Analysis of the Transcriptional Promoter Which Regulates the Latency-Related Transcript of Bovine Herpesvirus 1

Authors

Clinton J. Jones, University of Nebraska - LincolnFollow
G. Delhon, University of Nebraska-LincolnFollow
A. Bratanich, University of Nebraska - Lincoln
G. Kutish, University of Nebraska - Lincoln
D. Rock, University of Nebraska-LincolnFollow

Document Type

Article

Date of this Version

3-1-1990

Comments

Published in JOURNAL OF VIROLOGY, Mar. 1990, p. 1164-1170, Vol. 64, No. 3. Copyright © 1990, American Society for Microbiology. Used by permission.

Abstract

As a transcriptional promoter in primary cultures of sensory ganglionic neurons, DNA sequences near the 5' terminus of the latency-related (LR) gene of bovine herpesvirus 1 were at least 10 times more efficient than the simian virus 40 early promoter-enhancer. In contrast, as a promoter in bovine, rodent, or monkey cells, the LR promoter was approximately six times less efficient than the simian virus 40 early promoter-enhancer. The LR promoter had strict orientation preferences in neurons and all other mammalian cell lines tested. Removal of a 146-base-pair XhoI fragment from the LR promoter resulted in stimulation of LR promoter activity in bovine cells but not rabbit neurons, monkey fibroblasts, or rodent cells. LR promoter activity in bovine cells is stimulated by bovine herpesvirus 1 lytic infection, suggesting that viral gene products or virus-induced factors positively regulate the expression of the LR gene. A synthetic glucocorticoid, dexamethasone, repressed LR promoter activity in bovine cells. These results imply that a variety of factors can influence the expression of the LR gene during latent infections of neurons as well as during the lytic infection cycle.