Abstract
The U3 region of the human endogenous retrovirus W long terminal repeat (HERV-W LTR) contains several putative regulatory sequences that regulate the transcription of neighboring cellular genes, as well as viral genes. We found that the LTR-directed transcription of the HERV-W can be induced by the herpes simplex virus type 1 (HSV-1) infection. The effect was partly mediated by the action of the HSV-1 immediate early protein 1 (IE1), and required an Oct-1 binding site that is located in the LTR. Results from the gel shift assay also suggest that HSV-1 stimulates the LTR through enhancing the DNA binding activity of Oct-1. This effect might be important in understanding both the HERV-W- and HSV-1-mediated pathogenesis, because HERVs represent an important class of retro-transpositional mutagens, and could also provide a new regulatory element for the nearby cellular genes.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Carcinoma, Hepatocellular / pathology
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DNA / genetics
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DNA / metabolism
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DNA-Binding Proteins / metabolism
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Endogenous Retroviruses / genetics*
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Genes, Immediate-Early
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Genes, Reporter
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Genes, Viral
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HeLa Cells
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Herpesvirus 1, Human / genetics
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Herpesvirus 1, Human / physiology*
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Host Cell Factor C1
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Humans
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Immediate-Early Proteins / genetics
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Immediate-Early Proteins / physiology*
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Liver Neoplasms / pathology
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Luciferases / biosynthesis
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Luciferases / genetics
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Octamer Transcription Factor-1
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Plasmids / genetics
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Protein Binding
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Reverse Transcriptase Polymerase Chain Reaction
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Teratocarcinoma / pathology
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Terminal Repeat Sequences*
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Transcription Factors / metabolism
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Transcription, Genetic
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Tumor Cells, Cultured
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Viral Proteins / genetics
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Viral Proteins / physiology*
Substances
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DNA-Binding Proteins
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HCFC1 protein, human
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Host Cell Factor C1
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IE1 protein, Human herpesvirus 1
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Immediate-Early Proteins
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Octamer Transcription Factor-1
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POU2F1 protein, human
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Transcription Factors
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Viral Proteins
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DNA
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Luciferases