity. We found that the correlation between host genetic diversity and infection prevalence can be significantly positive for intermediate values of parasite virulence and fecundity. But the correlation can also be weak and statistically non-significant, even when parasite-mediated frequency-dependent selection is the sole force maintaining host diversity. Hence correlational analyses of field populations, while useful, might underestimate the role of parasites in maintaining host diversity. 

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4. Immunological feedback loops generate parasite persistence thresholds that explain variation in infection duration

   https://doi.org/10.1098/rspb.2024.0934  

   Cressler, Clayton E; Metz, Daniel_C G; Chang_van_Oordt, David A; Graham, Andrea L (September 2024, Proceedings of the Royal Society B: Biological Sciences)

   Infection duration affects individual host fitness and between-host transmission. Whether an infection is cleared or becomes chronic depends on the complex interaction between host immune responses and parasite growth. Empirical and theoretical studies have suggested that there are critical thresholds of parasite dose that can determine clearance versus chronicity, driven by the ability of the parasite to manipulate host immunity. However, the mammalian immune response is characterized by strong positive and negative feedback loops that could generate duration thresholds even in the absence of direct immunomodulation. Here, we derive and analyse a simple model for the interaction between T-cell subpopulations and parasite growth. We show that whether an infection is cleared or not is very sensitive to the initial immune state, parasite dose and strength of immunological feedbacks. In particular, chronic infections are possible even when parasites provoke a strong and effective immune response and lack any ability to immunomodulate. Our findings indicate that the initial immune state, which often goes unmeasured in empirical studies, is a critical determinant of infection duration. This work also has implications for epidemiological models, as it implies that infection duration will be highly variable among individuals, and dependent on each individual’s infection history. 

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5. Predation shifts coevolution toward higher host contact rate and parasite virulence

   https://doi.org/10.1098/rspb.2021.2800  

   Walsman, Jason C.; Cressler, Clayton E. (July 2022, Proceedings of the Royal Society B: Biological Sciences)

   Hosts can avoid parasites (and pathogens) by reducing social contact, but such isolation may carry costs, e.g. increased vulnerability to predators. Thus, many predator–host–parasite systems confront hosts with a trade-off between predation and parasitism. Parasites, meanwhile, evolve higher virulence in response to increased host sociality and consequently, increased multiple infections. How does predation shift coevolution of host behaviour and parasite virulence? What if predators are selective, i.e. predators disproportionately capture the sickest hosts? We answer these questions with an eco-coevolutionary model parametrized for a Trinidadian guppy–Gyrodactylusspp. system. Here, increased predation drives host coevolution of higher grouping, which selects for higher virulence. Additionally, higher predator selectivity drives the contact rate higher and virulence lower. Finally, we show how predation and selectivity can have very different impacts on host density and prevalence depending on whether hosts or parasites evolve, or both. For example, higher predator selectivity led to lower prevalence with no evolution or only parasite evolution but higher prevalence with host evolution or coevolution. These findings inform our understanding of diverse systems in which host behavioural responses to predation may lead to increased prevalence and virulence of parasites. 

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