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

来源：

VIRUS RESEARCH | 2002年 / 86卷 / 1-2期

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.

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页码：93 / 100

页数：8

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