MCB Joint Seminar Series: John Purdy "Metabolic Dynamics Feeding and Starving Human Cytomegalovirus"

From entry into and exit from cells, the replication of viruses requires metabolism. Since herpesviruses do not encode a metabolic network, successful virus infection depends on host metabolism. We focus on human cytomegalovirus (HCMV), a common herpesvirus that causes disease in the immunocompromised and is a leading cause of congenital disabilities. Our research defines the virus-host metabolism interactions that help HCMV to successfully replicate, specifically changes in lipid metabolism. We demonstrated that HCMV infection promotes lipid synthesis, altering the host lipidome to establish a lipid environment that favors the virus. Moreover, a virus's dependency on host metabolism is a weakness the host can exploit—or potentially scientists—to restrict virus replication. A more recent theme of our research is to understand how host cells regulate metabolism to reduce virus replication, i.e., metabolism as an intrinsic cellular antiviral defense. Overall, our studies reveal the dynamics between the host and HCMV in raising or lowering a metabolic barrier during virus replication.