A mutant deleted for most of the herpes simplex virus type 1 (HSV-1) UOL gene does not affect the spontaneous reactivation phenotype in rabbits.

TitleA mutant deleted for most of the herpes simplex virus type 1 (HSV-1) UOL gene does not affect the spontaneous reactivation phenotype in rabbits.
Publication TypeJournal Article
Year of Publication2006
AuthorsChan D, Cohen J, Naito J, Mott KR, Osorio N, Jin L, Fraser NW, Jones C, Wechsler SL, Perng GC
JournalJournal of neurovirology
Volume12
Issue1
Pagination5-16
Date Published2006 Feb
ISSN1355-0284
KeywordsAnimals, Disease Models, Animal, DNA, Viral, Gene Deletion, Genes, Viral, Herpes Simplex, Herpesvirus 1, Human, Mutation, Rabbits, Restriction Mapping, Virus Activation
Abstract

The mechanisms involved in the herpes simplex virus type 1 (HSV-1) latency-reactivation cycle are not fully understood. The latency-associated transcript (LAT) is the only HSV-1 RNA abundantly detected during neuronal latency. LAT plays a significant role in latency because LAT(-) mutants have a reduced reactivation phenotype. Several novel viral transcripts have been identified within the LAT locus, including UOL, which is located just upstream of LAT. The authors report here on a mutant, DeltaUOL, which has a 437-nucleotide deletion that deletes most of UOL. DeltaUOL replicated similarly to its wild-type parental McKrae HSV-1 strain in infected cells, the eyes, trigeminal ganglia, and brains of mice and rabbits. It was indistinguishable from wild-type virus as regards explant-induced reactivation in mice, and spontaneous reactivation in rabbits. In contrast, DeltaUOL was significantly less virulent in mice. Thus, UOL appears to be dispensable for the wild-type reactivation phenotype while appearing to play a role in neurovirulence in ocularly infected animals.

Alternate JournalJ. Neurovirol.