Evidence that transcriptional control is the major mechanism of regulation for the glycoprotein D gene in herpes simplex virus type 1-infected cells.
In this report, we demonstrate a close correlation between the levels of steady-state mRNA, polysome-associated RNA, and the rate of protein synthesis for glycoprotein D, a beta-gamma product of herpes simplex virus type 1, and for the model beta (ICP8), beta-gamma (glycoprotein B), and gamma (glycoprotein C) gene products included in this study as controls. No evidence was found for posttranscriptional control of expression of these products. We conclude from these results that the major regulatory control for these genes during herpes simplex virus type 1 infection is transcriptional.
Smith
I L
IL
Department of Microbiology and Molecular Genetics, College of Medicine, University of California, Irvine 92717.
Sandri-Goldin
R M
RM
D000818:Animals; D002460:Cell Line; D005786:Gene Expression Regulation; D005814:Genes, Viral; D006801:Humans; D007118:Immunoassay; D007700:Kinetics; D009693:Nucleic Acid Hybridization; D012333:RNA, Messenger / Q000235:genetics; D012367:RNA, Viral / Q000235:genetics; D018139:Simplexvirus / Q000235:genetics*; D014158:Transcription, Genetic; D014709:Vero Cells; D014759:Viral Envelope Proteins / Q000096:biosynthesis / Q000235:genetics*
D012333:RNA, Messenger; D012367:RNA, Viral; D014759:Viral Envelope Proteins; C039447:glycoprotein D, Human herpesvirus 1