Transactivation of the human endogenous retrovirus K long terminal repeat by herpes simplex virus type 1 immediate early protein 0

Virus Res. 2002 Jun;86(1-2):93-100. doi: 10.1016/s0168-1702(02)00058-8.

Abstract

We found that LTR-directed transcription of the human endogenous retrovirus K can be induced by HSV-1 infection. The effect was mediated by the action of a HSV-1 immediate early protein, ICP0 and required the AP-1 binding site present on the HERV-K LTR. In addition, ICP0 could up-regulate AP-1 activity, suggesting that ICP0 increases transcription of HERV-K through AP-1 site. This effect might be important to understand both HERV-K- and HSV-1-mediated pathogenesis because HERV-K LTR represents an important class of retrotranspositional mutagens and also could provide a new regulatory element for the linked DNA sequences.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Herpesvirus 1, Human / chemistry
  • Humans
  • Immediate-Early Proteins / physiology*
  • Luciferases / genetics
  • Luciferases / metabolism
  • Retroviridae / classification
  • Retroviridae / genetics*
  • Terminal Repeat Sequences / genetics*
  • Transcription, Genetic / genetics*
  • Transcriptional Activation / physiology*
  • Tumor Cells, Cultured

Substances

  • IE1 protein, Human herpesvirus 1
  • Immediate-Early Proteins
  • Luciferases