ABSTRACT
BoHV-4 replication cycle is dependent on the S-phase of the cell-cycle at the stage of viral DNA synthesis. Because p21 is a rate-limiting regulator of the G1/S-phase transition and up-regulated by DNA-damaging agents, in this study p21 expression in BoHV-4 infected cells was investigated. The p21 promoter was found to be highly activated in a dose- and time-dependent manner following BoHV-4 infection only in cells which are permissive for BoHV-4 replication. Thus p21 expression reports on BoHV-4 replication and could represent a host cell defensive response to infection-associated cellular damage.
Subject(s)
Cattle Diseases/virology , Cyclin-Dependent Kinase Inhibitor p21/biosynthesis , Herpesviridae Infections/veterinary , Herpesvirus 4, Bovine/physiology , Tumor Virus Infections/veterinary , Virus Replication , Animals , Biomarkers , Cattle , Cattle Diseases/metabolism , Cell Line , Genes, Reporter , Herpesviridae Infections/metabolism , Herpesviridae Infections/virology , Host-Pathogen Interactions , Mice , Promoter Regions, Genetic , Time Factors , Tumor Virus Infections/metabolism , Tumor Virus Infections/virologyABSTRACT
The CMV enhancer-promoter sequence is often used as a transcriptional regulatory element in vector systems. We have used this control element to drive expression of GFP in a lentivirus vector transgene in pigs and chickens. Promoted as a 'universal' enhancer/promoter element capable of transcriptional activity in a number of cells in vitro, CMV-GFP transgene expression in vivo is preferentially observed in exocrine cells. This expression profile validates the use of this transcriptional control sequence to target expression to exocrine cells in gene transfer strategies.
