During herpes simplex virus type 1 infection of rabbits, the ability to express the latency-associated transcript increases latent-phase transcription of lytic genes.
Trigeminal ganglia (TG) from rabbits latently infected with either wild-type herpes simplex virus type 1 (HSV-1) or the latency-associated transcript (LAT) promoter deletion mutant 17DeltaPst were assessed for their viral chromatin profile and transcript abundance. The wild-type 17syn+ genomes were more enriched in the transcriptionally permissive mark dimethyl H3 K4 than were the 17DeltaPst genomes at the 5' exon and ICP0 and ICP27 promoters. Reverse transcription-PCR analysis revealed significantly more ICP4, tk, and glycoprotein C lytic transcripts in 17syn+ than in 17DeltaPst. These results suggest that, for efficient reactivation from latency in rabbits, the LAT is important for increased transcription of lytic genes during latency.
Giordani
Nicole V
NV
Department of Molecular Genetics and Microbiology, Box 100266, University of Florida College of Medicine, Gainesville, FL 32610-0266, USA.
Neumann
Donna M
DM
Kwiatkowski
Dacia L
DL
Bhattacharjee
Partha S
PS
McAnany
Peterjon K
PK
Hill
James M
JM
Bloom
David C
DC
D000818:Animals; D003315:Cornea / Q000821:virology; D015870:Gene Expression / Q000235:genetics; D005814:Genes, Viral / Q000502:physiology*; D018259:Herpesvirus 1, Human / Q000235:genetics / Q000502:physiology*; D011817:Rabbits; D014158:Transcription, Genetic; D012668:Trigeminal Ganglion / Q000821:virology; D017735:Virus Latency / Q000502:physiology*