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PMID: 12407409 Published · ppublish English Journal Article Review

To kill or be killed: viral evasion of apoptosis.

Nature immunology ·Vol. 3 ·No. 11 ·2002-11-00 ·Pages 1013-8

Benedict CA, Norris PS, Ware CF

Abstract

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.

MeSH Terms
Animals Apoptosis/physiology Cysteine Endopeptidases/physiology Cytokines/physiology Humans Interferons/physiology Mice Models, Biological Molecular Mimicry Proto-Oncogene Proteins c-bcl-2/physiology Receptors, Tumor Necrosis Factor/physiology Signal Transduction Tumor Necrosis Factor-alpha/physiology Vertebrates/immunology,virology Virus Diseases/immunology,pathology,virology Virus Physiological Phenomena Virus Replication
Chemicals
Cytokines Proto-Oncogene Proteins c-bcl-2 Receptors, Tumor Necrosis Factor Tumor Necrosis Factor-alpha Interferons Cysteine Endopeptidases
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Benedict Chris A
Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA.
Norris Paula S
Ware Carl F
Article Info
Journal
Nature immunology
Abbr.
Nat Immunol
ISSN
1529-2908
Published
2002-11-00
Pages
1013-8
Language
English
Region
United States
NLM ID
100941354
Subset
IM
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