Epstein-Barr Virus: Diseases Linked to Infection and Transformation

被引:82
作者
Jha, Hem C. [2 ]
Pei, Yonggang
Robertson, Erle S. [1 ]
机构
[1] Univ Penn, Perelman Sch Med, Abramson Canc Ctr, Dept Otorhinolaryngol Head & Neck Surg, Philadelphia, PA 19104 USA
[2] Indian Inst Technol Indore, Ctr Biosci & Biomed Engn, Indore, Madhya Pradesh, India
基金
美国国家卫生研究院;
关键词
EBV; latency; lytic; transformation; B-cell; epithelial cell; cancer; infection; NASOPHARYNGEAL CARCINOMA-CELLS; SARCOMA-ASSOCIATED HERPESVIRUS; POSTTRANSPLANT LYMPHOPROLIFERATIVE DISORDERS; HODGKINS-LYMPHOMA NHL; NUCLEAR ANTIGEN 1; NF-KAPPA-B; TRANSCRIPTION FACTOR; BURKITTS-LYMPHOMA; C-MYC; RETINOBLASTOMA PROTEIN;
D O I
10.3389/fmicb.2016.01602
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Epstein-Barr virus (EBV) was first discovered in 1964, and was the first known human tumor virus now shown to be associated with a vast number of human diseases. Numerous studies have been conducted to understand infection, propagation, and transformation in various cell types linked to human diseases. However, a comprehensive lens through which virus infection, reactivation and transformation of infected host cells can be visualized is yet to be formally established and will need much further investigation. Several human cell types infected by EBV have been linked to associated diseases. However, whether these are a direct result of EBV infection or indirectly due to contributions by additional infectious agents will need to be fully investigated. Therefore, a thorough examination of infection, reactivation, and cell transformation induced by EBV will provide a more detailed view of its contributions that drive pathogenesis. This undoubtedly expand our knowledge of the biology of EBV infection and the signaling activities of targeted cellular factors dysregulated on infection. Furthermore, these insights may lead to identification of therapeutic targets and agents for clinical interventions. Here, we review the spectrum of EBV-associated diseases, the role of the encoded latent antigens, and the switch to latency or lytic replication which occurs in EBV infected cells. Furthermore, we describe the cellular processes and critical factors which contribute to cell transformation. We also describe the fate of B-cells and epithelial cells after EBV infection and the expected consequences which contribute to establishment of viral-associated pathologies.
引用
收藏
页数:16
相关论文
共 236 条
[1]   Epstein - Barr Virus Transforming Protein LMP-1 Alters B Cells Gene Expression by Promoting Accumulation of the Oncoprotein ΔNp73α [J].
Accardi, Rosita ;
Fathallah, Ikbal ;
Gruffat, Henri ;
Mariggio, Giuseppe ;
Le Calvez-Kelm, Florence ;
Voegele, Catherine ;
Bartosch, Birke ;
Hernandez-Vargas, Hector ;
McKay, James ;
Sylla, Bakary S. ;
Manet, Evelyne ;
Tommasino, Massimo .
PLOS PATHOGENS, 2013, 9 (03)
[2]   Epstein-Barr virus immediate-early proteins BZLF1 and BRLF1 activate the ATF2 transcription factor by increasing the levels of phosphorylated p38 and c-Jun N-terminal kinases [J].
Adamson, AL ;
Darr, D ;
Holley-Guthrie, E ;
Johnson, RA ;
Mauser, A ;
Swenson, J ;
Kenney, S .
JOURNAL OF VIROLOGY, 2000, 74 (03) :1224-1233
[3]   An epidemiologic study of index and family infectious mononucleosis and adult Hodgkin's disease (HD):: Evidence for a specific association with EBV+ve HD in young adults [J].
Alexander, FE ;
Lawrence, DJ ;
Freeland, J ;
Krajewski, AS ;
Angus, B ;
Taylor, GM ;
Jarrett, RF .
INTERNATIONAL JOURNAL OF CANCER, 2003, 107 (02) :298-302
[4]   How does Epstein-Barr virus (EBV) complement the activation of Myc in the pathogenesis of Burkitt's lymphoma? [J].
Allday, Martin J. .
SEMINARS IN CANCER BIOLOGY, 2009, 19 (06) :366-376
[5]  
Allen Upton, 2002, Can J Infect Dis, V13, P89
[6]   Reactivation of Epstein-Barr virus from latency [J].
Amon, W ;
Farrell, PJ .
REVIEWS IN MEDICAL VIROLOGY, 2005, 15 (03) :149-156
[7]  
ARVANITAKIS L, 1995, J IMMUNOL, V155, P1047
[8]  
Bajaj Bharat G, 2007, Cancer Treat Res, V133, P141
[9]   EBNA3C Augments Pim-1 Mediated Phosphorylation and Degradation of p21 to Promote B-Cell Proliferation [J].
Banerjee, Shuvomoy ;
Lu, Jie ;
Cai, Qiliang ;
Sun, Zhiguo ;
Jha, Hem Chandra ;
Robertson, Erle S. .
PLOS PATHOGENS, 2014, 10 (08)
[10]   The EBV Latent Antigen 3C Inhibits Apoptosis through Targeted Regulation of Interferon Regulatory Factors 4 and 8 [J].
Banerjee, Shuvomoy ;
Lu, Jie ;
Cai, Qiliang ;
Saha, Abhik ;
Jha, Hem Chandra ;
Dzeng, Richard Kuo ;
Robertson, Erle S. .
PLOS PATHOGENS, 2013, 9 (05)