title: The herpes simplex virus type 1 early gene (thymidine kinase) promoter is activated in neurons of brain, but not trigeminal ganglia, of transgenic mice in the absence of viral proteins.
abstract: Latent infection of sensory neurons and reactivation are necessary for maintenance of herpes simplex virus type 1 (HSV-1) in its host population. It has been proposed that the HSV-1 early gene, thymidine kinase (TK), may play an important regulatory role in this process. The authors used reporter transgenic mice to test whether sensory ganglia neurons could activate the HSV-1 TK reporter transgene in the absence of viral proteins. The reporter transgene was activated in subsets of neurons in the brain but was not activated in sensory ganglia neurons following a variety of experimental manipulations. These results do not support a role for TK in regulation of the latent viral genome.
authors.affiliation: Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri 65211, USA.
authors.forename: Christie M
authors.initials: CM
authors.lastname: Loiacono
authors.forename: Robert
authors.initials: R
authors.lastname: Myers
authors.forename: William J
authors.initials: WJ
authors.lastname: Mitchell
mesh_terms: D000818:Animals; D001921:Brain / Q000166:cytology* / Q000821:virology; D017930:Genes, Reporter; D006561:Herpes Simplex / Q000821:virology*; D018259:Herpesvirus 1, Human / Q000235:genetics*; D051379:Mice; D008822:Mice, Transgenic; D009475:Neurons, Afferent / Q000502:physiology* / Q000821:virology; D011401:Promoter Regions, Genetic; D013937:Thymidine Kinase / Q000235:genetics*; D019076:Transgenes / Q000235:genetics; D012668:Trigeminal Ganglion / Q000166:cytology* / Q000821:virology; D017735:Virus Latency
chemical_list: D013937:Thymidine Kinase