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

被引:48
作者
Kwun, HJ
Han, HJ
Lee, WJ
Kim, HS
Jang, KL [1 ]
机构
[1] Pusan Natl Univ, Dept Microbiol, Coll Nat Sci, Pusan 609735, South Korea
[2] Pusan Natl Univ, Dept Biol, Coll Nat Sci, Pusan 609735, South Korea
关键词
AP-1; HERV-K LTR; HSV; ICP0; transcriptional regulation;
D O I
10.1016/S0168-1702(02)00058-8
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:93 / 100
页数:8
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