Host-pathogen evolution modulates response to environmental change

University Of Maryland, College Park, College Park MD

Investigators

Abstract

Temperature can affect the severity and contagiousness of infectious diseases. For some diseases, warmer temperatures can increase severity, but for other diseases, especially those caused by fungal pathogens, high temperatures can lead to symptom reduction and improved health for the hosts. In such cases, warmer summers could bring a bit of climate ‘good news,’ releasing hosts populations from the burden of disease. However, the evolution of genetic changes in either host susceptibility to infection or pathogen sensitivity to heat have the potential to alter this outcome. This research will investigate the potential for such evolutionary change to buffer hosts and pathogens against rapidly changing seasonal temperatures using a combination of mathematical models and studies of a highly tractable model plant-disease system that naturally occurs across a large range of temperature variation. Results from this research will advance scientific knowledge of seasonally-dependent disease transmission, which is known to occur in humans, domesticated populations and wildlife, and lead to improved understanding of how evolutionary changes in hosts and pathogens feedback to affect risks posed by infectious diseases. Outcomes from this research could help improve temperature-based forecast models for disease spread, and will also inform management practices by identifying any unintended consequences of using heat to control disease symptoms and spread. This research will also result in the development of new educational material and opportunities for undergraduate students just entering studies in the life sciences. The research will investigate the central hypothesis that temperature-driven reductions in disease expression result in an evolutionary increase in host susceptibility by reducing selection for resistance. It will also explore the consequences of these host evolutionary shifts on the ability of disease to persist in habitats that would otherwise be too warm. To achieve this, new theoretical models will be developed that explore the impact of seasonal variation in temperature on host-pathogen evolutionary feedbacks for diseases that experience heat-induced curing. The team will also test the model predictions in a real-world disease system by quantifying susceptibility and transmission of the wild plant, Silene vulgaris, to its endemic fungal pathogen, Microbotryum silenes-inflatae, across an elevational gradient. This will determine whether populations at warmer, lower-elevation locations have increased susceptibility and that these shifts in susceptibility in turn impact the distribution and prevalence of disease. The research will also investigate whether pathogen populations are capable of evolving higher levels of heat tolerance, and exploring the impact of such evolution on disease transmission through a combination of models and field-based disease transmission experiments. This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.