Associate Professor, BIO5 Institute
Director, Graduate Program in Immunobiology
Associate Professor, Cellular and Molecular Medicine
Associate Professor, Cancer Biology - GIDP
Associate Professor, Genetics - GIDP
Associate Professor, Molecular and Cellular Biology
Felicia Goodrum graduated with her PhD from Wake Forest University and then trained as a postdoctoral fellow with Thomas Shenk at Princeton University where she was a Leukemia and Lymphoma Society Fellow and Special Fellow. Dr. Goodrum joined the faculty at the University of Arizona in the Department of Immunobiology and the BIO5 Institute in 2006 and is an Assoicate Professor. Dr. Goodrum is the recipient of the Pew Scholar in Biomedical Sciences Award and the Presidential Award for Early Career Scientists and Engineers. Dr. Goodrum's work throughout her career has focused on complex interaction between viruses and their host and is currently focused on the mechanisms of viral persistence of human cytomegalovirus
Dr. Goodrum's long-standing research focus is to understand the molecular virus-host interactions important to human cytomegalovirus (CMV) latency and persistence in the host. While the molecular basis of CMV latency is poorly understood, it is critical to controlling CMV pathology in the immunocompromised, as well as pathologies (e.g. CMV disease following stem cell transplantation in leukemia patients) that are linked to persistence of the virus in healthy individuals. She has developed a physiologically-relevant, in vitro model for the study of HCMV latency using primary CD34+ hematopoietic progenitor cells (HPCs). Using this model, she has investigated the affects of HCMV on hematopoiesis and defined profiles of viral gene expression in defined CD34+ hematopoietic subpopulations.
As a PI on several NIH-funded grants, Dr. Goodrum has further identified the first virus-coded determinants required for HCMV latency and reactivation from latency. Their recent work has defined the epidermal growth factor receptor (EGFR) as primary pathway targeted by these viral determinants to switch between latent and replicative states of infection. The goal of their research program is to define the mechanistic underpinnings of HCMV latency and lay the foundation for clinical interventions to control CMV disease in all settings.