Respiratory Syncytial Virus Mechanisms to Interfere with Type 1 Interferons

被引:56
作者
Barik, Sailen [1 ]
机构
[1] Cleveland State Univ, Ctr Gene Regulat Hlth & Dis, Dept Biol Geol & Environm Sci, Cleveland, OH 44115 USA
来源
CHALLENGES AND OPPORTUNITIES FOR RESPIRATORY SYNCYTIAL VIRUS VACCINES | 2013年 / 372卷
关键词
NONSTRUCTURAL PROTEINS NS1; NF-KAPPA-B; DOUBLE-STRANDED-RNA; TOLL-LIKE RECEPTORS; RIG-I; IMMUNE-RESPONSE; V-PROTEIN; EPITHELIAL-CELLS; INNATE IMMUNITY; PARAMYXOVIRUS SIMIAN-VIRUS-5;
D O I
10.1007/978-3-642-38919-1_9
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Respiratory syncytial virus (RSV) is a member of the Paramyxoviridae family that consists of viruses with nonsegmented negative-strand RNA genome. Infection by these viruses triggers the innate antiviral response of the host, mainly type I interferon (IFN). Essentially all other viruses of this family produce IFN suppressor functions by co-transcriptional RNA editing. In contrast, RSV has evolved two unique nonstructural proteins, NS1 and NS2, to effectively serve this purpose. Together, NS1 and NS2 degrade or sequester multiple signaling proteins that affect both IFN induction and IFN effector functions. While the mechanism of action of NS1 and NS2 is a subject of active research, their effect on adaptive immunity is also being recognized. In this review, we discuss various aspects of NS1 and NS2 function with implications for vaccine design.
引用
收藏
页码:173 / 191
页数:19
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