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Regulation of glycoprotein D synthesis: does alpha 4, the major regulatory protein of herpes simplex virus 1, regulate late genes both positively and negatively?


, : Regulation of glycoprotein D synthesis: does alpha 4, the major regulatory protein of herpes simplex virus 1, regulate late genes both positively and negatively?. Journal of Virology 62(1): 148-158

Earlier studies have described the .alpha.4/c113 baby hamster kidney cell line which constitutively expresses the .alpha.4 protein, the major regulatory protein of herpes simplex virus 1 (HSV-1). Introduction of the HSV-1 glycoprotein B (gB) gene, regulated as a .gamma.1 gene, into these cells yielded a cell line which constitutively expressed both the .alpha.4 and .gamma.1 gB genes. The expression of the gB gene was dependent on the presence of functional .alpha.4 protein. In this article we report that we introduced into the .alpha.4/c113 and into the parental BHK cells, the HSV-1 BamHI J fragment, which encodes the domains of four genes, including those of glycoproteins D, G, and I (gD, gG, and gI), and most of the coding sequences of the glycoprotein E (gE) gene. In contrast to the earlier studies, we obtained significant constitutive expression of gD (also a .gamma.1 gene) in a cell line (BJ) derived from parental BHK cells, but not in a cell line (.alpha.4/BJ) which expresses functional .alpha.4 protein. RNA homologous to the gD gene was present in significant amounts in the BJ cell line; smaller amounts of this RNA were detected in the .alpha.4/BJ cell line. RNA homologous to gE, presumed to be polyadenylated from signals in the vector sequences, was present in the BJ cells but not in the .alpha.4/BJ cells. The expression of the HSV-1 gD and gE genes was readily induced in the .alpha.4/BJ cells by superinfection with HSV-2. The BJ cell line was, in contrast, resistant to expression of HSV-1 and HSV-2 genes. The BamHI J DNA fragment copy number was approximately 1 per BJ cell genome equivalent and 30 to 50 per .alpha.4/BJ cell genome equivalent. We conclude that (i) the genes specifying gD and gB belong to different viral regulatory gene subsets, (ii) the gD gene is subject to both positive and negative regulation, (iii) both gD and gE mRNAs are subject to translational controls although they may be different, and (iv) the absence of expression of gD in the .alpha.4/BJ cells reflects the expression of the .alpha.4 protein in these cells.

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Accession: 006288221

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