Publications
164 results found
Brady G, Karstegl CE, Farrell PJ, 2013, Novel function of the unique N-terminal region of RUNX1c in B cell growth regulation, NUCLEIC ACIDS RESEARCH, Vol: 41, Pages: 1555-1568, ISSN: 0305-1048
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- Citations: 15
Tzellos S, Farrell PJ, 2012, Epstein-barr virus sequence variation-biology and disease., Pathogens, Vol: 1, Pages: 156-174, ISSN: 2076-0817
Some key questions in Epstein-Barr virus (EBV) biology center on whether naturally occurring sequence differences in the virus affect infection or EBV associated diseases. Understanding the pattern of EBV sequence variation is also important for possible development of EBV vaccines. At present EBV isolates worldwide can be grouped into Type 1 and Type 2, a classification based on the EBNA2 gene sequence. Type 1 EBV is the most prevalent worldwide but Type 2 is common in parts of Africa. Type 1 transforms human B cells into lymphoblastoid cell lines much more efficiently than Type 2 EBV. Molecular mechanisms that may account for this difference in cell transformation are now becoming clearer. Advances in sequencing technology will greatly increase the amount of whole EBV genome data for EBV isolated from different parts of the world. Study of regional variation of EBV strains independent of the Type 1/Type 2 classification and systematic investigation of the relationship between viral strains, infection and disease will become possible. The recent discovery that specific mutation of the EBV EBNA3B gene may be linked to development of diffuse large B cell lymphoma illustrates the importance that mutations in the virus genome may have in infection and human disease.
Hatzimichael E, Lo Nigro C, Lattanzio L, et al., 2012, The collagen prolyl hydroxylases are novel transcriptionally silenced genes in lymphoma, British Journal of Cancer, Vol: 107, Pages: 1423-1432, ISSN: 1532-1827
Tzartos J, Khan G, Cruz-Sadaba M, et al., 2012, Association of innate immune activation with latent Epstein - Barr virus infection in active multiple sclerosis lesions, European Congress of Immunology, Publisher: WILEY-BLACKWELL, Pages: 51-51, ISSN: 0019-2805
Kwok H, Tong AHY, Lin CH, et al., 2012, Genomic Sequencing and Comparative Analysis of Epstein-Barr Virus Genome Isolated from Primary Nasopharyngeal Carcinoma Biopsy, PLOS ONE, Vol: 7, ISSN: 1932-6203
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- Citations: 68
Buettner M, Lang A, Tudor CS, et al., 2012, Lytic Epstein-Barr virus infection in epithelial cells but not in B-lymphocytes is dependent on Blimp1, JOURNAL OF GENERAL VIROLOGY, Vol: 93, Pages: 1059-1064, ISSN: 0022-1317
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- Citations: 18
Tzartos JS, Khan G, Vossenkamper A, et al., 2012, Association of innate immune activation with latent Epstein-Barr virus in active MS lesions, NEUROLOGY, Vol: 78, Pages: 15-23, ISSN: 0028-3878
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- Citations: 103
Cancian L, Bosshard R, Lucchesi W, et al., 2011, C-terminal region of EBNA-2 determines the superior transforming ability of type 1 Epstein-Barr virus by enhanced gene regulation of LMP-1 and CXCR7., PLoS Pathog, Vol: 7
Type 1 Epstein-Barr virus (EBV) strains immortalize B lymphocytes in vitro much more efficiently than type 2 EBV, a difference previously mapped to the EBNA-2 locus. Here we demonstrate that the greater transforming activity of type 1 EBV correlates with a stronger and more rapid induction of the viral oncogene LMP-1 and the cell gene CXCR7 (which are both required for proliferation of EBV-LCLs) during infection of primary B cells with recombinant viruses. Surprisingly, although the major sequence differences between type 1 and type 2 EBNA-2 lie in N-terminal parts of the protein, the superior ability of type 1 EBNA-2 to induce proliferation of EBV-infected lymphoblasts is mostly determined by the C-terminus of EBNA-2. Substitution of the C-terminus of type 1 EBNA-2 into the type 2 protein is sufficient to confer a type 1 growth phenotype and type 1 expression levels of LMP-1 and CXCR7 in an EREB2.5 cell growth assay. Within this region, the RG, CR7 and TAD domains are the minimum type 1 sequences required. Sequencing the C-terminus of EBNA-2 from additional EBV isolates showed high sequence identity within type 1 isolates or within type 2 isolates, indicating that the functional differences mapped are typical of EBV type sequences. The results indicate that the C-terminus of EBNA-2 accounts for the greater ability of type 1 EBV to promote B cell proliferation, through mechanisms that include higher induction of genes (LMP-1 and CXCR7) required for proliferation and survival of EBV-LCLs.
Gregorovic G, Bosshard R, Karstegl CE, et al., 2011, Cellular Gene Expression That Correlates with EBER Expression in Epstein-Barr Virus-Infected Lymphoblastoid Cell Lines, JOURNAL OF VIROLOGY, Vol: 85, Pages: 3535-3545, ISSN: 0022-538X
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- Citations: 44
Lai IY-C, Farrell PJ, Kellam P, 2011, X-box binding protein 1 induces the expression of the lytic cycle transactivator of Kaposi's sarcoma-associated herpesvirus but not Epstein Barr virus in co-infected primary effusion lymphoma, Journal of General Virology, Vol: 92, Pages: 421-431, ISSN: 1465-2099
Cells of primary effusion lymphoma (PEL), a B-cell non-Hodgkin's lymphoma, are latently infected by Kaposi's sarcoma-associated herpesvirus (KSHV), with about 80 % of PEL also co-infected with Epstein–Barr virus (EBV). Both viruses can be reactivated into their lytic replication cycle in PEL by chemical inducers. However, simultaneous activation of both lytic cascades leads to mutual lytic cycle co-repression. The plasma cell-differentiation factor X-box binding protein 1 (XBP-1) transactivates the KSHV immediate–early promoter leading to the production of the replication and transcription activator protein (RTA), and reactivation of KSHV from latency. XBP-1 has been reported to act similarly on the EBV immediate–early promoter Zp, leading to the production of the lytic-cycle transactivator protein BZLF1. Here we show that activated B-cell terminal-differentiation transcription factor X-box binding protein 1 (XBP-1s) does not induce EBV BZLF1 and BRLF1 expression in PEL and BL cell lines, despite inducing lytic reactivation of KSHV in PEL. We show that XBP-1s transactivates the KSHV RTA promoter but does not transactivate the EBV BZLF1 promoter in non-B-cells by using a luciferase assay. Co-expression of activated protein kinase D, which can phosphorylate and inactivate class II histone deacetylases (HDACs), does not rescue XBP-1 activity on Zp nor does it induce BZLF1 and BRLF1 expression in PEL. Finally, chemical inducers of KSHV and EBV lytic replication in PEL, including HDAC inhibitors, do not lead to XBP-1 activation. We conclude that XBP-1 specifically reactivates the KSHV lytic cycle in dually infected PELs.
McDonald C, Karstegl CE, Kellam P, et al., 2010, Regulation of the Epstein-Barr virus Zp promoter in B lymphocytes during reactivation from latency, JOURNAL OF GENERAL VIROLOGY, Vol: 91, Pages: 622-629, ISSN: 0022-1317
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- Citations: 17
Brady G, Farrell PJ, 2009, RUNX3-Mediated Repression of RUNX1 in B Cells, JOURNAL OF CELLULAR PHYSIOLOGY, Vol: 221, Pages: 283-287, ISSN: 0021-9541
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- Citations: 15
Brady G, Whiteman HJ, Spender LC, et al., 2009, Downregulation of RUNX1 by RUNX3 Requires the RUNX3 VWRPY Sequence and Is Essential for Epstein-Barr Virus-Driven B-Cell Proliferation, JOURNAL OF VIROLOGY, Vol: 83, Pages: 6909-6916, ISSN: 0022-538X
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- Citations: 40
McDonald CM, Petosa C, Farrell PJ, 2009, Interaction of Epstein-Barr Virus BZLF1 C-Terminal Tail Structure and Core Zipper Is Required for DNA Replication but Not for Promoter Transactivation, JOURNAL OF VIROLOGY, Vol: 83, Pages: 3397-3401, ISSN: 0022-538X
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- Citations: 9
Al-Mozaini M, Bodelon G, Karstegl CE, et al., 2009, Epstein-Barr virus BART gene expression, JOURNAL OF GENERAL VIROLOGY, Vol: 90, Pages: 307-316, ISSN: 0022-1317
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- Citations: 49
Lucchesi W, Brady G, Dittrich-Breiholz O, et al., 2008, Differential gene regulation by Epstein-Barr virus type 1 and type 2 EBNA2, JOURNAL OF VIROLOGY, Vol: 82, Pages: 7456-7466, ISSN: 0022-538X
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- Citations: 52
Horner D, Lewis M, Farrell PJ, 2008, Novel hypotheses for the roles of EBNA-1 and BHRF1 in EBV-related cancers, INTERVIROLOGY, Vol: 38, Pages: 195-205, ISSN: 0300-5526
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- Citations: 28
Brady G, MacArthur GJ, Farrell PJ, 2008, Epstein-Barr virus and Burkitt lymphoma, POSTGRADUATE MEDICAL JOURNAL, Vol: 84, Pages: 372-377, ISSN: 0032-5473
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- Citations: 48
Brady G, MacArthur GJ, Farrell PJ, 2007, Epstein-Barr virus and Burkitt lymphoma, JOURNAL OF CLINICAL PATHOLOGY, Vol: 60, Pages: 1397-1402, ISSN: 0021-9746
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- Citations: 139
Farrell PJ, 2007, Role for HLA in susceptibility to infectious mononucleosis, JOURNAL OF CLINICAL INVESTIGATION, Vol: 117, Pages: 2756-2758, ISSN: 0021-9738
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- Citations: 8
Pattle SB, Farrell PJ, 2006, The role of Epstein-Barr virus in cancer, EXPERT OPINION ON BIOLOGICAL THERAPY, Vol: 6, Pages: 1193-1205, ISSN: 1471-2598
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- Citations: 114
Spender LC, Lucchesi W, Bodelon G, et al., 2006, Cell target genes of Epstein-Barr virus transcription factor EBNA-2:: induction of the p55α regulatory subunit of PI3-kinase and its role in survival of EREB2.5 cells, JOURNAL OF GENERAL VIROLOGY, Vol: 87, Pages: 2859-2867, ISSN: 0022-1317
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- Citations: 47
Amon W, White RE, Farrell PJ, 2006, Epstein-Barr virus origin of lytic replication mediates association of replicating episomes with promyelocytic leukaemia protein nuclear bodies and replication compartments, JOURNAL OF GENERAL VIROLOGY, Vol: 87, Pages: 1133-1137, ISSN: 0022-1317
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- Citations: 17
Syed N, Smith P, Sullivan A, et al., 2006, Transcriptional silencing of Polo-like kinase 2 (<i>SNK/PLK2</i>) is a frequent event in B-cell malignancies, BLOOD, Vol: 107, Pages: 250-256, ISSN: 0006-4971
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- Citations: 100
Whiteman HJ, Farrell PJ, 2006, RUNX expression and function in human B cells, CRITICAL REVIEWS IN EUKARYOTIC GENE EXPRESSION, Vol: 16, Pages: 31-44, ISSN: 1045-4403
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- Citations: 16
Spender LC, Whiteman HJ, Karstegl CE, et al., 2005, Transcriptional cross-regulation of RUNX1 by RUNX3 in human B cells, ONCOGENE, Vol: 24, Pages: 1873-1881, ISSN: 0950-9232
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- Citations: 79
Farrell PJ, 2005, Can plasma Epstein-Barr virus DNA levels be used to monitor nasopharyngeal carcinoma progression?, NATURE CLINICAL PRACTICE ONCOLOGY, Vol: 2, Pages: 14-15, ISSN: 1743-4254
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- Citations: 1
Amon W, Farrell PJ, 2005, Reactivation of Epstein-Barr virus from latency, REVIEWS IN MEDICAL VIROLOGY, Vol: 15, Pages: 149-156, ISSN: 1052-9276
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- Citations: 145
Amon W, Binné UK, Bryant H, et al., 2004, Lytic cycle gene regulation of Epstein-Barr virus, JOURNAL OF VIROLOGY, Vol: 78, Pages: 13460-13469, ISSN: 0022-538X
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- Citations: 43
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