Regulation of herpes simplex virus 1 genes: α gene sequence requirements for transient induction of indicator genes regulated by β or late (γ2) promoters

A specific 15-bp TATA box promoter element is required for expression of a herpes simplex virus type 1 late gene.

“…Post-transcriptional regulation would more likely involve specific sequences found in the transcribed region. The A8LS-45 results would also argue against a repressor model for inhibition of late gene transcription at early times during infection, as has been suggested previously (Homa et al 1986a;Mavromara-Nazos et al 1986). However, late promoters can be activated by IE proteins in the absence of viral DNA replication in transfection experiments (Mavomara-Nazos et al 1986;Shapira et al 1987).…”

Herpes Simplex Virus Genes Involved in Latency in vitro

“…This polypeptide might act alone or in conjunction with one or more of the virion components and/or the other IE polypeptides, excluding Vmw175. Polypeptide Vmw 110 is capable of stimulating the expression, presumably at the transcriptional level, of a variety of genes introduced into cells by transfection (Everett, 1984;O'Hare & Hayward, 1985;Gelman & Silverstein, 1985;Mavromara-Nazos et al, 1986). The degree of 'transactivation' can be increased when Vmw175 is present, but to date there are no examples of eukaryotic or animal virus genes which fail to respond to Vmwll0.…”

Herpes simplex virus type-1 infection upregulates cellular promoters and telomerase activity in both tumor and nontumor human cells

“…53 Despite not being essential for viral replication, lacking ICP0 gene significantly hampers the viral replication in cultured cells, especially infected with low MOIs. 54,55 ICP0 is a potent transactivator of all three kinetic classes of HSV promoters, 56,57 and its transactivating activity has been shown to increase synergistically in the presence of ICP4, [19][20][21][22]58,59 which may explain the fact that the ICP0+/ICP4À mutant (such as CgalD3 and TOZ.1) had a markedly lower magnitude of enhancement in tyrosinase promoter activity than the wild-type or other ICP0+/ICP4+ mutants (Fig.4a). Similarly, since VP16 can activate the transcription of all IE genes 60,61 deletion of the VP16 gene could significantly abolish HSVinduced increase in the activity of cellular promoters as shown by infection with the VP16(À) mutant V422.…”

“…10,13,14 All IE proteins except ICP47 are nuclear phosphoproteins 15 and act to regulate their own synthesis as well as the synthesis of proteins of later kinetic classes. [16][17][18][19][20][21][22] Since the genes of HSV are standard polymerase II transcription units, 23 exogenous polymerase II promoters used to express transgenes may be affected by HSV IE gene products in the same way as viral promoters are. If the expression of a transgene could be augmented by viral IE proteins, the specificity of tissue-or tumor-targeted therapy might thus be jeopardized.…”