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中华耳鼻咽喉头颈外科杂志 2011年第8期46卷 675-680页

作者：万仁强李湘平王路鲁娟罗花南李刚刘雄张宝南方医科大学南方医院耳鼻咽喉头颈外科广州510515

目的研究EB病毒核抗原1（Epstein—Barr virus nuclear antigen1，EBNAI）对人鼻咽癌细胞增殖及细胞周期的影响。方法构建特异性的短发夹RNA（short hairpin RNA，shRNA）EBNA1慢病毒干扰载体，包装慢病毒后感染过表达EBNA1的鼻咽癌细胞... 详细信息

目的研究EB病毒核抗原1（Epstein—Barr virus nuclear antigen1，EBNAI）对人鼻咽癌细胞增殖及细胞周期的影响。方法构建特异性的短发夹RNA（short hairpin RNA，shRNA）EBNA1慢病毒干扰载体，包装慢病毒后感染过表达EBNA1的鼻咽癌细胞C666－EBNA1（简写为CE）。应用四甲基偶氮唑蓝法（MTT）和细胞计数法检测细胞增殖状态，流式细胞术、荧光定量PCR及蛋白免疫印迹法检测细胞周期及相关调控因子变化。结果成功构建含shRNA EBNA1的重组慢病毒，其感染可显著下调CE细胞中EBNA1表达。细胞计数和MTF均证明CE—shRNA细胞的增殖能力较CE-对照组显著下降（P值均〈0．05）。细胞周期提示干扰EBNAl后cE细胞G0．G1期比例由（62．43±6．62）％升高到（89．66±0．64）％，两者比较差异有统计学意义（t=-7．091，P=0．002），S期比例由（34．93±7．36）％下降为（7．824-2．44）％，两者比较差异有统计学意义（t=6．095，P=0．004），G2-M期无明显变化（t=0．090，P=0．933）。抑制EBNA1后，c—myc、CDK4、CDK6、pRb的mRNA水平分别下调65．60％、34．06％、41．05％、55．29％。蛋白免疫印迹法证实抑制EBNA1后4种蛋白的表达亦下凋。结论沉默EBNA1基因可抑制鼻咽癌细胞增殖，其机制之一可能是通过影响c—myc、CDK4、CDK6、pRb等基因的表达使鼻咽癌细胞阻滞于G0-G1期。

关键词：爱泼斯坦巴尔病毒核抗原鼻咽肿瘤细胞增殖细胞周期

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系统性红斑狼疮EB病毒潜伏期基因与Ⅰ型干扰素诱导基因的相关关系研究

系统性红斑狼疮EB病毒潜伏期基因与Ⅰ型干扰素诱导基因的相关关系...

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作者：韩丽青岛大学

学位级别：硕士

目的研究Epstein-Barr(EB)病毒潜伏期表达基因EB病毒核心抗原1(EBNA-1)、潜伏膜蛋白-1(LMP-1)、EB病毒编码小RNA(EBER)以及多个Ⅰ型干扰素诱导基因在SLE患者和健康对照体内的表达,分析EB病毒潜伏期感染各基因表达与各Ⅰ型干扰素诱导基... 详细信息

目的研究Epstein-Barr(EB)病毒潜伏期表达基因EB病毒核心抗原1(EBNA-1)、潜伏膜蛋白-1(LMP-1)、EB病毒编码小RNA(EBER)以及多个Ⅰ型干扰素诱导基因在SLE患者和健康对照体内的表达,分析EB病毒潜伏期感染各基因表达与各Ⅰ型干扰素诱导基因表达之间的关系及其与SLE的相关性。对象与方法共入选68例SLE患者和40例健康对照者。实时荧光定量PCR(Real-time PCR)检测研究对象外周血淋巴细胞中EB病毒潜伏感染相关基因(EBNA-1、LMP-1、EBER)及各Ⅰ型干扰素诱导基因2’-5’寡腺甘酸样合成酶(0ASL)、干扰素刺激基因15(ISG15)和淋巴细胞抗原6复合体E(LY6E)m RNA表达水平。统计分析采用非参数U检验、方差分析、卡方检验及Spearman相关检验。结果***患者中EB病毒EBNA-1和LMP-1 m RNA水平高于健康对照(分别为U=1681,P<0.05,U=213,P<0.05);两组间EBER的表达水平没有显著差异。病情活动组与肾炎组潜伏期基因无明显差异。***患者各Ⅰ型干扰素诱导基因OASL、ISG15、LY6E,m RNA的表达水平高于正常对照组(U=377.5～725.0,P<0.05);两组间MX1表达无显著差异。肾炎组ISG15m RNA表达水平高于非肾炎组(U=387.5,P<0.05),OASL、LY6E和MX1的表达在肾炎、非肾炎组之间没有显著差异。***-1与MX1、LY6E表达呈正相关(r=0.24、0.34,P<0.05);EBER与ISG15表达呈正相关(r=0.27,P<0.05);LMP-1与MX1、OASL、ISG15表达呈正相关(r=0.054、0.219、0.003,P<0.05)。结论***病毒潜伏感染可能是SLE的致病因素之一。2.Ⅰ型干扰素诱导基因表达水平与SLE发病有关。***病毒潜伏感染基因可能通过I型干扰素诱导下游基因通路引起SLE发病和发展。

关键词：红斑狼疮,系统性疱疹病毒4型,人爱泼斯坦巴尔病毒核抗原病毒基质蛋白质类干扰素Ⅰ型

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Evidence that protein binding specifies sites of DNA demethylation

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MOLECULAR AND CELLULAR BIOLOGY 1999年第1期19卷 46-56页

作者： Hsieh, CL Univ So Calif Dept Urol Norris Canc Ctr Los Angeles CA 90033 USA Univ So Calif Dept Biochem & Mol Biol Los Angeles CA 90033 USA

It has been hypothesized that protein factors may protect CpG islands from methyltransferase during development and that demethylation may involve protein-DNA interactions at demethylated sites. However, direct evidence has been lacking. In this study, demethylation at the EBNA-1 binding sites of the Epstein-Barr virus latent replication origin, oriP, was investigated by using human cells. Several novel findings are discussed, First, there are specific preferential demethylation sites within the oriP region. Second, the DNA sequence of oriP alone is not the target of an active demethylation process. Third, EBNA-1 binding is required for the site specific demethylation in oriP, Interestingly, CpG sites adjacent to and between the FBNA-1 sites do not become demethylated. Fourth, demethylation of the first DNA strand in oriP at the EBNA-1 binding sites involves a passive (replication dependent) mechanism. The second-strand demethylation appears to occur through an active mechanism. That is, EBNA-1 protein binding prevents the FBNA-1 binding sites from being remethylated after one round of DNA replication, and it appears that an active demethylase then demethylates these hemimethylated sites. This study provides clear evidence that protein binding specifies sites of DNA demethylation and provides insights into the sequence of steps and the mechanism of demethylation.

关键词： DNA Methylation Epstein-Barr Virus Nuclear Antigens Replication Origin DNA甲基化爱泼斯坦巴尔病毒核抗原复制起点 EBV-encoded nuclear antigen 1 Epstein-Barr Virus Nuclear Antigens demethylation Protein Binding DNA Methylation DNA demethylation Replication Origin

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Loss of EBNA1-specific memory CD4⁺ and CD8⁺ T cells in HIV-infected patients progressing to AIDS-related non-hodgkin lymphoma

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BLOOD 2005年第9期106卷 3166-3174页

作者： Piriou, E van Dort, K Nanlohy, NM van Oers, MHJ Miedema, F van Baarle, D Univ Med Ctr Utrecht Dept Immunol NL-3584 EA Utrecht Netherlands Univ Amsterdam Acad Med Ctr Dept Clin Viroimmunol Sanquin Res CLB & Landsteiner Lab NL-1105 AZ Amsterdam Netherlands Univ Amsterdam Acad Med Ctr Dept Hematol NL-1105 AZ Amsterdam Netherlands

We previously observed a loss of Epstein-Barr virus (EBV)-specific CD8(+) T cells in subjects progressing to EBV-related non-Hodgkin lymphoma (NHL), correlating with loss of CD4(+) T cells. The aim of the present study was to determine the role of EBV-specific CD4(+) T cells in the development of NHL during chronic HIV infection. To this end, CD4(+) and CD8(+) memory T cells, capable of both proliferation and subsequent interferon gamma (IFN-gamma) production, directed against a latent (Epstein-Barr virus nuclear antigen 1 [EBNA1]) and a lytic (BamH fragment Z left frame 1 [BZLF1]) EBV antigen were studied longitudinally in 9 progressors to NHL, 4 progressors to non-EBV-related AIDS, and 4 slow progressors to AIDS. In all 3 groups we observed a decline of EBV-specific memory CD4(+) and CD8(+) T-cell responses during HIV infection. However, whereas latent antigen EBNA1-specific CD4(+) T cells were lost well before diagnosis in all subjects who developed an AIDS-related NHL (and EBNA1-specific CD8(+) T cells were significantly lower compared with the other groups), these cells were better preserved in progressors to non-EBV-related disease and slow progressors. Loss of EBNA1-specific T-cell immunity thus might be important for progression to NHL. Interestingly, BZLF1-specific T cells were not lost in all progressors to NHL, suggesting a different function of these cells in the surveillance of EBV-infected B cells.

关键词： CD4-Positive T-Lymphocytes CD8-Positive T-Lymphocytes Epstein-Barr VirusNuclear Antigens CD4阳性T淋巴细胞 CD8阳性T淋巴细胞爱泼斯坦巴尔病毒核抗原免疫记忆淋巴瘤艾滋病相关

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Requirement of replication licensing for the dyad symmetry element-dependent replication of the Epstein-Barr virus oriP minichromosome

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VIROLOGY 1999年第1期263卷 42-54页

作者： Shirakata, M Imadome, K Hirai, K Tokyo Med & Dent Univ Med Res Inst Dept Tumor Virol Div Virol & ImmunolBunkyo Ku Tokyo 1148510 Japan

Latent Epstein-Barr virus genome is maintained in cells by the viral oriP-binding factor EBNA1 and cellular replication factors. EBNA1 binds to the dyad symmetry (DS) element in oriP and initiates DNA replication once in a single S phase, but the mechanism by which this DS-dependent replication is initiated is unknown. Replication licensing of cellular chromatins occurs during early GI phase. Because licensing is essential for the next round of replication in S phase, it facilitates once-in-a-cell-cycle replication of the cellular genome. Using the transient replication assay with HeLa/EB1 cell, we demonstrate that the oriP plasmid required a cell cycle window including early G1 phase for replication in the next S phase. The plasmid containing only the DS element had a similar requirement of early G1 phase for replication. Analysis using sucrose density gradient centrifugation revealed that the oriP minichromosome existed in two distinct states: one formed at late G1 and the other formed at G2/M. These results suggest that the DS-dependent DNA replication from oriP requires the replication licensing, implying a possible involvement of the cellular licensing factor MCM in the DNA replication from oriP. (C) 1999 Academic Press.

关键词：细胞周期离心法梯密度 DNA复制爱泼斯坦巴尔病毒核抗原基因表达调控病毒 HeLa细胞疱疹病毒4型人/遗传学疱疹病毒4型人/生理学质粒/遗传学复制起点 S期转染肿瘤细胞培养的病毒复制人类

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Epstein-Barr virus nuclear protein 2 interacts with p300, CBP, and PCAF histone acetyltransferases in activation of the LMP1 promoter

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第1期97卷 430-435页

作者： Wang, L Grossman, SR Kieff, E Brigham & Womens Hosp Dept Microbiol Project Virol Boston MA 02115 USA Brigham & Womens Hosp Dept Mol Genet Project Virol Boston MA 02115 USA Harvard Univ Sch Med Channing Lab Boston MA 02115 USA Brigham & Womens Hosp Dept Med Project Virol Boston MA 02115 USA Dana Farber Canc Inst Dept Adult Oncol Boston MA 02115 USA

The Epstein-Barr virus (EBV) nuclear protein 2 (EBNA2) and herpes simplex virion protein 16 (VP16) acidic domains that mediate transcriptional activation now are found to have affinity for p300, CBP, and PCAF histone acetyltransferases (HATs). Transcriptionally inactive point mutations in these domains lack affinity for p300, CBP. or PCAF, P300 and CBP copurify with the principal HAT activities that bind to EBNA2 or VP16 acidic domains through velocity sedimentation and anion-exchange chromatography. EBNA2 binds to both the N- and C-terminal domains of p300 and coimmune-precipitates from transfected 293T cells with p300, In EBV-infected Akata Burkitt's tumor cells that do not express the EBV encoded oncoproteins EBNA2 or LMP1, p300 expression enhances the ability of EBNA2 to up-regulate LMP? expression. Through its intrinsic: HAT activity, PCAF can further potentiate the p300 effect. In 293 T cells, P300 and CBP (but not PCAF) can also coactivate transcription mediated by the EBNA2 or VP16 acidic domains and HAT-negative mutants of p300 have partial activity. Thus, the EBNA2 and VP16 acidic domains can utilize the intrinsic HAT or scaffolding properties of p300 to activate transcription.

关键词：乙酰基转移酶类/代谢伯基特淋巴瘤 CREB结合蛋白质细胞周期蛋白质类/代谢 DNA结合蛋白质类爱泼斯坦巴尔病毒核抗原真菌蛋白质类/遗传学真菌蛋白质类/代谢基因表达调控病毒/遗传学基因报告单纯疱疹病毒蛋白质Vmw65/代谢疱疹病毒4型人/代谢组蛋白酰基转移酶突变核蛋白质类/代谢启动区遗传蛋白质结合酿酒酵母蛋白质类反式激活因子类/代谢转录因子/遗传学转录因子/代谢转录激活/遗传学肿瘤细胞培养的病毒基质蛋白质类/遗传学病毒蛋白质类/代谢 p300-CBP转录因子人类

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Characterization of intertypic recombinants of the Epstein-Barr virus from the body-cavity-based lymphomas cell lines BC-1 and BC-2

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VIROLOGY 1999年第2期264卷 359-369页

作者： Aguirre, AJ Robertson, ES Univ Michigan Sch Med Dept Microbiol & Immunol Ann Arbor MI 48109 USA Univ Michigan Sch Med Ctr Comprehens Canc Ann Arbor MI 48109 USA

Epstein-Barr Virus (EBV) can infect and transform human B-lymphocytes and has been associated with numerous human malignancies. Two distinct types of EBV have been described, EBV-1 and EBV-2. Whereas type 1 is known to be most widespread throughout the healthy adult population, type 2 EBV has been shown to be significantly present in certain T-cell immunocompromised patients. Some evidence also suggests that such immune impairment promotes coinfection with multiple strains of EBV and fosters the development of intertypic recombinant viruses. In this work, we have analyzed two established body-cavity-based lymphoma or primary effusion lymphoma cell lines, BC-1 and BC-2, for the presence of intertypic EBV recombinants. Using PCR primers to amplify across several markers in the genome, we have typed the BC-1 and BC-2 EBV at these loci. Immunoblot analysis of the EBNA1 protein expressed by these cell lines also suggests a change in EBV typing at this locus in these genomes. Additionally, we have analyzed the expression patterns of the latent EBNA proteins from these viruses and performed Southern blot analysis of the BamHI- and EcoRI-digested genomes to detect variations occurring from type I and II genomes. On the basis of these data, we suggest that the genomes of EBV in BC-l and BC-2 are intertypic recombinants of type 1 and type 2 EBV genomes. This work corroborates other reports that intertypic EBV recombinants occur in the immunocompromised population. It is likely that intertypic recombination is a mechanism by which novel variants of EBV emerge having selective advantages over a strictly type 1 or type 2 strain. (C) 1999 Academic Press.

关键词： Epstein-Barr Virus Nuclear Antigens Herpesvirus 4 Human Recombination Genetic 爱泼斯坦巴尔病毒核抗原疱疹病毒4型人重组遗传

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In vivo gene transfer into rat hearts with Epstein-Barr virus-based episomal vectors using a gene gun

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TRANSPLANTATION PROCEEDINGS 2000年第7期32卷 2413-2414页

作者： Nishizaki, K Mazda, O Dohi, Y Satoh, E Kawata, T Mizuguchi, K Yonemasu, K Kitamura, S Taniguchi, S Nara Med Univ Dept Surg 3 Kashihara Nara 6348522 Japan Nara Med Univ Dept Publ Hlth Kashihara Nara 6348522 Japan Kyoto Prefectural Univ Med Dept Microbiol Kyoto 602 Japan Natl Cardiovasc Ctr Div Cardiovasc Surg Osaka Japan

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Human RPA (hSSB) interacts with EBNA1, the latent origin binding protein of Epstein-Barr virus

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NUCLEIC ACIDS RESEARCH 1998年第2期26卷 631-637页

作者： Zhang, D Frappier, L Gibbs, E Hurwitz, J O'Donnell, M Rockefeller Univ Howard Hughes Med Inst Lab DNA Replicat New York NY 10021 USA Univ Toronto Dept Med Genet & Microbiol Toronto ON M5S 1A8 Canada Mem Sloan Kettering Canc Ctr Program Mol Biol New York NY 10021 USA

RPA is the replicative single-strand DNA (ssDNA) binding protein of eukaryotic chromosomes. This report shows that human RPA interacts with EBNA1, the latent origin binding protein of Epstein-Barr virus (EBV), RPA binds to EBNA1 both in solution, and when EBNA1 is bound to the EBV origin. RPA is a heterotrimer, and the main contact with EBNA1 is formed through the 70 kDa subunit of RPA, the subunit which binds to ssDNA, We propose that this interaction between RPA and EBNA1 is an early step in activation of the latent origin of EBV.

关键词： DNA-Binding Proteins Epstein-Barr Virus Nuclear Antigens DNA Viral Peptide Fragments DNA结合蛋白质类爱泼斯坦巴尔病毒核抗原 DNA-Binding Proteins peptide fragment DNA drone honey bees Epstein-Barr Virus Nuclear Antigens Human Herpesvirus 4 Binding Protein

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Epstein-Barr virus nuclear antigen (EBNA)-1 carboxy-terminal and EBNA-4 sequence polymorphisms in nasal natural killer/T-cell lymphoma in the United States

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LABORATORY INVESTIGATION 2002年第7期82卷 957-962页

作者： Gaal, K Weiss, LM Chen, WG Chen, YY Arber, DA City Hope Natl Med Ctr Dept Pathol Div Pathol Duarte CA 91010 USA

Epstein-Barr virus (EBV) polymorphisms were examined in 12 cases of nasal natural killer (NK)/T-cell lymphoma diagnosed in the United States (U.S.-NL) with respect to the EBV-associated nuclear antigen (EBNA)-1 carboxy (C)-terminal region and the EBNA-4 region. A single dominant EBV strain was found in all cases. EBNA-1 sequences were remarkably homogeneous, showing either a P-ala (2/12) or P-ala variant (9/12) sequence. Other EBNA-1 subtypes known to be common in U.S.-reactive samples, such as P-thr or V-leu, were not identified. The final case had a base deletion with frame shift and premature stop codon. EBNA-1 C-terminal amino acid substitutions were common at codons 499 (10/12 cases), 502 (7/12), 524 (9/12), and 528 (6/12), all previously reported "hot spots." However, unlike previous reports of other EBV-associated neoplastic and reactive tissues, mutations were absent at residues 487 and 492. Mutations within HLA-A11-restricted immunogenic EBNA-4 epitopes 399-408 and 416-424 occurred in 3 of 12 cases but were not associated with HLA-A11 status. In summary, the exclusive finding of P-ala variant or P-ala EBNA-1 sequences in U.S.-NL cases differs from that reported in U.S.-reactive and non-U.S.-NL cases. Although the significance of this difference is not known for certain, it may be related to geographic and/or site-specific variations, rather than oncogenicity per se.

关键词： Epstein-Barr Virus Nuclear Antigens Herpesvirus 4 Human Killer Cells Natural 爱泼斯坦巴尔病毒核抗原疱疹病毒4型人杀伤细胞天然淋巴瘤 T细胞鼻肿瘤 EBV-encoded nuclear antigen 1 killer cell United States Carcinogenicity Epstein-Barr Virus Nuclear Antigens

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