The herpes simplex virus type 1 strain 17 open reading frame RL1 encodes a polypeptide of apparent Mr 37K equivalent to ICP34.5 of herpes simplex virus type 1 strain F

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

“…However, since the 734.5 gene is by definition expressed late in infection and appears not to be a component of the virion (McKay et al, 1993), it is difficult to envisage a role in the reactivation process. A novel regulatory pathway in neurons has recently been proposed in which limited e,/~ and 7 gene expression stimulates a second more vigorous round of viral replication (Kosz-Vnenchak et al, 1993).…”

Cell type and cell state determine differential in vitro growth of non-neurovirulent ICP34.5-negative herpes simplex virus types 1 and 2

“…The protein ICP34.5 (Ackermann et al, 1986;McKay et al, 1993) encoded by RL1 is the only specific HSV neurovirulence factor. Mutants that fail to make ICP34.5 are totally non-neurovirulent in the CNS of mice (Taha et al, 1989a, b;Chou & Roizman, 1992;MacLean et al, 1991 a, b) but are capable of establishing and reactivating from latent infections in the PNS following peripheral inoculation (MacLean et al, 1991b;Robertson et al, 1992).…”

“…Infected cell extracts were prepared as described previously (McKay et al, 1993). After transfer, the nitrocellulose was blocked for 1 h in PBS containing 5 % dried milk and incubated with the various antisera, diluted as described below in PBS containing 1% BSA.…”

“…The deletions were mapped to a region of the genome subsequently shown to encode a gene (RL1) both in HSV-1 strain F (Chou & Roizman, 1990) and strain 17 + (Dolan et al, 1992) and in HSV-2 strain HG52 (McGeoch et al, 1991). RL1 encodes the protein ICP34.5 (Ackermann et al, 1986;McKay et al, 1993) which is the only identified, specific HSV neurovirulence factor. As well as being unable to replicate productively ?…”

Functional analysis of the herpes simplex virus type 2 strain HG52 RL1 gene: the intron plays no role in virulence.

“…Sequence analysis of the region between IE1 and the ' a ' sequence in HSV-2 strain HG52 by demonstrated the presence of an open reading frame (ORF) predicted to encode an ICP34.5 homologue ; however, none of our antisera against the HSV-1 protein cross-react with the HSV-2 strain HG52 gene product which has yet to be identified (McKay et al, 1993 ;Brown et al, 1997). The organization of the HSV-2 strain HG52 RL1 gene differs from that of HSV-1: although both initiation codons are in equivalent positions, the HSV-2 strain HG52 coding sequence lacks the central (PAT) & -"!…”