Antagonism of Innate Immunity by Paramyxovirus Accessory Proteins

被引:18
作者
Chambers, Raychel [1 ]
Takimoto, Toru [1 ]
机构
[1] Univ Rochester, Med Ctr, Dept Microbiol & Immunol, Rochester, NY 14642 USA
来源
VIRUSES-BASEL | 2009年 / 1卷 / 03期
关键词
interferon; paramyxoviruses; innate immunity; apoptosis; VIRUS-V-PROTEIN; NEWCASTLE-DISEASE-VIRUS; VIRAL-RNA SYNTHESIS; INTERFERON SIGNAL-TRANSDUCTION; RECOMBINANT MEASLES VIRUSES; UBIQUITIN LIGASE COMPLEXES; CYSTEINE-RICH DOMAIN; SENDAI-VIRUS; C-PROTEINS; RIG-I;
D O I
10.3390/v1030574
中图分类号
Q93 [微生物学];
学科分类号
071005 [微生物学];
摘要
Paramyxovirinae, a subfamily of Paramyxoviridae, are negative strand RNA viruses comprised of many important human and animal pathogens, which share a high degree of genetic and structural homology. The accessory proteins expressed from the P/V/C gene are major factors in the pathogenicity of the viruses, because of their ability to abrogate various facets of type I interferon (IFN) induction and signaling. Most of the paramyxoviruses exhibit a commonality in their ability to antagonize innate immunity by blocking IFN induction and the Jak/STAT pathway. However, the manner in which the accessory proteins inhibit the pathway differs among viruses. Similarly, there are variations in the capability of the viruses to counteract intracellular detectors (RNA helicases, mda-5 and RIG-I). Furthermore, a functional specificity in the antagonism of the IFN response has been reported, suggesting that specificity in the circumvention of innate immunity restricts viral host range. Available evidence indicates that paramyxoviruses employ specific strategies to antagonize the IFN response of their specific hosts, which is one of the major factors that determine viral pathogenicity and host range.
引用
收藏
页码:574 / 593
页数:20
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