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