Vaccinia virus immune evasion: mechanisms, virulence and immunogenicity

被引:262
作者
Smith, Geoffrey L. [1 ]
Benfield, Camilla T. O. [1 ]
de Motes, Carlos Maluquer [1 ]
Mazzon, Michela [1 ]
Ember, Stuart W. J. [1 ]
Ferguson, Brian J. [1 ]
Sumner, Rebecca P. [1 ]
机构
[1] Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England
基金
英国惠康基金; 英国医学研究理事会;
关键词
NF-KAPPA-B; NECROSIS-FACTOR RECEPTOR; COMPLEMENT CONTROL PROTEINS; CHEMOKINE-BINDING-PROTEIN; MURINE INTRADERMAL MODEL; HERPES-SIMPLEX-VIRUS; DOUBLE-STRANDED-RNA; GENETICALLY-ENGINEERED POXVIRUSES; INTERFERON-INDUCED RESISTANCE; POTENTIAL THERAPEUTIC TARGET;
D O I
10.1099/vir.0.055921-0
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Virus infection of mammalian cells is. sensed by pattern recognition receptors and leads to an innate immune response that restricts virus replication and induces adaptive immunity. In response, viruses have evolved many countermeasures that enable them to replicate and be transmitted to new hosts, despite the host innate immune response. Poxviruses, such as vaccinia virus (VACV), have large DNA genomes and encode many proteins that are dedicated to host immune evasion. Some of these proteins are secreted from the infected cell, where they bind and neutralize complement factors, interferons, cytokines and chemokines. Other VACV proteins function inside cells to inhibit apoptosis or signalling pathways that lead to the production of interferons and pro-inflammatory cytokines and chemokines. In this review, these VACV immunomodulatory proteins are described and the potential to create more immunogenic VACV strains by manipulation of the gene encoding these proteins is discussed.
引用
收藏
页码:2367 / 2392
页数:26
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