rjdana0@pop.uky.edu

The focus of the laboratory is the mechanism by which herpes simplex virus (HSV) reactivates from latently infected cells. We employ a novel in vitro latency model consisting of neurally differentiated PC12 cells latently infected with HSV. The latent state is characterized by the lack of infectious virus production and minimal viral gene expression. Virus can be induced to reactivate by a variety of means including physical and chemical trauma. Current emphasis is targeted to changes in viral and host gene expression during reactivation events. Real-time reverse transcription polymerase chain reaction (RT-PCR) is routinely performed to address these goals.

Danaher R. J., A. D. Savells-Arb, S. A. Black, R. J. Jacob, and C. S. Miller. 2001. Herpesvirus quiescence in neuronal cells IV: Virus activation induced by pituitary adenylate cyclase-activating polypeptide (PACAP) involves the protein kinase A pathway. J NeuroVirol 7:163-168.

Danaher R. J., R. J. Jacob, and C. S. Miller. 2000. Herpesvirus quiescence in neuronal cells III: Antiviral conditions not required to establish and maintain HSV-2 quiescence. J. NeuroVirol. 6:296-302.

Danaher R. J., R. J. Jacob, M. D. Chorak, C. Freeman, and C. S. Miller. 1999. Heat stress activates production of herpes simplex virus type 1 from quiescently infected neurally differentiated PC12 cells. J. NeuroVirol. 5:374-383. 

Danaher R. J., R. J. Jacob, and C. S. Miller. 1999. Establishment of a quiescent herpes simplex virus type 1 infection in PC12 cells. J. NeuroVirol. 5:258-267.

Miller C. S., R. J. Danaher, and R. J. Jacob. 1998. Molecular aspects of herpes simplex virus 1 latency, reactivation, and recurrence. Crit. Rev. Oral Biol. Oral Med. 9:541-562.