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You are located on Craig Miller, D.M.D., M.S. webpage.

Craig Miller, D.M.D., M.S.

Photo of Craig Miller, D.M.D., M.S.

University of Kentucky, Lexington, Kentucky, 
Bachelor of General Studies "with High Distinction"

University of Kentucky, College of Dentistry, Lexington, Kentucky, 
Doctor of Dental Medicine "with Distinction"

University of Texas Health Science Center, 
San Antonio, Texas
Master of Science & Certificate in Dental Diagnostic Science
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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


Miller, C.S., Danaher, R.J., Jacob, R.J. Molecular aspects of herpes simplex virus 1 latency, reactivation and recurrence. Crit 
Rev Oral Biol Med 9(4):541-562, 1998.

Danaher, R.J., Jacob, R.J., Miller, C.S. Establishment of a quiescent herpes simplex virus type 1 infection in nuerally 
differentiated PC12 cells. J Neuro Virol 5(3):258-267, 1999.

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

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

Danaher R.J., Savells-Arb AD, Black Jr SA, Jacob R.J., Miller C.S. Herpesvirus quiescence in neuronal cells IV: reactivation 
induced by pituitary adenylate cyclase activating polypeptide (PACAP) involves the protein kinase A pathway. J NeuroVirol 7: 
1-6, 2001.

Miller CS, Bhattacharjee PS, Higaki S, Jacob RJ, Danaher RJ, Thompson HW, Hill JM. Herpesvirus Quiescence (QIF) in
Neuronal Cells VI: Correlative Analysis Demonstrates Usefulness of QIF-PC12 Cells to Examine HSV-1 Latency and
Reactivation and Deregulated LAT ORF Expression. Curr Eye Research 26(3-4):239-48, 2003.

Danaher RJ, Jacob RJ, Miller CS. Herpesvirus quiescence in neuronal cells
α promoter and αV: Forskolin-responsiveness of the
herpes simplex virus type 1 contribution of the putative CRE element. J NeuroVirol 9:489-497, 2003.

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