Multiple pathways for Epstein-Barr virus episome loss from nasopharyngeal carcinoma

被引:37
作者
Dittmer, Dirk P. [1 ,2 ]
Hilscher, Chelsey J. [1 ,2 ]
Gulley, Margaret L. [3 ]
Yang, Eric V. [4 ]
Chen, Min [4 ]
Glaser, Ronald [4 ,5 ]
机构
[1] Univ N Carolina, Lineberger Comprehens Canc Ctr, Ctr AIDS Res, Chapel Hill, NC 27599 USA
[2] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA
[3] Univ N Carolina, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA
[4] Ohio State Univ, Med Ctr, Inst Behav Med Res, Columbus, OH 43210 USA
[5] Ctr Comprehens Canc, Dept Mol Virol Immunol & Med Genet, Columbus, OH USA
关键词
episome; real-time QPCR; Epstein-Barr virus; nasopharyngeal carcinoma; epithelial cells;
D O I
10.1002/ijc.23685
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Epstein-Barr virus (EBV) is the prototypical example for episomal persistence of genetic information. Yet, little is known about how this viral episome is lost. Episome loss occurs naturally in nasopharyngeal carcinoma (NPC) upon explantation into culture. Using whole-genome profiling, we found evidence for 2 different pathways of episome loss: (i) rapid loss of the entire episome or (ii) successive mutation/deletion of the episome until at least 1 essential cis-element is destroyed. This second phenotype was seen in a clone of HONE-1 NPC cells that maintains the EBV episome for prolonged time in culture. The conceptual insights provided by our quantitative analysis should aid our understanding of mammalian episomes, as well as lead to designs to cure latent viral infection. (c) 2008 Wiley-Liss, Inc.
引用
收藏
页码:2105 / 2112
页数:8
相关论文
共 49 条
[1]   Long-term-infected telomerase-immortalized endothelial cells: a model for Kaposi's sarcoma-associated herpesvirus latency in vitro and in vivo [J].
An, Feng-Qi ;
Folarin, Hope Merlene ;
Compitello, Nicole ;
Roth, Justin ;
Gerson, Stanton L. ;
McCrae, Keith R. ;
Fakhari, Farnaz D. ;
Dittmer, Dirk P. ;
Renne, Rolf .
JOURNAL OF VIROLOGY, 2006, 80 (10) :4833-4846
[2]  
Bankier A T, 1983, Mol Biol Med, V1, P21
[3]  
Bowtell D., 2003, DNA MICROARRAYS MOL
[4]  
BROACH JR, 1981, MOL BIOL YEAST SACCH, P445
[5]   Dynamic chromatin boundaries delineate a latency control region of Epstein-Barr virus [J].
Chau, CM ;
Lieberman, PM .
JOURNAL OF VIROLOGY, 2004, 78 (22) :12308-12319
[6]  
Cheung ST, 1999, INT J CANCER, V83, P121, DOI 10.1002/(SICI)1097-0215(19990924)83:1<121::AID-IJC21>3.0.CO
[7]  
2-F
[8]  
Dittmer DP, 2003, CANCER RES, V63, P2010
[9]   Cluster analysis and display of genome-wide expression patterns [J].
Eisen, MB ;
Spellman, PT ;
Brown, PO ;
Botstein, D .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (25) :14863-14868
[10]   VIRUS PARTICLES IN CULTURED LYMPHOBLASTS FROM BURKITTS LYMPHOMA [J].
EPSTEIN, MA ;
ACHONG, BG ;
BARR, YM .
LANCET, 1964, 1 (733) :702-+