To kill or be killed: viral evasion of apoptosis

被引:358
作者
Benedict, CA [1 ]
Norris, PS [1 ]
Ware, CF [1 ]
机构
[1] La Jolla Inst Allergy & Immunol, Div Mol Immunol, San Diego, CA 92121 USA
关键词
D O I
10.1038/ni1102-1013
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
In the struggle between virus and host, control over the cell's death machinery is crucial for survival. Viruses are obligatory intracellular parasites and, as such, must modulate apoptotic pathways to control the lifespan of their host in order to complete their replication cycle. Many of the counter-assaults mounted by the immune system incorporate activation of the apoptotic pathway-particularly by members of the tumor necrosis factor cytokine family-as a mechanism to restrict viral replication. Thus, apoptosis serves as a powerful selective pressure for the virus to evade. However, for the host, success is harsh and potentially costly, as apoptosis often contributes to pathogenesis. Here we examine some of the molecular mechanisms by which viruses manipulate the apoptotic machinery to their advantage and how we (as vertebrates) have evolved and learned to cope with viral evasion.
引用
收藏
页码:1013 / 1018
页数:6
相关论文
共 80 条
[1]
Apoptosis control by death and decoy receptors [J].
Ashkenazi, A ;
Dixit, VM .
CURRENT OPINION IN CELL BIOLOGY, 1999, 11 (02) :255-260
[2]
Host defense, viruses and apoptosis [J].
Barber, GN .
CELL DEATH AND DIFFERENTIATION, 2001, 8 (02) :113-126
[3]
Benedict CA, 1999, J IMMUNOL, V162, P6967
[4]
Lymphotoxins and cytomegalovirus cooperatively induce interferon-β, establishing host-virus detente [J].
Benedict, CA ;
Banks, TA ;
Senderowicz, L ;
Ko, M ;
Britt, WJ ;
Angulo, A ;
Ghazal, P ;
Ware, CF .
IMMUNITY, 2001, 15 (04) :617-626
[5]
Three adenovirus E3 proteins cooperate to evade apoptosis by tumor necrosis factor-related apoptosis-inducing ligand receptor-1 and-2 [J].
Benedict, CA ;
Norris, PS ;
Prigozy, TI ;
Bodmer, JL ;
Mahr, JA ;
Garnett, CT ;
Martinon, F ;
Tschopp, J ;
Gooding, LR ;
Ware, CF .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (05) :3270-3278
[6]
Death effector domain-containing herpesvirus and poxvirus proteins inhibit both Fas- and TNFR1-induced apoptosis [J].
Bertin, J ;
Armstrong, RC ;
Ottilie, S ;
Martin, DA ;
Wang, Y ;
Banks, S ;
Wang, GH ;
Senkevich, TG ;
Alnemri, ES ;
Moss, B ;
Lenardo, MJ ;
Tomaselli, KJ ;
Cohen, JI .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (04) :1172-1176
[7]
CAR1, a TNFR-related protein, is a cellular receptor for cytopathic avian leukosis sarcoma viruses and mediates apoptosis [J].
Brojatsch, J ;
Naughton, J ;
Rolls, MM ;
Zingler, K ;
Young, JAT .
CELL, 1996, 87 (05) :845-855
[8]
Altered cellular mRNA levels in human cytomegalovirus-infected fibroblasts: Viral block to the accumulation of antiviral mRNAs [J].
Browne, EP ;
Wing, B ;
Coleman, D ;
Shenk, T .
JOURNAL OF VIROLOGY, 2001, 75 (24) :12319-12330
[9]
A study of the interferon antiviral mechanism: Apoptosis activation by the 2-5A system [J].
Castelli, JC ;
Hassel, BA ;
Wood, KA ;
Li, XL ;
Amemiya, K ;
Dalakas, MC ;
Torrence, PF ;
Youle, RJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (06) :967-972
[10]
Modulation of the NF-κB pathway by virally encoded death effector domains-containing proteins [J].
Chaudhary, PM ;
Jasmin, A ;
Eby, MT ;
Hood, L .
ONCOGENE, 1999, 18 (42) :5738-5746