title: Expression of beta-galactosidase in neurons of dorsal root ganglia which are latently infected with herpes simplex virus type 1.
abstract: Explanation into culture of dorsal root ganglia (DRG) latently infected with herpes simplex virus type 1 (HSV-1) causes reactivation of the virus. Previous studies have suggested that either latency-associated transcripts (LATs) were removed as an early consequence of reactivation or, alternatively, there was a population of latently infected cells which did not contain LATs. We have now attempted to detect this population of neurons by inserting a reporter gene (Escherichia coli lacZ gene), under the control of promoters other than LAT, into the HSV-1 strain 17 mutant in 1814, which was used in the earlier studies. One of these promoters, the human cytomegalovirus enhancer, resulted in weak expression of beta-galactosidase in DRG neurons for at least 5 months. The pattern of staining was predominantly homogeneous in neurons at 3 or 5 days post-infection or at 3 days post-explanation, and was predominantly speckled in latently infected neurons (1 to 5 months post-infection). About 30% of the beta-galactosidase-positive neurons did not contain LATs by in situ hybridization. However, the detergents used to enable penetration of the substrate for beta-galactosidase had also reduced the levels of the LATs; in neurons which originally had only small numbers of LATs this may have reduced levels to below those detectable by the methods used. There was, therefore, no unequivocal evidence for a population of latently HSV-1-infected cells which did not express LATs.
authors.affiliation: University of Glasgow Department of Neurology, Southern General Hospital, UK.
authors.forename: M S
authors.initials: MS
authors.lastname: Ecob-Prince
authors.forename: K
authors.initials: K
authors.lastname: Hassan
authors.forename: M T
authors.initials: MT
authors.lastname: Denheen
authors.forename: C M
authors.initials: CM
authors.lastname: Preston
mesh_terms: D000818:Animals; D003587:Cytomegalovirus / Q000235:genetics; D004742:Enhancer Elements, Genetic; D004926:Escherichia coli / Q000201:enzymology / Q000235:genetics; D005727:Ganglia, Spinal / Q000201:enzymology / Q000821:virology*; D018259:Herpesvirus 1, Human / Q000254:growth & development / Q000502:physiology*; D006801:Humans; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009474:Neurons / Q000201:enzymology / Q000821:virology*; D009924:Organ Culture Techniques; D011401:Promoter Regions, Genetic; D014158:Transcription, Genetic; D014162:Transfection; D014775:Virus Activation; D001616:beta-Galactosidase / Q000096:biosynthesis*
chemical_list: D001616:beta-Galactosidase