Necroptosis: The Trojan horse in cell autonomous antiviral host defense

被引:86
作者
Mocarski, Edward S. [1 ]
Guo, Hongyan [1 ]
Kaiser, William J. [1 ]
机构
[1] Emory Univ, Emory Vaccine Ctr, Dept Microbiol & Immunol, Sch Med, Atlanta, GA 30322 USA
关键词
Programmed necrosis; FADD; cFLIP; Serine/threonine protein kinase; Ribonucleotide reductase; MIXED LINEAGE KINASE; NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; PROGRAMMED NECROSIS; PROTEIN-KINASE; RIBONUCLEOTIDE REDUCTASE; DOMAIN-LIKE; HUMAN CYTOMEGALOVIRUS; BLOCKS APOPTOSIS; CASPASE-8; ACTIVATION;
D O I
10.1016/j.virol.2015.03.016
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Herpesviruses suppress cell death to assure sustained infection in their natural hosts. Murine cytomegalovirus (MCMV) encodes suppressors of apoptosis as well as M45-encoded viral inhibitor of RIP activation (vIRA) to block RIP homotypic interaction motif (RHIM)-signaling and recruitment of RIP3 (also called RIPK3), to prevent necroptosis. MCMV and human cytomegalovirus encode a viral inhibitor of caspase (Casp)8 activation to block apoptosis, an activity that unleashes necroptosis. Herpes simplex virus (HSV)1 and HSV2 incorporate both RHIM and Casp8 suppression strategies within UL39-encoded ICP6 and ICP10, respectively, which are herpesvirus-conserved homologs of MCMV M45. Both HSV proteins sensitize human cells to necroptosis by blocking Casp8 activity while preventing RHIM-dependent RIP3 activation and death. In mouse cells, HSV1 ICP6 interacts with RIP3 and, surprisingly, drives necroptosis. Thus, herpesviruses have illuminated the contribution of necoptosis to host defense in the natural host as well as its potential to restrict cross-species infections in nonnatural hosts. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:160 / 166
页数:7
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