Felicia Goodrum

Professor of Microbiology and Immunology

Our laboratory is broadly interested in complex interactions between DNA viruses and their host cells that allow viruses to subvert or co-opt cellular processes for viral objectives. Through co-evolution, herpesviruses have mastered our biology, skillfully manipulating the host to achieve an extraordinary coexistent latent state that enables the virus to persist indefinitely in the immunocompetent host. Human cytomegalovirus (HCMV) is the largest, most complex virus known to infect humans and asymptomatically infects most of the population worldwide. In addition to the risks to human health, HCMV is a powerful tool for understanding biological host process as it has evolved to target or manipulate the most pivotal points in almost and host process. Our laboratory seeks to define the virus-host interactions important for the virus to "sense" and "respond" to host cues and filter noise in the system to switch between latent and replicative states. This foundational knowledge is key to controlling HCMV pathology and will broadly define strategies by which viruses integrate into host cell biology. Our research interests include:

1. The molecular switch controlling HCMV latency and reactivation. Define the complex transcriptional patterns and the virus-host interactions differentially controlling them, as well as their dependence on cell type (e.g., epithelial, endothelial, hematopoietic) or differentiation state, to regulate the entry into and exit from latency.

2. DNA damage repair and replication: Define how HCMV hijacks and modulates host DNA repair and replication pathways to maintain viral genome integrity and modulate viral genome conformation for replication and latency. This work also provides novel insights into DNA replication and repair strategies in human cells that have been primarily understood in yeast.

3. Innate signaling. Define how the virus subverts and commandeers interferon signaling in navigating decisions to establish latency or reactivate from latency.

4. Liver X receptor (sterol) signaling. Define how HCMV regulates and is regulated by cholesterol signaling to make decisions to enter into or exit from latency.

5. HCMV modulation of barrier function and intestinal health. Using human intestinal organoids, define how HCMV impacts differentiation, proliferation, and function of the colonic epithelial cellular barrier through the modulation of host signaling pathways important to differentiation, proliferation and repair.

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