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	Varicella-zoster virus immediate-early protein orf61 abrogates the irf3-mediated innate immune response through degradation of activated irf3
	Zhu, Huifang1; Zheng, Chunfu1; Xing, Junji1; Wang, Shuai1; Li, Shuping2,3; Lin, Rongtuan4; Mossman, Karen L.5
刊名	Journal of virology
	2011-11-01
卷号	85期号:21页码:11079-11089
ISSN号	0022-538X
DOI	10.1128/jvi.05098-11
通讯作者	Zheng, chunfu(zheng.alan@hotmail.com)
英文摘要	Varicella-zoster virus (vzv) infection of differentiated cells within the host and establishment of latency likely requires evasion of innate immunity and limits secretion of antiviral cytokines. here we report that its immediate-early protein orf61 antagonizes the beta interferon (ifn-beta) pathway. vzv infection down-modulated the sendai virus (sev)-activated ifn-beta pathway, including mrna of ifn-beta and its downstream interferon-stimulated genes (isgs), isg54 and isg56. through a primary screening of vzv genes, we found that orf61 inhibited sev-mediated activation of ifn-beta and isre (ifn-stimulated response element) promoter activities but only slightly affected nf-kappa b promoter activity, implying that the ifn-beta pathway may be blocked in the irf3 branch. an indirect immunofluorescence assay demonstrated that ectopic expression of orf61 abrogated the detection of irf3 in sev-infected cells; however, it did not affect endogenous dormant irf3 in noninfected cells. additionally, orf61 was shown to be partially colocalized with activated irf3 in the nucleus upon treatment with mg132, an inhibitor of proteasomes, and the direct interaction between orf61 and activated irf3 was confirmed by a coimmunoprecipitation assay. furthermore, western blot analysis demonstrated that activated irf3 was ubiquitinated in the presence of orf61, suggesting that orf61 degraded phosphorylated irf3 via a ubiquitin-proteasome pathway. semiquantitative reverse transcription-pcr (rt-pcr) analysis demonstrated that the level of isg54 and isg56 mrnas was also downregulated by orf61. taken together, our results convincingly demonstrate that orf61 down-modulates the irf3-mediated ifn-beta pathway by degradation of activated irf3 via direct interaction, which may contribute to the pathogenesis of vzv infection.
WOS关键词	HERPES-SIMPLEX-VIRUS ; INTERFERON REGULATORY FACTOR-3 ; RING FINGER DOMAIN ; KAPPA-B ; SIGNALING PATHWAYS ; ANTIVIRAL RESPONSE ; MAMMALIAN-CELLS ; BETA-INTERFERON ; INFECTED-CELLS ; HOST-DEFENSE
WOS研究方向	Virology
WOS类目	Virology
语种	英语
出版者	AMER SOC MICROBIOLOGY
WOS记录号	WOS:000296254400015
内容类型	期刊论文
URI标识	http://www.corc.org.cn/handle/1471x/2375947
专题	武汉病毒研究所
通讯作者	Zheng, Chunfu
作者单位	1.Chinese Acad Sci, Wuhan Inst Virol, Mol Virol & Viral Immunol Res Grp, State Key Lab Virol, Wuhan 430071, Peoples R China 2.Zhejiang Univ, Sch Med, Affiliated Hosp 1, State Key Lab Diag & Treatment Infect Dis, Hangzhou 310058, Zhejiang, Peoples R China 3.Key Lab Infect Dis, Hangzhou 310058, Zhejiang, Peoples R China 4.McGill Univ, Dept Med, Lady Davis Inst Med Res, Terry Fox Mol Oncol Grp, Montreal, PQ H3T 1E2, Canada 5.McMaster Univ, Dept Pathol & Mol Med, Inst Infect Dis Res, Hamilton, ON L8N 3Z5, Canada
推荐引用方式 GB/T 7714	Zhu, Huifang,Zheng, Chunfu,Xing, Junji,et al. Varicella-zoster virus immediate-early protein orf61 abrogates the irf3-mediated innate immune response through degradation of activated irf3[J]. Journal of virology,2011,85(21):11079-11089.
APA	Zhu, Huifang.,Zheng, Chunfu.,Xing, Junji.,Wang, Shuai.,Li, Shuping.,...&Mossman, Karen L..(2011).Varicella-zoster virus immediate-early protein orf61 abrogates the irf3-mediated innate immune response through degradation of activated irf3.Journal of virology,85(21),11079-11089.
MLA	Zhu, Huifang,et al."Varicella-zoster virus immediate-early protein orf61 abrogates the irf3-mediated innate immune response through degradation of activated irf3".Journal of virology 85.21(2011):11079-11089.

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