Repression of gene expression upon infection of cells with herpes simplex virus type 1 mutants impaired for immediate-early protein synthesis. – PubMed

Repression of gene expression upon infection of cells with herpes simplex virus type 1 mutants impaired for immediate-early protein synthesis. - PubMed

Repression of gene expression upon infection of cells with herpes simplex virus type 1 mutants impaired for immediate-early protein synthesis. - PubMed
At early times after infection with herpes simplex virus, transcription from β-promoters is initiated only in the presence of a functional 174,000 Mr phosphoprotein (ICP4), encoded by an immediate early (α) gene (IE4). When cells are simultaneously infected with syn+ and syn− strains of HSV-1, the morphology of the syn+ strain is dominant. A virus derived from HSV-1(U(L)17-stop) but containing a restored U(L)17 gene was also constructed and was designated HSV-1(U(L)17-restored). When cell samples were treated with IFNα or IFNγ prior to viral infection, transcription of the CAT gene was greatly inhibited. A 395-bp upstream sequence encompassing all UL9 transcription initiation sites was active in expressing a reporter gene and was induced by viral immediate-early proteins. The hemagglutinin (HA) surface protein of the influenza virus is highly immunogenic and thus widely considered to be the antigen of choice for an influenza vaccine. The strongest homologies were observed in two segments of the ectodomain, the transmembrane domain, and sequences adjacent to the transmembrane domain.

Both elements remained available for transactivation by HSV-1 IE proteins at 24 h postinfection, showing that the in1820K genome was not irreversibly inactivated. The levels of accumulated mRNA and transcription of the early–late gD gene also showed parallel reductions in infected V2.6 cells (about 6-fold). The ICP0 promoter was induced when hexamethylene bisacetamide was added to cultures at the time of infection, but the response to this agent was also lost by 24 h after infection. Therefore, promoter elements within the HSV-1 genome are actively repressed in the absence of IE gene expression, and repression is not restricted specifically to HSV-1 IE promoters.

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