cmiller@pop.uky.edu

Our long-term goal is to understand how herpes simplex virus 1 and 2 (HSV) reactivate from a latent state. Following epithelial cell infection, HSV spreads to sensory neurons where it remains latent for the life of the host. Periodically, the virus reactivates from latency following stress and trauma. Our laboratory is interested in understanding the stress-associated regulatory processes that allow the virus to reactivate. Ongoing studies use neurally differentiated PC12 cells as hosts of HSV-1 latent-like infection. Genes and proteins critical to reactivation are evaluated by exposing quiescently-infected cells and transfected cells to stimulatory agents associated with reactivation. Genes and proteins activated and/or repressed are identified using viral deletion mutants, Western, Southern and Northern blotting, reverse transcriptase polymerase chain reaction (RT-PCR), the chloramphenicol acetyl transferase (CAT) and luciferase assays, and enhanced green fluorescence. Other technologies used routinely are cell culture, direct plaque assay, mutant construction, immunocytochemistry, in situ hybridization, Northern blot analyses, electrophoretic mobility shift assay, the polymerase chain reaction, and confocal and electron microscopy.

Collaboration with Robert J. Jacob