My lab is interested in how human cytomegalovirus (HCMV) manipulates host metabolic pathways to ensure efficient replication. HCMV is ubiquitous in humans and like all herpesviruses, infects the host for life. The main focus of my 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 to inform novel antiviral and therapeutic measures associated with viral infections or mitochondrial dysfunction. Our metabolic observations are also being applied to diverse fields such as cancer and aging. We are exploring how HCMV may contribute to these pathologies by altering the metabolic microenvironment or contributing to mitochondrial dysfunction.
Research interests: cytomegalovirus; mitochondria; metabolism; adipose tissue; antivirals; aging