The main focus of the lab is to understand the role of host mitochondria during HCMV infection. HCMV relies on host metabolic machinery to supply the bioenergetic and biosynthetic intermediates needed for replication. This includes DNA, protein, and lipid synthesis and the energy required for these processes. Our data suggests that by controlling the mitochondria, HCMV can dictate ATP production, reactive oxygen species release, signaling to the nucleus, and, importantly, apoptotic pathways. We exploit multiple models to define the mechanistic interactions between the virus and host pathways that contribute to successful viral replication. The ultimate goal is to identify mechanisms utilized by HCMV to alter mitochondrial function and inform novel antiviral and therapeutic measures associated with viral infections or mitochondrial dysfunction.