Octamer motif mediates transcriptional repression of HSV immediate-early genes and octamer-containing cellular promoters in neuronal cells

Establishment of latency in vitro by the herpes simplex virus type 1 mutant in 1814

“…The properties of in1814 in tissue culture and animal systems demonstrate that Vmw65 is important for the initiation of infection, especially at low m.o.i., and that the lack of trans-activation of IE genes does not prevent the establishment or reactivation of latency. The results support the attractive, but unproven, hypothesis that the block leading to latency is at the level of IE gene transcription (Kristie & Roizman, 1988;Kemp et al, 1990).…”

“…This may reflect an overall 'silencing' of the genome, perhaps by conversion to a chromatin-like structure (Deshmane & Fraser, 1989), the presence of a specific inhibitor of IE transcription, as exists in mouse C1300 neuroblastoma cells (Kemp et al, 1990), or a combination of the two. Whatever the cause of silencing, gene expression remains sensitive to trans-activation by Vmw 110.…”

In vitro reactivation of latent equid herpesvirus-1 from CD5+/CD8+ leukocytes indirectly by IL-2 or chorionic gonadotrophin.

“…It seems most likely that IL-2 and eCG indirectly stimulate host factors and therefore initiate immediate early transcription leading to the reactivation of the virus via host factors (Jones et al, 1985 ;Everett, 1987 ;Goding & O'Hare, 1989 ;Kemp et al, 1990 ;Lin et al, 1991 ;Purewal et al, 1992). The model of reactivation described will be useful for future studies in defining the interaction of infected DAAC leukocytes and endothelial cells in EHV-1 infections of the horse and will also be a useful model for further defining mechanisms involved in alphaherpesvirus latency.…”

Quiescent viral genomes in human fibroblasts after infection with herpes simplex virus type 1 Vmw65 mutants

“…It has been suggested that a block to IE transcription, possibly imposed by inhibitory TAATGARAT-binding proteins, is primarily responsible for the abortion of lytic replication and hence the establishment of latency (Roizrnan & Sears, 1987;Kristie & Roizmam 1988;Kemp et al, 1990;Lillycrop et al, 1991Lillycrop et al, , 1994Sears et al, 1991). In support of this hypothesis, in1814 establishes latency after inoculation into mice even though productive infection in neurons is impaired, suggesting that IE gene expression is not required for latency (Steiner et al, 1990;Valyi-Nagy et al, 1991;Ecob-Prince et al, 1993).…”