Differential gene regulation by Epstein-Barr virus type 1 and type 2 EBNA2

被引：57

作者：

Lucchesi, Walter ^{[1
]}

Brady, Gareth ^{[1
]}

Dittrich-Breiholz, Oliver ^{[2
]}

Kracht, Michael ^{[3
]}

Russ, Rainer ^{[4
]}

Farrell, Paul J. ^{[1
]}

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Dept Virol, Fac Med, London W2 1PG, England

[2] Hannover Med Sch, Inst Biochem, D-30625 Hannover, Germany

[3] Rudolf Buchheim Inst Pharmakol, D-35392 Giessen, Germany

[4] Genedata AG, CH-4058 Basel, Switzerland

来源：

JOURNAL OF VIROLOGY | 2008年 / 82卷 / 15期

关键词：

D O I：

10.1128/JVI.00223-08

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

A transfection assay with a lymphoblastoid cell line infected with Epstein-Barr virus was used to compare the abilities of type 1 and type 2 EBNA2 to sustain cell proliferation. The reduced proliferation in cells expressing type 2 EBNA2 correlated with loss of expression of some cell genes that are known to be targets of type I EBNA2. Microarray analysis of EBNA2 target genes identified a small number of genes that are more strongly induced by type 1 than by type 2 EBNA2, and one of these genes (CXCR7) was shown to be required for proliferation of lymphoblastoid cell lines. The Epstein-Barr virus LMP1 gene was also more strongly induced by type I EBNA2 than by type 2, but this effect was transient. Type 1 and type 2 EBNA2 were equally effective at arresting cell proliferation of Burkitt's lymphoma cell lines lacking Epstein-Barr virus and were also shown to cause apoptosis in these cells. The results indicate that differential gene regulation by Epstein-Barr virus type 1 and type 2 EBNA2 may be the basis for the much weaker B-cell transformation activity of type 2 Epstein-Barr virus strains compared to type 1 strains.

引用

页码：7456 / 7466

页数：11

共 52 条

[1] THE MARCKS BROTHERS - A FAMILY OF PROTEIN-KINASE-C SUBSTRATES [J].

ADEREM, A .

CELL, 1992, 71 (05) :713-716

[2] Lytic cycle gene regulation of Epstein-Barr virus [J].

Amon, W ;

Binné, UK ;

Bryant, H ;

Jenkins, PJ ;

Karstegl, CE ;

Farrell, PJ .

JOURNAL OF VIROLOGY, 2004, 78 (24) :13460-13469

[3] 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

[4] The chemokine SDF-1/CXCL12 binds to and signals through the orphan receptor RDC1 in T lymphocytes [J].

Balabanian, K ;

Lagane, B ;

Infantino, S ;

Chow, KYC ;

Harriague, J ;

Moepps, B ;

Arenzana-Seisdedos, F ;

Thelen, M ;

Bachelerie, F .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (42) :35760-35766

[5] The ADAMDEC1 (decysin) gene structure: evolution by duplication in a metalloprotease gene cluster on Chromosome 8p12 [J].

Bates, EEM ;

Fridman, WH ;

Mueller, CGF .

IMMUNOGENETICS, 2002, 54 (02) :96-105

[6] EPSTEIN-BARR VIRUS-INDUCED GENES - 1ST LYMPHOCYTE-SPECIFIC G-PROTEIN-COUPLED PEPTIDE RECEPTORS [J].

BIRKENBACH, M ;

JOSEFSEN, K ;

YALAMANCHILI, R ;

LENOIR, G ;

KIEFF, E .

JOURNAL OF VIROLOGY, 1993, 67 (04) :2209-2220

[7]

Brady G, 2007, J CLIN PATHOL, V60, P1397, DOI 10.1136/jcp.2007.047977

[8] Intracellular interleukin-1α functionally interacts with histone acetyltransferase complexes [J].

Buryskova, M ;

Pospisek, M ;

Grothey, A ;

Simmet, T ;

Burysek, L .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (06) :4017-4026

[9] EPSTEIN-BARR VIRUS NUCLEAR PROTEIN-2 IS A KEY DETERMINANT OF LYMPHOCYTE-TRANSFORMATION [J].

COHEN, JI ;

WANG, F ;

MANNICK, J ;

KIEFF, E .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (23) :9558-9562

[10] U2 REGION OF EPSTEIN-BARR VIRUS-DNA MAY ENCODE EPSTEIN-BARR NUCLEAR ANTIGEN-2 [J].

DAMBAUGH, T ;

HENNESSY, K ;

CHAMNANKIT, L ;

KIEFF, E .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1984, 81 (23) :7632-7636

← 1 2 3 4 5 6 →