Epstein-Barr virus LMP2A: regulating cellular ubiquitination processes for maintenance of viral latency?

被引：23

作者：

Portis, T ^{[1
]}

Ikeda, M ^{[1
]}

Longnecker, R ^{[1
]}

机构：

[1] Northwestern Univ, Dept Microbiol & Immunol, Feinberg Sch Med, Chicago, IL 60611 USA

来源：

TRENDS IN IMMUNOLOGY | 2004年 / 25卷 / 08期

关键词：

D O I：

10.1016/j.it.2004.05.009

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Epstein-Barr virus (EBV) is a potentially oncogenic herpesvirus that persists in the B lymphocytes of most individuals. LMP2A might function as a central mediator of viral latency, allowing for long-term survival of infected B cells by providing a surrogate B-cell receptor signal. Recent studies support a model in which LMP2A utilizes ubiquitin-dependent processes to modulate cellular signaling pathways, including the Wnt and Notch pathways. Whether these pathways are exploited by LMP2A to maintain cell survival or to regulate viral gene expression during viral latency remains to be determined. These processes must be further explored to identify the factors that contribute to the maintenance of viral latency and possibly the development of EBV-associated malignancies.

引用

页码：422 / 426

页数：5

共 53 条

[1] Degradation of the Epstein-Barr virus latent membrane protein 1 (LMP1) by the ubiquitin-proteasome pathway - Targeting via ubiquitination of the N-terminal residue [J].

Aviel, S ;

Winberg, G ;

Massucci, M ;

Ciechanover, A .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (31) :23491-23499

[2] EBV persistence in memory B cells in vivo [J].

Babcock, GJ ;

Decker, LL ;

Volk, M ;

Thorley-Lawson, DA .

IMMUNITY, 1998, 9 (03) :395-404

[3] Epstein-Barr virus LMP2A-induced B-cell survival in two unique classes of EμLMP2A transgenic mice [J].

Caldwell, RG ;

Brown, RG ;

Longnecker, R .

JOURNAL OF VIROLOGY, 2000, 74 (03) :1101-1113

[4] Epstein-Barr virus LMP2A drives B cell development and survival in the absence of normal B cell receptor signals [J].

Caldwell, RG ;

Wilson, JB ;

Anderson, SJ ;

Longnecker, R .

IMMUNITY, 1998, 9 (03) :405-411

[5] 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

[6] The B cell antigen receptor regulates the transcriptional activator β-catenin via protein kinase C-mediated inhibition of glycogen synthase kinase-3 [J].

Christian, SL ;

Sims, PV ;

Gold, MR .

JOURNAL OF IMMUNOLOGY, 2002, 169 (02) :758-769

[7]

Cornell M, 1999, GENETICS, V152, P567

[8] Reed-Sternberg cell genome expression supports a B-cell lineage [J].

Cossman, J ;

Annunziata, CM ;

Barash, S ;

Staudt, L ;

Dillon, P ;

He, WW ;

Ricciardi-Castagnoli, P ;

Rosen, CA ;

Carter, KC .

BLOOD, 1999, 94 (02) :411-416

[9] EPSTEIN-BARR VIRUS-ENCODED NUCLEAR ANTIGEN-2 ACTIVATES THE VIRAL LATENT MEMBRANE-PROTEIN PROMOTER BY MODULATING THE ACTIVITY OF A NEGATIVE REGULATORY ELEMENT [J].

FAHRAEUS, R ;

JANSSON, A ;

RICKSTEN, A ;

SJOBLOM, A ;

RYMO, L .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (19) :7390-7394

[10] Tyrosine 112 of latent membrane protein 2A is essential for protein tyrosine kinase loading and regulation of Epstein-Barr virus latency [J].

Fruehling, S ;

Swart, R ;

Dolwick, KM ;

Kremmer, E ;

Longnecker, R .

JOURNAL OF VIROLOGY, 1998, 72 (10) :7796-7806

← 1 2 3 4 5 6 →