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	Genetic disruption of kshv major latent nuclear antigen lana enhances viral lytic transcriptional program
	Li, Qiuhua1,3; Zhou, Fuchun1,2; Ye, Fengchun1,2; Gao, Shou-Jiang1,2,3,4,5,6,7
刊名	Virology
	2008-09-30
卷号	379期号:2页码:234-244
关键词	Kshv Lana Viral latency Lytic replication Vital transcriptional program Reverse genetics
ISSN号	0042-6822
DOI	10.1016/j.virol.2008.06.043
通讯作者	Gao, shou-jiang(gaos@uthscsa.edu)
英文摘要	Following primary infection, kshv establishes a lifelong persistent latent infection in the host. the mechanism of kshv latency is not fully understood. the latent nuclear antigen (lana or lna) encoded by orf73 is one of a few vital genes expressed during kshv latency, and is consistently detected in all kshv-related malignancies. lana is essential for kshv episome persistence, and regulates the expression of viral lytic genes through epigenetic silencing, and inhibition of the expression and transactivation function of the key kshv lytic replication initiator rta (orf50). in this study, we used a genetic approach to examine the role of lana in regulating kshv lytic replication program. deletion of lana did not affect the expression of its adjacent genes vcyclin (orf72) and vflip (orf71). in contrast, the expression levels of viral lytic genes including immediate-early gene rta, early genes mta (orf57), vil-6 (orf-k2) and orf59, and late gene orf-k8.1 were increased before and after vital lytic induction with 12-o-tetradecanoyl-phorbol-13-acetate and sodium butyrate. this enhanced expression of vital lytic genes was also observed following overexpression of rta with or without simultaneous chemical induction. consistent with these results, the lana mutant cells produced more infectious virions than the wild-type virus cells did, furthermore, genetic repair of the mutant virus reverted the phenotypes to those of wild-type virus. together, these results have demonstrated that, in the context of vital genome, lana contributes to kshv latency by regulating the expression of rta and its downstream genes. (c) 2008 elsevier inc. all rights reserved.
WOS关键词	SARCOMA-ASSOCIATED HERPESVIRUS ; BACTERIAL ARTIFICIAL CHROMOSOME ; PROTEIN-KINASE PATHWAYS ; KAPOSIS-SARCOMA ; ENDOTHELIAL-CELLS ; PRIMARY INFECTION ; EPISOME PERSISTENCE ; DNA-REPLICATION ; HUMAN-HERPESVIRUS-8 ; EXPRESSION
WOS研究方向	Virology
WOS类目	Virology
语种	英语
出版者	ACADEMIC PRESS INC ELSEVIER SCIENCE
WOS记录号	WOS:000259549500008
内容类型	期刊论文
URI标识	http://www.corc.org.cn/handle/1471x/2375525
专题	武汉病毒研究所
通讯作者	Gao, Shou-Jiang
作者单位	1.Univ Texas Hlth Sci Ctr San Antonio, Tumor Virol Program, Greehey Childrens Canc Res Inst, San Antonio, TX 78229 USA 2.Univ Texas Hlth Sci Ctr San Antonio, Dept Pediat, San Antonio, TX 78229 USA 3.Univ Texas Hlth Sci Ctr San Antonio, Dept Microbiol & Immunol, San Antonio, TX 78229 USA 4.Univ Texas Hlth Sci Ctr San Antonio, Dept Med, San Antonio, TX 78229 USA 5.Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78229 USA 6.Univ Texas Hlth Sci Ctr San Antonio, Canc Therapy & Res Ctr, San Antonio, TX 78229 USA 7.Chinese Acad Sci, Tumor Virol Grp, Wuhan Inst Virol, Wuhan, Peoples R China
推荐引用方式 GB/T 7714	Li, Qiuhua,Zhou, Fuchun,Ye, Fengchun,et al. Genetic disruption of kshv major latent nuclear antigen lana enhances viral lytic transcriptional program[J]. Virology,2008,379(2):234-244.
APA	Li, Qiuhua,Zhou, Fuchun,Ye, Fengchun,&Gao, Shou-Jiang.(2008).Genetic disruption of kshv major latent nuclear antigen lana enhances viral lytic transcriptional program.Virology,379(2),234-244.
MLA	Li, Qiuhua,et al."Genetic disruption of kshv major latent nuclear antigen lana enhances viral lytic transcriptional program".Virology 379.2(2008):234-244.

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