Epstein, M. A., Barr, Y. M. & Achong, B. G. Virus particles in cultured lymphoblasts from Burkitt's lymphoma. Lancet15, 702–703 (1964). The discovery of EBV — the first description of a virus based on the use of the electron microscope. Article Google Scholar
Nemerow, G. R., Mold, C., Schwend, V. K., Tollefson, V. & Cooper, N. R. Identification of gp350 as the viral glycoprotein mediating attachment of Epstein–Barr virus (EBV) to the EBV/C3d receptor of B cells: sequence homology of gp350 and C3 complment fragment C3d. J. Virol.61, 1416–1420 (1987). CASPubMedPubMed Central Google Scholar
Borza, C. M. & Hutt-Fletcher, L. M. Alternate replication in B-cells and epithelial cells switches tropism of Epstein–Barr virus. Nature Med.8, 594–599 (2002). ArticleCASPubMed Google Scholar
Kieff, E. & Rickinson, A. B. in Fields Virology (eds Knipe, D. M. & Howley, P. M.) 2511–2574 (Lippincott Williams and Wilkins, Philadelphia, 2001). Google Scholar
Kieff, E. & Rickinson, A. B. in Fields Virology (eds Knipe, D. M. & Howley, P. M.) 2575–2627 (Lippincott Williams and Wilkins, Philadelphia, 2001). Google Scholar
Rowe, M. et al. Differences in B cell growth phenotype reflect novel patterns of Epstein–Barr virus latent gene expression in Burkitt's lymphoma cells. EMBO J.6, 2743–2751 (1987). First description of distinct forms of EBV latency in Burkitt's lymphoma cells, as compared to EBV-transformed B-cell lines. ArticleCASPubMedPubMed Central Google Scholar
Wang, F. et al. Epstein–Barr virus latent membrane protein (LMP1) and nuclear proteins 2 and 3C are effectors of phenotypic changes in B lymphocytes: EBNA-2 and LMP1 cooperatively induce CD23. J. Virol.64, 2309–2318 (1990). CASPubMedPubMed Central Google Scholar
Levitskaya, J. et al. Inhibition of antigen processing by the internal repeat region of the Epstein–Barr virus nuclear antigen-1. Nature375, 685–688 (1995). Demonstration that the Gly-Ala-repeat domain of EBNA1 protects the protein from proteasome-mediated degradation. ArticleCASPubMed Google Scholar
Voo, K. S. et al. Evidence for the presentation of major histocompatibility complex class I-restricted Epstein–Barr virus nuclear antigen 1 peptides to CD8+ T lymphocytes. J. Exp. Med.199, 459–470 (2004). ArticleCASPubMedPubMed Central Google Scholar
Lee, S. P. et al. CD8 T cell recognition of endogenously expressed Epstein–Barr virus nuclear antigen 1. J. Exp. Med.199, 1409–1420 (2004). ArticleCASPubMedPubMed Central Google Scholar
Tellam, J. et al. Endogenous presentation of CD8+ T cell epitopes from Epstein–Barr virus-encoded nuclear antigen 1. J. Exp. Med.199, 1421–1431 (2004). ArticleCASPubMedPubMed Central Google Scholar
Humme, S. et al. The EBV nuclear antigen1 (EBNA1) enhances B cell immortalisation several thousandfold. Proc. Natl Acad. Sci. USA100, 10989–10994 (2003). ArticleCASPubMedPubMed Central Google Scholar
Wilson, J. B., Bell, J. L. & Levine, A. J. Expression of Epstein–Barr virus nuclear antigen-1 induces B cell neoplasia in transgenic mice. EMBO J.15, 3117–3126 (1996). ArticleCASPubMedPubMed Central Google Scholar
Kennedy, G., Komano, J. & Sugden, B. Epstein–Barr virus provides a survival factor to Burkitt's lymphomas. Proc. Natl Acad. Sci. USA100, 14269–14274 (2003). ArticleCASPubMedPubMed Central Google Scholar
Hammerschmidt, W. & Sugden, B. Genetic analysis of immortalizing functions of Epstein–Barr virus in human B lymphocytes. Nature340, 393–397 (1989). ArticleCASPubMed Google Scholar
Cohen, J. I., Wang, F., Mannick, J. & Kieff, E. Epstein–Barr virus nuclear protein 2 is a key determinant of lymphocyte transformation. Proc. Natl Acad. Sci. USA86, 9558–9562 (1989). ArticleCASPubMedPubMed Central Google Scholar
Grossman, S. R., Johannsen, E., Tong, R., Yalamanchili, R. & Kieff, E. The Epstein–Barr virus nuclear antigen 2 transactivator is directed to response elements by the Jκ recombination signal binding protein. Proc. Natl Acad. Sci. USA91, 7568–7572 (1994). ArticleCASPubMedPubMed Central Google Scholar
Hsieh, J. J. & Hayward, S. D. Masking of the CBF1/RBPJκ transcriptional repression domain by Epstein–Barr virus EBNA2. Science268, 560–563 (1995). This and the previous paper were the first to show that EBNA2 influences gene transcription by affecting the notch/RBP–Jκ pathway. ArticleCASPubMed Google Scholar
Mannick, J. B., Cohen, J. I., Birkenbach, M., Marchini, A. & Kieff, E. The Epstein–Barr virus nuclear protein encoded by the leader of the EBNA RNAs is important in B-lymphocyte transformation. J. Virol.65, 6826–6837 (1991). CASPubMedPubMed Central Google Scholar
Sinclair, A. J., Palmero, I., Peters, G. & Farrell, P. J. EBNA-2 and EBNA-LP cooperate to cause G0 and G1 transition during immortalization of resting human B lymphocytes by Epstein–Barr virus. EMBO J.13, 3321–3328 (1994). ArticleCASPubMedPubMed Central Google Scholar
Robertson, E., Lin, J. & Kieff, E. The amino-terminal domains of Epstein–Barr virus nuclear proteins 3A, 3B and 3C interact with RBPJκ. J. Virol.70, 3068–3074 (1996). CASPubMedPubMed Central Google Scholar
Zhao, B., Marshall, D. R. & Sample, C. E. A conserved domain of the Epstein–Barr virus nuclear antigens 3A and 3C binds to a discrete domain of Jκ. J. Virol.70, 4228–4236 (1996). CASPubMedPubMed Central Google Scholar
Tomkinson, B., Robertson, E. & Kieff, E. Epstein–Barr virus nuclear proteins EBNA-3A and EBNA-3C are essential for B-lymphocyte growth transformation. J. Virol.67, 2014–2025 (1993). CASPubMedPubMed Central Google Scholar
Parker, G. A. et al. Epstein–Barr virus nuclear antigen (EBNA)3C is an immortalizing oncoprotein with similar properties to adenovirus E1A and papillomavirus E7. Oncogene13, 2541–2549 (1996). CASPubMed Google Scholar
Parker, G. A., Touitou, R. & Allday, M. J. Epstein–Barr virus EBNA3C can disrupte multiple cell cycle checkpoints and induce nuclear division divorced from cytokinesis. Oncogene19, 700–709 (2000). ArticleCASPubMed Google Scholar
Radkov, S. A. et al. Epstein–Barr virus nuclear antigen 3C interacts with histone deacetylase to repress transcription. J. Virol.73, 5688–5697 (1999). CASPubMedPubMed Central Google Scholar
Wang, D., Liebowitz, D. & Kieff, E. An EBV membrane protein expressed in immortalised lymphocytes transforms established rodent cells. Cell43, 831–840 (1985). First study to show that LMP1 functions as a classic oncogene in a rodent cell-transformation assay. ArticleCASPubMed Google Scholar
Kaye, K. M., Izumi, K. M. & Kieff, E. Epstein–Barr virus latent membrane protein 1 is essential for B-lymphocyte growth transformation. Proc. Natl Acad. Sci. USA90, 9150–9154 (1993). ArticleCASPubMedPubMed Central Google Scholar
Henderson, S. et al. Induction of bcl-2 expression by Epstein–Barr virus latent membrane protein 1 protects infected B cells from programmed cell death. Cell65, 1107–1115 (1991). ArticleCASPubMed Google Scholar
Laherty, C. D., Hu, H. M., Opipari, A. W., Wang, F. & Dixit, V. M. The Epstein–Barr virus LMP1 gene product induces A20 zinc finger protein expression by activating nuclear factor κB. J. Biol. Chem.267, 24157–24160 (1992). CASPubMed Google Scholar
Eliopoulos, A. G., Gallagher, N. J., Blake, S. M., Dawson, C. W. & Young, L. S. Activation of the p38 mitogen-activated protein kinase pathway by Epstein–Barr virus-encoded latent membrane protein 1 coregulates interleukin-6 and interleukin-8 production. J. Biol. Chem.274, 16085–16096 (1999). ArticleCASPubMed Google Scholar
Eliopoulos, A. G. et al. Epstein–Barr virus-encoded LMP1 and CD40 mediate IL-6 production in epithelial cells via an NF-κB pathway involving TNF receptor-associated factors. Oncogene14, 2899–2916 (1997). ArticleCASPubMed Google Scholar
Mosialos, G. et al. The Epstein–Barr virus transforming protein LMP1 engages signalling proteins for the tumour necrosis factor receptor family. Cell80, 389–399 (1995). Important study showing that LMP1 functions as a constitutively activated member of the TNF receptor family by interacting with common accessory proteins. ArticleCASPubMed Google Scholar
Gires, O. et al. Latent membrane protein 1 of Epstein–Barr virus mimics a constitutively active receptor molecule. EMBO J.16, 6131–6140 (1997). ArticleCASPubMedPubMed Central Google Scholar
Kilger, E., Kieser, A., Baumann, M. & Hammerschmidt, W. Epstein–Barr virus-mediated B-cell proliferation is dependent upon latent membrane protein 1, which simulates an activated CD40 receptor. EMBO J.17, 1700–1709 (1998). ArticleCASPubMedPubMed Central Google Scholar
Uchida, J. et al. Mimicry of CD40 signals by Epstein–Barr virus LMP1 in B lymphocyte responses. Science286, 300–303 (1999). In vivodemonstration that LMP1 can partially substitute for absence of the CD40 receptor. ArticleCASPubMed Google Scholar
Eliopoulos, A. G. & Young, L. S. LMP1 structure and signal transduction. Semin. Cancer Biol.11, 435–444 (2001). ArticleCASPubMed Google Scholar
Longnecker, R. Epstein–Barr virus latency: LMP2, a regulator or means for Epstein–Barr virus persistence? Adv. Cancer Res.79, 175–200 (2000). ArticleCASPubMed Google Scholar
Caldwell, R. G., Wilson, J. B., Anderson, S. J. & Longnecker, R. Epstein–Barr virus LMP2A drives B cell development and survival in the absence of normal B cell receptor signals. Immunity9, 405–411 (1998). ArticleCASPubMed Google Scholar
Scholle, F., Bendt, K. M. & Raab-Traub, N. Epstein–Barr virus LMP2A transforms epithelial cells, inhibits cell differentiation, and activates Akt. J. Virol.74, 10681–10689 (2000). ArticleCASPubMedPubMed Central Google Scholar
Portis, T., Dyck, P. & Longnecker, R. Epstein–Barr virus (EBV) LMP2A induces alterations in gene transcription similar to those observed in Reed-Sternberg cells of Hodgkin lymphoma. Blood102, 4166–4178 (2003). ArticleCASPubMed Google Scholar
Portis, T. & Longnecker, R. Epstein–Barr virus LMP2A interferes with global transcription factor regulation when expressed during B-lymphocyte development. J. Virol.77, 105–114 (2003). ArticleCASPubMedPubMed Central Google Scholar
Takada, K. & Nanbo, A. The role of EBERs in oncogenesis. Semin. Cancer Biol.11, 461–467 (2001). ArticleCASPubMed Google Scholar
Nanbo, A., Inoue, K., Adachi-Takasawa, K. & Takada, K. Epstein–Barr virus RNA confers resistance to interferon-α-induced apoptosis in Burkitt's lymphoma. EMBO J.21, 954–965 (2002). ArticleCASPubMedPubMed Central Google Scholar
Ruf, I. K., Rhyne, P. W., Yang, C., Cleveland, J. L. & Sample, J. T. Epstein–Barr virus small RNAs potentiate tumourigenicity of Burkitt lymphoma cells independently of an effect on apoptosis. J. Virol.74, 10223–10228 (2000). ArticleCASPubMedPubMed Central Google Scholar
Deacon, E. M. et al. Epstein–Barr virus and Hodgkin's disease: transcriptional analysis of virus latency in the malignant cells. J. Exp. Med.177, 339–349 (1993). ArticleCASPubMed Google Scholar
Chen, H., Smith, P., Ambinder, R. F. & Hayward, S. D. Expression of Epstein–Barr virus BamHI-A rightward transcripts in latently infected B cells from peripheral blood. Blood93, 3026–3032 (1999). CASPubMed Google Scholar
Karran, L., Gao, Y., Smith, P. R. & Griffin, B. E. Expression of a family of complementary-strand transcripts in Epstein–Barr virus-infected cells. Proc. Natl Acad. Sci. USA89, 8058–8062 (1992). ArticleCASPubMedPubMed Central Google Scholar
Decaussin, G., Sbih-Lammali, F., de Turenne-Tessier, M., Bouguermouh, A. & Ooka, T. Expression of BARF1 gene encoded by Epstein–Barr virus in nasopharyngeal carcinoma biopsies. Cancer Res.60, 5584–5588 (2000). CASPubMed Google Scholar
zur Hausen, A. et al. Unique transcription pattern of Epstein–Barr virus (EBV) in EBV-carrying gastric adenocarcinomas: expression of the transforming BARF1 gene. Cancer Res.60, 2745–2748 (2000). CASPubMed Google Scholar
Sheng, W., Decaussin, G., Sumner, S. & Ooka, T. N-terminal domain of BARF1 gene encoded by Epstein–Barr virus is essential for malignant transformation of rodent fibroblasts and activation of BCL-2. Oncogene20, 1176–1185 (2001). ArticleCASPubMed Google Scholar
Anagnostopoulos, I., Hummel, M., Kreschel, C. & Stein, H. Morphology, immunophenotype and distribution of latently and/or productively Epstein–Barr virus-infected cells in acute infectious mononucleosis: implications for the interindividual infection route of Epstein–Barr virus. Blood85, 744–750 (1995). CASPubMed Google Scholar
Kurth, J. et al. Epstein–Barr virus-infected B cells in infectious mononucleosis: viral strategies for spreading in the B cell compartment and establishing latency. Immunity13, 485–495 (2000). ArticleCASPubMed Google Scholar
Babcock, G. J., Decker, L. L., Volk, M. & Thorley-Lawson, D. A. EBV persistence in memory B cells in vivo. Immunity9, 395–404 (1998). Important series of papers from the same group suggesting that EBV exploits the physiology of normal B-cell differentiation to persist within the memory-B-cell pool of the immunocompetent host. ArticleCASPubMed Google Scholar
Hochberg, D. et al. Acute infection with Epstein–Barr virus targets and overwhelms the peripheral memory B-cell compartment with resting, latently infected cells. J. Virol.78, 5194–5204 (2004). ArticleCASPubMedPubMed Central Google Scholar
Babcock, G. J., Hochberg, D. & Thorley-Lawson, D. A. The expression pattern of Epstein–Barr virus latent genes in vivo is dependent upon the differentiation stage of the infected B cell. Immunity13, 497–506 (2000). ArticleCASPubMed Google Scholar
Laichalk, L. L., Hochberg, D., Babcock, G. J., Freeman, R. B. & Thorley-Lawson, D. A. The dispersal of mucosal memory B cells: evidence from persistent EBV infection. Immunity16, 745–754 (2002). ArticleCASPubMed Google Scholar
Hislop, A. D., Annels, N. E., Gudgeon, N. H., Leese, A. M. & Rickinson, A. B. Epitope-specific evolution of human CD8+ T cell responses from primary to persistent phases of Epstein–Barr virus infection. J. Exp. Med.195, 893–905 (2002). ArticleCASPubMedPubMed Central Google Scholar
Young, L. et al. Expression of Epstein–Barr virus transformation-associated genes in tissues of patients with EBV lymphoproliferative disease. N. Engl. J. Med.321, 1080–1085 (1989). First demonstration of EBV latent protein expression in post-transplantation lymphomas. ArticleCASPubMed Google Scholar
Timms, J. M. et al. Target cells of Epstein–Barr virus (EBV)-positive post-transplant lymphoproliferative disease: similarities to EBV-positive Hodgkin's lymphoma. Lancet361, 217–223 (2003). ArticlePubMed Google Scholar
Capello, D. et al. Molecular histogenesis of post-transplantation lymphoproliferative disorders. Blood102, 3775–3785 (2003). ArticleCASPubMed Google Scholar
Hsu, J. L. & Glaser, S. L. Epstein–Barr virus-associated malignancies: epidemiologic patterns and etiologic implications. Crit. Rev. Oncol. Hematol.34, 27–53 (2000). ArticleCASPubMed Google Scholar
Kanzler, H., Kuppers, R., Hansmann, M. L. & Rajewsky, K. Hodgkin and Reed-Sternberg cells in Hodgkin's disease represent the outgrowth of a dominant tumour clone derived from (crippled) germinal center B cells. J. Exp. Med.184, 1495–1505 (1996). One of the first studies to isolate the malignant cells of Hodgkin's lymphoma and definitively determine the origin of these cells by immunoglobulin-gene sequencing. ArticleCASPubMed Google Scholar
Kuppers, R. Molecular biology of Hodgkin's lymphoma. Adv. Cancer Res.84, 277–312 (2002). ArticlePubMed Google Scholar
Schwering, I. et al. Loss of the B lineage-specific gene expression program in Hodgkin and Reed-Sternberg cells of Hodgkin lymphoma. Blood101, 1505–1512 (2003). ArticleCASPubMed Google Scholar
Polack, A. et al. c-myc activation renders proliferation of Epstein–Barr virus (EBV)-transformed cells independent of EBV nuclear antigen 2 and latent membrane protein 1. Proc. Natl Acad. Sci. USA93, 10411–10416 (1996). ArticleCASPubMedPubMed Central Google Scholar
Li, Z. et al. A global transcriptional regulatory role for c-myc in Burkitt's lymphoma. Proc. Natl Acad. Sci. USA100, 8146–8169 (2003). ArticleCAS Google Scholar
Lindstrom, M. S. & Wiman, K. G. Role of genetic and epigenetic changes in Burkitt lymphoma. Semin. Cancer Biol.12, 381–387 (2002). ArticleCASPubMed Google Scholar
Chapman, C. J., Mockridge, C. I., Rowe, M., Rickinson, A. B. & Stevenson, F. K. Analysis of V-H genes used by neoplastic B cells in endemic Burkitts lymphoma shows somatic hypermutation and intraclonal heterogeneity. Blood85, 2176–2181 (1995). CASPubMed Google Scholar
Klein, U., Klein, G., Ehlin-Henriksson, B., Rajewsky, K. & Kuppers, R. Burkitt's lymphoma is a malignancy of mature B cells expressing somatically mutated V-region genes. Mol. Med.1, 495–505 (1995). ArticleCASPubMedPubMed Central Google Scholar
Harris, R. S., Croom-Carter, D., Rickinson, A. B. & Neuberger, M. S. Epstein–Barr virus and the somatic hypermutation of immunoglobulin genes in Burkitt's lymphoma cells. J. Virol.75, 10488–10492 (2001). ArticleCASPubMedPubMed Central Google Scholar
Kelly, G., Bell, A. & Rickinson, A. B. Epstein–Barr virus-associated Burkitt lymphomagenesis selects for downregulation of the nuclear antigen EBNA1. Nature Med.8, 1098–1104 (2002). ArticleCASPubMed Google Scholar
Pajic, A. et al. Antagonistic effects of c-myc and Epstein–Barr virus latent genes on the phenotype of human B cells. Int. J. Cancer93, 810–816 (2001). ArticleCASPubMed Google Scholar
Kang, M. S., Hung, S. C. & Kieff, E. Epstein–Barr virus nuclear antigen 1 activates transcription from episomal but not integrated DNA and does not alter lymphocyte growth. Proc. Natl Acad. Sci. USA98, 15233–15238 (2001). ArticleCASPubMedPubMed Central Google Scholar
Kiss, C. et al. T cell leukaemia I oncogene expression depends on the presence of Epstein–Barr virus in the virus-carrying Burkitt lymphoma lines. Proc. Natl Acad. Sci. USA100, 4813–4818 (2003). ArticleCASPubMedPubMed Central Google Scholar
Boshoff, C. & Weiss, R. AIDS-related malignancies. Nature Rev. Cancer2, 373–382 (2002). ArticleCAS Google Scholar
Araujo, I. et al. Frequent expansion of Epstein–Barr virus (EBV) infected cells in germinal centres of tonsils from an area with a high incidence of EBV-associated lymphoma. J. Pathol.187, 326–330 (1999). ArticleCASPubMed Google Scholar
Jones, J. F. et al. T-cell lymphomas containing Epstein–Barr viral DNA in patients with chronic Epstein–Barr virus infections. N. Engl. J. Med.318, 733–741 (1988). ArticleCASPubMed Google Scholar
Harabuchi, Y. et al. Epstein–Barr virus in nasal T-cell lymphomas in patients with lethal midline granuloma. Lancet335, 128–130 (1990). ArticleCASPubMed Google Scholar
Kanegane, H., Nomura, K., Miyawaki, T. & Tosato, G. Biological aspects of Epstein–Barr virus (EBV)-infected lymphocytes in chronic active EBV infection and associated malignancies. Crit. Rev. Oncol. Haematol.44, 239–249 (2002). Article Google Scholar
Kikuta, H. et al. Epstein–Barr virus genome-positive T lymphocytes in a boy with chronic active EBV infection associated with Kawaski-like disease. Nature333, 455–457 (1988). ArticleCASPubMed Google Scholar
Kanavaros, P. et al. Nasal T-cell lymphoma: a clinicopathologic entity associated with peculiar phenotype and with Epstein–Barr virus. Blood81, 2688–2695 (1993). CASPubMed Google Scholar
Raab-Traub, N. Epstein–Barr virus in the pathogenesis of NPC. Semin. Cancer Biol.12, 431–441 (2002). ArticleCASPubMed Google Scholar
Yu, M. C. & Yuan, J. M. Epidemiology of nasopharyngeal carcinoma. Semin. Cancer Biol.12, 421–429 (2002). ArticlePubMed Google Scholar
Yu, M. C., Ho, J. H., Lai, S. H. & Henderson, B. E. Cantonese-style salted fish as a cause of nasopharyngeal carcinoma: report of a case–control study in Hong Kong. Cancer Res.46, 956–961 (1986). CASPubMed Google Scholar
Raab-Traub, N. & Flynn, K. The structure of the termini of the Epstein–Barr virus as a marker of clonal cellular proliferation. Cell47, 883–889 (1986). ArticleCASPubMed Google Scholar
Zeng, Y. Seroepidemiological studies on nasopharyngeal carcinoma in China. Adv. Cancer Res.44, 121–138 (1985). ArticleCASPubMed Google Scholar
Chan, A. T. C. et al. Plasma Epstein–Barr virus DNA and residual disease after radiotherapy for undifferentiated nasopharyngeal carcinoma. J. Natl Cancer Inst.94, 1614–1619 (2002). ArticleCASPubMed Google Scholar
Pathmanathan, R. et al. Undifferentiated, non-keratinising, and squamous cell carcinoma of the nasopharynx. Variants of Epstein–Barr virus-infected neoplasia. Am. J. Pathol.146, 1355–1367 (1995). CASPubMedPubMed Central Google Scholar
Shibata, D. & Weiss, L. M. Epstein–Barr virus-associated gastric adenocarcinoma. Am. J. Pathol.140, 769–774 (1992). CASPubMedPubMed Central Google Scholar
Imai, S. et al. Gastric carcinoma: monoclonal epithelial malignant cells expressing Epstein–Barr virus latent infection protein. Proc. Natl Acad. Sci. USA91, 9131–9135 (1994). ArticleCASPubMedPubMed Central Google Scholar
Schneider, B. G. et al. Loss of p16/CDKN2A tumour suppressor protein in gastric adenocarcinoma is associated with Epstein–Barr virus and antomic location in the body of the stomach. Hum. Pathol.31, 45–50 (2000). ArticleCASPubMed Google Scholar
Lee, H. S., Chang, M. S., Yang, H. K., Lee, B. L. & Kim, W. H. Epstein–Barr virus-positive gastric carcinoma has a distinct protein expression profile in comparison with Epstein–Barr virus-negative carcinoma. Clin. Cancer Res.10, 1698–1705 (2004). ArticleCASPubMed Google Scholar
zur Hausen, A. et al. Epstein–Barr virus in gastric carcinomas and gastric stump carcinomas: a late event in gastric carcinogenesis. J. Clin. Pathol.57, 487–491 (2004). ArticleCASPubMedPubMed Central Google Scholar
Bonnet, M. et al. Detection of Epstein–Barr virus in invasive breast cancers. J. Natl Cancer Inst.91, 1376–1381 (1999). ArticleCASPubMed Google Scholar
Sugawara, Y. et al. Detection of Epstein–Barr virus (EBV) in hepatocellular carcinoma tissue: a novel EBV latency characterised by the absence of EBV-encoded small RNA expression. Virology256, 196–202 (1999). ArticleCASPubMed Google Scholar
Murray, P. G. et al. Reactivity with a monoclonal antibody to Epstein–Barr virus (EBV) nuclear antigen 1 defines a subset of aggressive breast cancers in the absence of the EBV genome. Cancer Res.63, 2338–2343 (2003). CASPubMed Google Scholar
Li, J. -H. et al. Tumour-targeted gene therapy for nasopharyngeal carcinoma. Cancer Res.62, 171–178 (2002). CASPubMed Google Scholar
Li, J. -H. et al. Efficacy of targeted FasL in nasopharyngeal carcinoma. Mol. Ther.8, 964–973 (2003). ArticleCASPubMed Google Scholar
Israel, B. F. & Kenney, S. C. Virally targeted therapies for EBV-associated malignancies. Oncogene22, 5122–5130 (2003). ArticleCASPubMed Google Scholar
Feng, W. -H., Hong, G., Delecluse, H. J. & Kenney, S. C. Lytic induction therapy for Epstein–Barr virus-positive B-cell lymphomas. J. Virol.78, 1893–1902 (2004). ArticleCASPubMedPubMed Central Google Scholar
Ambinder, R. F., Robertson, K. D. & Tao, Q. DNA methylation and the Epstein–Barr virus. Semin. Cancer Biol.9, 369–375 (1999). ArticleCASPubMed Google Scholar
Chan, A. T. C. et al. Azacitidine induces demethylation of the Epstein–Barr virus genome in tumours. J. Clin. Oncol.22, 1373–1381 (2004). ArticleCASPubMed Google Scholar
Chodosh, J. et al. Eradication of latent Epstein–Barr virus by hydroxyurea alters the growth-transformed cell phenotype. J. Infect. Dis.177, 1194–1201 (1998). ArticleCASPubMed Google Scholar
Slobod, K. S. et al. Epstein–Barr virus-targeted therapy for AIDS-related primary lymphoma of the central nervous system. Lancet356, 1493–1494 (2000). ArticleCASPubMed Google Scholar
Piche, A., Kasono, K., Johanning, F., Curiel, T. J. & Curiel, D. T. Phenotypic knockout of the latent membrane protein 1 of Epstein–Barr virus by an intracellular single-chain antibody. Gene Ther.5, 1171–1179 (1998). ArticleCASPubMed Google Scholar
Kenney, J. L., Guinness, M. E., Curiel, T. & Lacy, J. Antisense to the Epstein–Barr virus (EBV)-encoded latent membrane protein 1 (LMP-1) suppresses LMP-1 and Bcl-2 expression and promotes apoptosis in EBV-immortalised B cells. Blood92, 1721–1727 (1998). CASPubMed Google Scholar
Cahir-McFarland, E. D., Davidson, D. M., Schauer, S. L., Duong, J. & Kieff, E. NFκB inhibition causes spontaneous apoptosis in Epstein–Barr virus-transformed lymphoblastoid cells. Proc. Natl Acad. Sci. USA97, 6055–6060 (2000). ArticleCASPubMedPubMed Central Google Scholar
Farrell, C. J. et al. Inhibition of Epstein–Barr virus-induced growth proliferation by a nuclear antigen EBNA2-TAT peptide. Proc. Natl Acad. Sci. USA101, 4625–4630 (2004). ArticleCASPubMedPubMed Central Google Scholar
Kirchmaier, A. L. & Sugden, B. Dominant-negative inhibitors of EBNA-1 of Epstein–Barr virus. J. Virol.71, 1766–1775 (1997). CASPubMedPubMed Central Google Scholar
Rooney, C. M. et al. Use of gene-modified virus-specific T lymphocytes to control Epstein–Barr virus-related lymphoproliferation. Lancet345, 9–13 (1995). First study to use adoptive transfer of EBV-specific T cells for the treatment of lymphoproliferative disease. ArticleCASPubMed Google Scholar
Khanna, R. et al. Activation and adoptive transfer of Epstein–Barr virus-specific cytotoxic T cells in solid organ transplant patients with post-transplant lymphoproliferative disease. Proc. Natl Acad. Sci. USA96, 10391–10396 (1999). ArticleCASPubMedPubMed Central Google Scholar
Haque, T. et al. Treatment of Epstein–Barr virus-positive post-transplantation lymphoproliferative disease with partly HLA-matched allogeneic cytotoxic T cells. Lancet360, 436–442 (2002). ArticlePubMed Google Scholar
Roskrow, M. A. et al. Epstein–Barr virus (EBV)-specific cytotoxic T lymphocytes for the treatment of patients with EBV-positive relapsed Hodgkin's disease. Blood91, 2925–2934 (1998). CASPubMed Google Scholar
Wagner, H. J. et al. Expansion of EBV latent membrane protein 2a specific cytotoxic T cells for the adoptive immunotherapy of EBV latency type 2 malignancies: influence of recombinant IL12 and IL15. Cytotherapy5, 231–240 (2003). ArticleCASPubMed Google Scholar
Paludan, C. et al. Epstein–Barr nuclear antigen 1-specific CD4+ Th1 cells kill Burkitt's lymphoma cells. J. Immunol.169, 1593–1603 (2002). ArticleCASPubMed Google Scholar
Taylor, G. S. et al. Dual stimulation of Epstein–Barr virus (EBV)-specific CD4+/− and CD8+/− T cell responses by a chimeric antigen construct: Potential therapeutic vaccine for EBV-positive nasopharyngeal carcinoma. J. Virol.78, 768–778 (2004). ArticleCASPubMedPubMed Central Google Scholar
Frisan, T. et al. Local suppression of Epstein–Barr virus (EBV)-specific cytotoxicity in biopsies of EBV-positive Hodgkin's disease. Blood86, 1493–1501 (1995). CASPubMed Google Scholar
Wagner, H. J. et al. A strategy for treatment of Epstein–Barr virus-positive Hodgkin's disease by targeting interleukin 12 to the tumour environment using tumour antigen-specific T cells. Cancer Gene Ther.11, 81–91 (2004). ArticleCASPubMed Google Scholar
Baer, R. et al. DNA sequence and expression of the B95-8 Epstein–Barr virus genome. Nature310, 207–211 (1984). Sequencing of the prototype strain of EBV — at the time, this was the largest region of DNA ever sequenced and the first human virus to be fully sequenced. ArticleCASPubMed Google Scholar
Brauninger, A. et al. Epstein–Barr virus (EBV)-positive lymphoproliferations in post-transplant patients show immunoglobulin V gene mutation patterns suggesting interference of EBV with normal B cell differentiation processes. Eur. J. Immunol.33, 1593–1602 (2003). ArticlePubMedCAS Google Scholar
Brauninger, A. et al. Survival and clonal expansion of mutating 'forbidden' (immunoglobulin receptor-deficient) Epstein–Barr virus-infected B cells in angioimmunoblastic T cell lymphoma. J. Exp. Med.194, 927–940 (2001). ArticleCASPubMedPubMed Central Google Scholar
Pathmanathan, R., Prasad, U., Sadler, R., Flynn, K. & Raab-Traub, N. Clonal proliferations of cells infected with Epstein–Barr virus in preinvasive lesions related to nasopharyngeal carcinoma. N. Engl. J. Med.333, 693–698 (1995). First demonstration of clonal EBV infection in pre-malignant lesions of the nasopharynx. ArticleCASPubMed Google Scholar
Lo, K. -W. & Huang, D. P. Genetic and epigenetic changes in nasopharyngeal carcinoma. Semin. Cancer Biol.12, 451–462 (2002). Important review summarizing the genetic and epigenetic events that contribute to the pathogenesis of NPC and indicating that some of these occur before EBV infection. ArticleCASPubMed Google Scholar
Knox, P. G., Li, Q. X., Rickinson, A. B. & Young, L. S. In vitro production of stable Epstein–Barr virus-positive epithelial cell clones which resemble the virus: cell interaction observed in nasopharyngeal carcinoma. Virology215, 40–50 (1996). ArticleCASPubMed Google Scholar
Zhou, S., Fujimuro, M., Hsieh, J. J., Chen, L. & Hayward, S. D. A role for SKIP in EBNA2 activation of CBF1-repressed promoters. J. Virol.74, 1939–1947 (2000). ArticleCASPubMedPubMed Central Google Scholar
Artavanis-Tsakonas, S., Matsuno, K. & Fortini, M. E. Notch signaling. Science268, 225–232 (1995). ArticleCASPubMed Google Scholar
Sakai, T. et al. Functional replacement of the intracellular region of the Notch1 receptor by Epstein–Barr virus nuclear antigen 2. J. Virol.72, 6034–6039 (1998). CASPubMedPubMed Central Google Scholar
Huen, D. S., Henderson, S. A., Croom-Carter, D. & Rowe, M. The Epstein–Barr virus latent membrane protein-1 (LMP1) mediates activation of NF-κB and cell surface phenotype via two effector regions in its carboxy-terminal cytoplasmic domain. Oncogene10, 549–560 (1995). CASPubMed Google Scholar
Eliopoulos, A. G. et al. Epstein–Barr virus-encoded latent infection membrane protein 1 regulates the processing of p100 NFκB2 to p52 via an IKKγ/NEMO-independent signalling pathway. Oncogene22, 7557–7569 (2003). ArticleCASPubMed Google Scholar
Dykstra, M. L., Longnecker, R. & Pierce, S. K. Epstein–Barr virus coopts lipid rafts to block the signalling and antigen transport functions of the BCR. Immunity14, 57–67 (2001). ArticleCASPubMed Google Scholar
Ikeda, M., Ikeda, A., Longan, L. C. & Longnecker, R. The Epstein–Barr virus latent membrane protein 2A PY motif recruits WW domain-containing ubiquitin-protein ligases. Virology268, 178–191 (2000). ArticleCASPubMed Google Scholar
Chen, S. -Y., Lu, J., Shih, Y. -C. & Tsai, C. -H. Epstein–Barr virus latent membrane protein 2A regulates c-Jun protein through extracellular signal-regulated kinase. J. Virol.76, 9556–9561 (2002). ArticleCASPubMedPubMed Central Google Scholar
Young, L. S. & Murray, P. G. Epstein–Barr virus and oncogenesis: from latent genes to tumours. Oncogene22, 5108–5121 (2003). ArticleCASPubMed Google Scholar