Epstein-Barr virus: Induction and control of cell transformation

被引：54

作者：

Dolcetti, R

Masucci, MG

机构：

[1] NCI, IRCCS, Dept Preclin & Epidemiol Res, Immunovirol & Biotherapy Unit,CRO, I-33081 Aviano, PN, Italy

[2] Karolinska Inst, Ctr Microbiol & Tumor Biol, Stockholm, Sweden

[3] Int Canc Ctr, IOV, Rovigo, Italy

来源：

JOURNAL OF CELLULAR PHYSIOLOGY | 2003年 / 196卷 / 02期

关键词：

D O I：

10.1002/jcp.10263

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Epstein-Barr virus (EBV), a ubiquitous human herpes virus, is associated with an increasing number of lymphoid and epithelial malignancies. The ability of the virus to establish life-long persistent infections and induce growth transformation is related to the function of a set of viral proteins that are variously expressed in both normal and malignant cells. Recent evidence indicates that these viral proteins are able to usurp cellular pathways that promote the cell growth and survival, while impairing anti-viral immune responses. Elucidation of the mechanisms by which EBV induces cell transformation and escapes host immune control provides the rational background for the design of new strategies of intervention for EBV-related malignancies. (C) 2003 Wiley-Liss, Inc.

引用

收藏

页码：207 / 218

页数：12

相关论文

共 148 条

[51] THE EPSTEIN-BARR-VIRUS NUCLEAR ANTIGEN-2 TRANSACTIVATOR IS DIRECTED TO RESPONSE ELEMENTS BY THE J-KAPPA RECOMBINATION SIGNAL BINDING-PROTEIN [J].

GROSSMAN, SR ;

JOHANNSEN, E ;

TONG, X ;

YALAMANCHILI, R ;

KIEFF, E .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (16) :7568-7572

[52] Isolation and characterization of transformed human T-cell lines infected by Epstein-Barr virus [J].

Groux, H ;

Cottrez, F ;

Montpellier, C ;

Quatannens, B ;

Coll, J ;

Stehelin, D ;

Auriault, C .

BLOOD, 1997, 89 (12) :4521-4530

[53] Molecular biology of Burkitt's lymphoma [J].

Hecht, JL ;

Aster, JC .

JOURNAL OF CLINICAL ONCOLOGY, 2000, 18 (21) :3707-3721

[54] Functional p53 chimeras containing the Epstein-Barr virus Gly-Ala repeat are protected from Mdm2-and HPV-E6-induced proteolysis [J].

Heessen, S ;

Leonchiks, A ;

Issaeva, N ;

Sharipo, A ;

Selivanova, G ;

Masucci, MG ;

Dantuma, NP .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (03) :1532-1537

[55] INDUCTION OF BCL-2 EXPRESSION BY EPSTEIN-BARR-VIRUS LATENT MEMBRANE PROTEIN-1 PROTECTS INFECTED B-CELLS FROM PROGRAMMED CELL-DEATH [J].

HENDERSON, S ;

ROWE, M ;

GREGORY, C ;

CROOMCARTER, D ;

WANG, F ;

LONGNECKER, R ;

KIEFF, E ;

RICKINSON, A .

CELL, 1991, 65 (07) :1107-1115

[56] MEDIATION OF EPSTEIN-BARR-VIRUS EBNA2 TRANSACTIVATION BY RECOMBINATION SIGNAL-BINDING PROTEIN J(K) [J].

HENKEL, T ;

LING, PD ;

HAYWARD, SD ;

PETERSON, MG .

SCIENCE, 1994, 265 (5168) :92-95

[57] Horizontal transfer of DNA by the uptake of apoptotic bodies [J].

Holmgren, L ;

Szeles, A ;

Rajnavölgyi, E ;

Folkman, J ;

Klein, G ;

Ernberg, I ;

Falk, KI .

BLOOD, 1999, 93 (11) :3956-3963

[58] THE ROLE OF EPSTEIN-BARR-VIRUS IN LYMPHOEPITHELIOMA-LIKE CARCINOMAS [J].

IEZZONI, JC ;

GAFFEY, MJ ;

WEISS, LM .

AMERICAN JOURNAL OF CLINICAL PATHOLOGY, 1995, 103 (03) :308-315

[59] The Epstein-Barr virus latent membrane protein 2A PY motif recruits WW domain-containing ubiquitin-protein ligases [J].

Ikeda, M ;

Ikeda, A ;

Longan, LC ;

Longnecker, R .

VIROLOGY, 2000, 268 (01) :178-191

[60] Epstein-Barr virus (EBV)-carrying and -expressing T-cell lines established from severe chronic active EBV infection [J].

Imai, S ;

Sugiura, M ;

Oikawa, O ;

Koizumi, S ;

Hirao, M ;

Kimura, H ;

Hayashibara, H ;

Terai, N ;

Tsutsumi, H ;

Oda, T ;

Chiba, S ;

Osato, T .

BLOOD, 1996, 87 (04) :1446-1457

← 1 2 3 4 5 6 7 8 9 10 →