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 retrotranspositional mutagens, and could also provide a new regulatory element for the nearby cellular genes.
|Original language||English (US)|
|Number of pages||6|
|Journal||Molecules and cells|
|State||Published - Feb 2003|
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology