Acute invasive infections caused by fungi are a well-established cause of morbidity and mortality in neutropenic individuals, heavily immunosuppressed patients, and patients in the ICU due to severe viral infection, but these invasive infections occur only in a small proportion of the population. However, chronic fungal infections, such as severe asthma with fungal sensitization (SAFS) and allergic bronchopulmonary aspergillosis (ABPA), are much more prevalent and associated with prolonged healthcare needs and costs. While our understanding of how the immune system keeps invasive fungal infections at bay is rapidly emerging, there is a critical gap in our understanding of the early host-fungal interactions that are necessary for the establishment of fungal persistence and allergic disease observed during chronic fungal disease. Through pilot grant funding from DartCF and the Cystic Fibrosis Foundation, our laboratory, in collaboration with The Cramer Laboratory, has developed a robust small animal ABPA model that has all the hallmark features of human ABPA disease including robust Th2 immunity, severe IgE elevation, and, most importantly, fungal persistence. We hope to use this new ABPA model to dissect the molecular mechanism(s) by which A. fumigatus persists in vivo to drive Th2/IgE hypersensitivity and ABPA disease.