Transactivation of the human endogenous retrovirus K long terminal repeat by herpes simplex virus type 1 immediate early protein 0.
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.
Kwun
Hyun Jin
HJ
Department of Microbiology, College of Natural Sciences, Pusan National University, Pusan, South Korea.
Han
Hae Jin
HJ
Lee
Woo Jung
WJ
Kim
Hee Soo
HS
Jang
Kyung Lib
KL
D018259:Herpesvirus 1, Human / Q000737:chemistry; D006801:Humans; D017874:Immediate-Early Proteins / Q000502:physiology*; D008156:Luciferases / Q000235:genetics / Q000378:metabolism; D012190:Retroviridae / Q000145:classification / Q000235:genetics*; D020079:Terminal Repeat Sequences / Q000235:genetics*; D014158:Transcription, Genetic / Q000235:genetics*; D015533:Transcriptional Activation / Q000502:physiology*; D014407:Tumor Cells, Cultured
C050678:IE1 protein, Human herpesvirus 1; D017874:Immediate-Early Proteins; D008156:Luciferases