The type I interferon system represents the primary innate response pathway initiated upon viral infection. Type I interferons elicit potent cell-intrinsic and cell-extrinsic mechanisms to combat infection. However, when improperly regulated, these responses can lead to devastating immunopathologies. Polymorphisms in genes responsible for regulation of the type I interferon response can therefore have a profound effect on the outcome of viral infections. Our group is interested in understanding how host genetics contribute to the pathological outcome of viral infections. Identification and characterization of these factors will be used to inform more personalized approaches to the treatment of infectious diseases.
Abnormal inflammation is a signature of many neurodegenerative diseases. However, the way in which inflammation contributes to the pathology of these diseases is poorly defined. We are interested in understanding the role of inflammation in the etiology of neurodegenerative diseases, with a specific focus on its role in amyotrophic lateral sclerosis (ALS).