Reactivation of Epstein-Barr virus from latency

被引:153
作者
Amon, W
Farrell, PJ
机构
[1] Univ London Imperial Coll Sci Technol & Med, Fac Med, Ludwig Inst Canc Res, London W2 1PG, England
[2] Univ London Imperial Coll Sci Technol & Med, Fac Med, Dept Virol, London W2 1PG, England
关键词
D O I
10.1002/rmv.456
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The general problem in cancer treatment centres on finding agents that specifically affect cancer cells without damaging normal cells. The differences between cancer cells and normal cells are usually very subtle but about 15% of all human cancers involve a virus infection, for example the Epstein-Barr virus associated cancers. In these cancers, every tumour cell carries the virus in a latent infection but the number of normal cells infected is very low. So a treatment that could somehow cause the elimination of EBV infected cells would be very specific for the cancer in such cases. One potential approach could involve finding ways to reactivate the latent virus in cancer cells into the early part of the lytic cycle, impeding cell proliferation, targeting chemotherapeutic agents to the cancer and causing the cancer cells to become targets for immune surveillance. This review considers the mechanisms by which EBV reactivation is controlled and discusses possible therapeutic approaches. Copyright (c) 2004 John Wiley & Sons, Ltd.
引用
收藏
页码:149 / 156
页数:8
相关论文
共 68 条
[1]   RELATIONSHIP BETWEEN THE EPSTEIN-BARR VIRUS GENOME AND NASOPHARYNGEAL CARCINOMA IN CAUCASIAN PATIENTS [J].
ANDERSSONANVRET, M ;
FORSBY, N ;
KLEIN, G ;
HENLE, W ;
BIORKLUND, A .
INTERNATIONAL JOURNAL OF CANCER, 1979, 23 (06) :762-767
[2]   Tonsillar memory B cells, latently infected with Epstein-Barr virus, express the restricted pattern of latent genes previously found only in Epstein-Barr virus-associated tumors [J].
Babcock, GJ ;
Thorley-Lawson, DA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (22) :12250-12255
[3]   EBV persistence in memory B cells in vivo [J].
Babcock, GJ ;
Decker, LL ;
Volk, M ;
Thorley-Lawson, DA .
IMMUNITY, 1998, 9 (03) :395-404
[4]   DNA-SEQUENCE AND EXPRESSION OF THE B95-8 EPSTEIN-BARR VIRUS GENOME [J].
BAER, R ;
BANKIER, AT ;
BIGGIN, MD ;
DEININGER, PL ;
FARRELL, PJ ;
GIBSON, TJ ;
HATFULL, G ;
HUDSON, GS ;
SATCHWELL, SC ;
SEGUIN, C ;
TUFFNELL, PS ;
BARRELL, BG .
NATURE, 1984, 310 (5974) :207-211
[5]   ACTIVATION OF THE EPSTEIN-BARR VIRUS GENOME BY 5-AZA-CYTIDINE IN LATENTLY INFECTED HUMAN LYMPHOID LINES [J].
BENSASSON, SA ;
KLEIN, G .
INTERNATIONAL JOURNAL OF CANCER, 1981, 28 (02) :131-135
[6]   EPSTEIN-BARR-VIRUS GENE-EXPRESSION IN P3HR1-SUPERINFECTED RAJI CELLS [J].
BIGGIN, M ;
BODESCOT, M ;
PERRICAUDET, M ;
FARRELL, P .
JOURNAL OF VIROLOGY, 1987, 61 (10) :3120-3132
[7]   Promoter sequences required for reactivation of Epstein-Barr virus from latency [J].
Binné, UK ;
Amon, W ;
Farrell, PJ .
JOURNAL OF VIROLOGY, 2002, 76 (20) :10282-10289
[8]   EPSTEIN-BARR-VIRUS LATENT GENE-TRANSCRIPTION IN NASOPHARYNGEAL CARCINOMA-CELLS - COEXPRESSION OF EBNA1, LMP1, AND LMP2 TRANSCRIPTS [J].
BROOKS, L ;
YAO, QY ;
RICKINSON, AB ;
YOUNG, LS .
JOURNAL OF VIROLOGY, 1992, 66 (05) :2689-2697
[9]   Signal transduction and transcription factor modification during reactivation of Epstein-Barr virus from latency [J].
Bryant, H ;
Farrell, PJ .
JOURNAL OF VIROLOGY, 2002, 76 (20) :10290-10298
[10]   B cell receptor signal strength determines B cell fate [J].
Casola, S ;
Otipoby, KL ;
Alimzhanov, M ;
Humme, S ;
Uyttersprot, N ;
Kutok, JL ;
Carroll, MC ;
Rajewsky, K .
NATURE IMMUNOLOGY, 2004, 5 (03) :317-327