My research interests are centered on understanding the mechanisms by which type I interferons mediate their biological effects during the host response to viral infections and in the development of autoimmune diseases. Type I interferons regulate a wide array of biological responses, including the induction of an antiviral state, regulation of programmed cell death, inhibition of cell growth, and the modulation of both the innate and adaptive immune responses. Interferons mediate these effects through the induction of hundreds of interferon stimulated genes (ISGs). Over the years, we have worked to identify and characterize the functions of different ISGs during viral infection, including interferon stimulated gene 15 (ISG15) and the differential functions of type I interferon subtypes. In addition, we have worked to understand the pathogenesis of emerging viral infections, including Chikungunya virus, and now SARS-CoV-2. Chikungunya virus is a re-emerging alphavirus that causes fever, rash, and arthritis in infected patients. Through the utilization of patient cohorts, clinical samples, and the development of mouse models of virus-induced arthritis, we are investigating the immune factors that regulate disease pathogenesis, working to develop therapeutics, and exploring how this virus causes chronic disease long after acute infection has been resolved.