
doi: 10.1292/jvms.58.715
pmid: 8877967
We analyzed the mechanism for feline herpesvirus type 1 (FHV-1) immediate early (IE) gene expression. We demonstrated that (i) the transcription initiation site of the FHV-1 IE transcript lies in the putative FHV-1 ICP4 binding site, (ii) the FHV-1 IE transcript is spliced to remove 906 bp intron from the leader region, (iii) cis-acting elements of the FHV-1 IE promoter map both down- and upstream of the transcription initiation site, and (iv) a deletion of a 58 bp sequence which includes the putative FHV-1 ICP4 binding site in the IE promoter resulted in significant induction of promoter activity by a FHV-1 IE gene product although the FHV-1 IE gene product slightly stimulates the FHV-1 IE promoter, indicating that the FHV-1 IE gene product down-regulates its own promoter via the region.
Chloramphenicol O-Acetyltransferase, Gene Expression Regulation, Viral, promoter, Base Sequence, Transcription, Genetic, FHV-1, Molecular Sequence Data, Alphaherpesvirinae, Regulatory Sequences, Nucleic Acid, Transfection, Polymerase Chain Reaction, Recombinant Proteins, Cell Line, Immediate-Early Proteins, gene expression, Cats, Animals, IE gene, Amino Acid Sequence, Promoter Regions, Genetic, Genes, Immediate-Early, DNA Primers
Chloramphenicol O-Acetyltransferase, Gene Expression Regulation, Viral, promoter, Base Sequence, Transcription, Genetic, FHV-1, Molecular Sequence Data, Alphaherpesvirinae, Regulatory Sequences, Nucleic Acid, Transfection, Polymerase Chain Reaction, Recombinant Proteins, Cell Line, Immediate-Early Proteins, gene expression, Cats, Animals, IE gene, Amino Acid Sequence, Promoter Regions, Genetic, Genes, Immediate-Early, DNA Primers
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