Vaccinia virus-induced apoptosis in immature B lymphocytes:: role of cellular Bcl-2

被引:20
作者
Baixeras, E
Cebrián, A
Albar, J
Salas, J
Martínez, C
Viñuela, E
Revilla, Y [1 ]
机构
[1] Univ Autonoma Madrid, CSIC, Ctr Biol Mol Severo Ochoa, E-28049 Madrid, Spain
[2] Univ Autonoma Madrid, CSIC, Ctr Nacl Biotecnol, E-28049 Madrid, Spain
关键词
vaccinia virus; apoptosis; B lymphocytes; Bcl-2;
D O I
10.1016/S0168-1702(98)00105-1
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Apoptosis is a form of physiological cell death which can be initiated in response to various stimuli including virus infections. We show that vaccinia virus (VV) infection induces apoptosis in an immature B lymphocyte line, WEHI-231. In these cells, several VV-specific proteins were synthesized during the infection, bur neither virus production nor viral DNA synthesis were detected. The intracellular levels of the proto-oncogene Bcl-2, which effectively protects cells from programmed cell death, were found to be down-regulated by the VV infection, suggesting that this down-regulation might be involved in the viral induction of apoptosis in WEHI-231 cells. Stable transfectants overexpressing human Bcl-2 were shown to be resistant to the apoptosis produced by the infection, a finding consistent with the proposed role for the down-regulation of endogenous Bcl-2 in W-induced apoptotic death. (C) 1998 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:107 / 113
页数:7
相关论文
共 26 条
[1]   An African swine fever virus Bcl-2 homolog, 5-HL, suppresses apoptotic cell death [J].
Afonso, CL ;
Neilan, JG ;
Kutish, GF ;
Rock, DL .
JOURNAL OF VIROLOGY, 1996, 70 (07) :4858-4863
[2]   HIGHLY EFFICIENT EXPRESSION OF PROTEINS ENCODED BY RECOMBINANT VACCINIA VIRUS IN LYMPHOCYTES [J].
ALONSO, JM ;
RODRIGUEZ, J ;
VINUELA, E ;
KROEMER, G ;
MARTINEZA, C .
SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 1991, 34 (05) :619-626
[3]   SIGNAL-TRANSDUCTION PATHWAYS INVOLVED IN B-CELL INDUCTION [J].
BAIXERAS, E ;
KROEMER, G ;
CUENDE, E ;
MARQUEZ, C ;
BOSCA, L ;
MARTINEZ, JEA ;
MARTINEZ, AC .
IMMUNOLOGICAL REVIEWS, 1993, 132 :5-47
[4]   PROGRAMMED CELL-DEATH BY BCL-2-DEPENDENT AND INDEPENDENT MECHANISMS IN B-LYMPHOMA CELLS [J].
CUENDE, E ;
ALESMARTINEZ, JE ;
DING, LY ;
GONZALEZGARCIA, M ;
MARTINEZA, C ;
NUNEZ, G .
EMBO JOURNAL, 1993, 12 (04) :1555-1560
[5]   HIV-1 INDUCES DOWN-REGULATION OF BCL-2 EXPRESSION AND DEATH BY APOPTOSIS OF EBV-IMMORTALIZED B-CELLS - A MODEL FOR A PERSISTENT SELF-LIMITING HIV-1 INFECTION [J].
DEROSSI, A ;
OMETTO, L ;
RONCELLA, S ;
DANDREA, E ;
MENIN, C ;
CALDERAZZO, F ;
ROWE, M ;
FERRARINI, M ;
CHIECOBIANCHI, L .
VIROLOGY, 1994, 198 (01) :234-244
[6]  
EASTMAN A, 1995, CELL DEATH DIFFER, P41
[7]   BCL-2 IS AN INNER MITOCHONDRIAL-MEMBRANE PROTEIN THAT BLOCKS PROGRAMMED CELL-DEATH [J].
HOCKENBERY, D ;
NUNEZ, G ;
MILLIMAN, C ;
SCHREIBER, RD ;
KORSMEYER, SJ .
NATURE, 1990, 348 (6299) :334-336
[8]   IDENTIFICATION AND CHARACTERIZATION OF THE P35-GENE OF BOMBYX-MORI NUCLEAR POLYHEDROSIS-VIRUS THAT PREVENTS VIRUS-INDUCED APOPTOSIS [J].
KAMITA, SG ;
MAJIMA, K ;
MAEDA, S .
JOURNAL OF VIROLOGY, 1993, 67 (01) :455-463
[9]  
KORSMEYER SJ, 1992, CANCER SURV, V15, P105
[10]   CLEAVAGE OF STRUCTURAL PROTEINS DURING ASSEMBLY OF HEAD OF BACTERIOPHAGE-T4 [J].
LAEMMLI, UK .
NATURE, 1970, 227 (5259) :680-+