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.