A herpes simplex virus type 1 variant, deleted in the promoter region of the latency-associated transcripts, does not produce any detectable minor RNA species during latency in the mouse trigeminal ganglion

Abstract

In peripheral sensory ganglia latently infected with herpes simplex virus type 1 (HSV-1) transcription is restricted. A set of viral latency-associated transcripts, the LATs, have been characterized by Northern blotting and in situ hybridization. These transcripts have previously been mapped to a 3 kb region of the viral genome within the repeat long region. However, transcription from adjacent regions of the genome can be detected by in situ hybridization, which cannot be detected by Northern blotting. These RNAs are termed minor LATs or m-LAT. In this study we show that in ganglia latently infected with the HSV-1 variant 1704, which is deleted in one complete copy of the LAT gene and in the promoter and 5' portion of the other copy, m-LATs are not detected by in situ hybridization. Furthermore, the levels of DNA in nervous system tissue latently infected with the parental and the 1704 variant virus are similar. Thus we propose that the sequence elements necessary for initiating transcription or stabilizing m-LATs are within the region deleted in variant 1704 that codes for the promoter and the 5' end of the LATs.

Intranuclear foci containing low abundance herpes simplex virus latency-associated transcripts visualized by non-isotopic in situ hybridization

“…It has been proposed that major LATs are stable introns derived from a single 8'3 kb poly(A) + primary transcript (Devi-Rao et al, 1991 ;Farrell et al, 1991). In support of this proposal, a single promoter element located at the 5' end of the in situ positive region (almost 700 nucleotides upstream of the major LATs) accounts for all HSV-1 transcription during latency (Dobson et aL, 1989;Mitchell et al, 1990b). However, detection of a primary transcript and its putative spliced products (approx.…”

Replication, establishment of latent infection, expression of the latency-associated transcripts and explant reactivation of herpes simplex virus type 1 34.5 mutants in a mouse eye model

“…LAT promoter deletion mutants are replication competent in mice and reactivate with higher efficiency than 1716 or 1771 from explanted TG (Leib et al, 1989b;Steiner et al, 1989;Trousdale et al, 1991), even though deletion of the LAT promoter abolishes LAT expression during latent infection (Mitchell et al, 1990b;Steiner et al, 1989;Trousdale et al, 1991). Stable LAT expression is not required for efficient reactivation; there are HSV-1 deletion mutants that do not produce a stable LAT in either tissue culture or latent infections, yet reactivate normally Block et al, 1990).…”

Regions of the Herpes Simplex Virus Type 1 Latency-Associated Transcript That Protect Cells from Apoptosis In Vitro and Protect Neuronal Cells In Vivo

“…1A and B). The primary LAT (mLAT or minor LAT), which has been detected by in situ hybridization, is an 8.3-kb transcript that maps from nucleotide 118803.to a polyadenylation site at nucleotide 127140 and beyond on the viral genome (9,31). However, the most abundant LAT species from this region is a 2.0-kb stable intron (2.0-kb LAT; Fig.…”