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1. Coevolutionary theory of hosts and parasites

   https://doi.org/10.1111/jeb.13981  

   Buckingham, Lydia J.; Ashby, Ben (April 2022, Journal of Evolutionary Biology)
2. Fast-lived Hosts and Zoonotic Risk

   https://doi.org/10.1016/j.pt.2020.10.012  

   Albery, Gregory F.; Becker, Daniel J. (February 2021, Trends in Parasitology)
3. The visual ecology of selective predation: Are unhealthy hosts less stealthy hosts?

   https://doi.org/10.1002/ece3.8464  

   Wale, Nina; Fuller, Rebecca_C; Johnsen, Sönke; Turrill, McKenna_L; Duffy, Meghan_A (December 2021, Ecology and Evolution)

   Abstract Predators can strongly influence disease transmission and evolution, particularly when they prey selectively on infected hosts. Although selective predation has been observed in numerous systems, why predators select infected prey remains poorly understood. Here, we use a mathematical model of predator vision to test a long‐standing hypothesis about the mechanistic basis of selective predation in aDaphnia–microparasite system, which serves as a model for the ecology and evolution of infectious diseases. Bluegill sunfish feed selectively onDaphniainfected by a variety of parasites, particularly in water uncolored by dissolved organic carbon. The leading hypothesis for selective predation in this system is that infection‐induced changes in the transparency ofDaphniarender them more visible to bluegill. Rigorously evaluating this hypothesis requires that we quantify the effect of infection on the visibility of prey from the predator's perspective, rather than our own. Using a model of the bluegill visual system, we show that three common parasites,Metschnikowia bicuspidata,Pasteuria ramosa, andSpirobacillus cienkowskii, decrease the transparency ofDaphnia, rendering infectedDaphniadarker against a background of bright downwelling light. As a result of this increased brightness contrast, bluegill can see infectedDaphniaat greater distances than uninfectedDaphnia—between 19% and 33% further, depending on the parasite.PasteuriaandSpirobacillusalso increase the chromatic contrast ofDaphnia. These findings lend support to the hypothesis that selective predation by fish on infectedDaphniacould result from the effects of infection onDaphnia's visibility. However, contrary to expectations, the visibility ofDaphniawas not strongly impacted by water color in our model. Our work demonstrates that models of animal visual systems can be useful in understanding ecological interactions that impact disease transmission. 

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4. Molecular Dialog Between Parasitic Plants and Their Hosts

   https://doi.org/10.1146/annurev-phyto-082718-100043  

   Clarke, Christopher R.; Timko, Michael P.; Yoder, John I.; Axtell, Michael J.; Westwood, James H. (August 2019, Annual Review of Phytopathology)

   Parasitic plants steal sugars, water, and other nutrients from host plants through a haustorial connection. Several species of parasitic plants such as witchweeds ( Striga spp.) and broomrapes ( Orobanche and Phelipanche spp.) are major biotic constraints to agricultural production. Parasitic plants are understudied compared with other major classes of plant pathogens, but the recent availability of genomic and transcriptomic data has accelerated the rate of discovery of the molecular mechanisms underpinning plant parasitism. Here, we review the current body of knowledge of how parasitic plants sense host plants, germinate, form parasitic haustorial connections, and suppress host plant immune responses. Additionally, we assess whether parasitic plants fit within the current paradigms used to understand the molecular mechanisms of microbial plant–pathogen interactions. Finally, we discuss challenges facing parasitic plant research and propose the most urgent questions that need to be answered to advance our understanding of plant parasitism. 

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5. Hosts, microbiomes, and the evolution of critical windows

   https://doi.org/10.1002/evl3.298  

   Metcalf, C. Jessica E.; Tepekule, Burcu; Bruijning, Marjolein; Koskella, Britt (December 2022, Evolution Letters)

   Abstract The absence of microbial exposure early in life leaves individuals vulnerable to immune overreaction later in life, manifesting as immunopathology, autoimmunity, or allergies. A key factor is thought to be a “critical window” during which the host's immune system can “learn” tolerance, and beyond which learning is no longer possible. Animal models indicate that many mechanisms have evolved to enable critical windows, and that their time limits are distinct and consistent. Such a variety of mechanisms, and precision in their manifestation suggest the outcome of strong evolutionary selection. To strengthen our understanding of critical windows, we explore their underlying evolutionary ecology using models encompassing demographic and epidemiological transitions, identifying the length of the critical window that would maximize fitness in different environments. We characterize how direct effects of microbes on host mortality, but also indirect effects via microbial ecology, will drive the optimal length of the critical window. We find that indirect effects such as magnitude of transmission, duration of infection, rates of reinfection, vertical transmission, host demography, and seasonality in transmission all have the effect of redistributing the timing and/or likelihood of encounters with microbial taxa across age, and thus increasing or decreasing the optimal length of the critical window. Declining microbial population abundance and diversity are predicted to result in increases in immune dysfunction later in life. We also make predictions for the length of the critical window across different taxa and environments. Overall, our modeling efforts demonstrate how critical windows will be impacted over evolution as a function of both host-microbiome/pathogen interactions and dispersal, raising central questions about potential mismatches between these evolved systems and the current loss of microbial diversity and/or increases in infectious disease. 

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