Innate Immunity and Immune Evasion by Enterovirus 71

被引:73
|
作者
Pathinayake, Prabuddha S. [1 ,2 ]
Hsu, Alan C-Y. [1 ,2 ]
Wark, Peter A. B. [1 ,2 ,3 ]
机构
[1] Univ Newcastle, Prior Res Ctr Asthma & Resp Dis, Newcastle, NSW 2305, Australia
[2] Hunter Med Res Inst, New Lambton Hts, NSW 2305, Australia
[3] John Hunter Hosp, Dept Resp & Sleep Med, New Lambton Hts, NSW 2305, Australia
来源
VIRUSES-BASEL | 2015年 / 7卷 / 12期
关键词
Enterovirus; 71; innate immunity; Interferon antagonist; HEPATITIS-C-VIRUS; NF-KAPPA-B; EARLY VIRAL REPLICATION; TOLL-LIKE RECEPTOR-3; PRE-MESSENGER-RNAS; INDUCIBLE GENE-I; RIG-I; IFN-LAMBDA; PATHOGEN RECOGNITION; ANTIVIRAL RESPONSES;
D O I
10.3390/v7122961
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Enterovirus 71 (EV71) is a major infectious disease affecting millions of people worldwide and it is the main etiological agent for outbreaks of hand foot and mouth disease (HFMD). Infection is often associated with severe gastroenterological, pulmonary, and neurological diseases that are most prevalent in children. Currently, no effective vaccine or antiviral drugs exist against EV71 infection. A lack of knowledge on the molecular mechanisms of EV71 infection in the host and the virus-host interactions is a major constraint to developing specific antiviral strategies against this infection. Previous studies have identified and characterized the function of several viral proteins produced by EV71 that interact with the host innate immune proteins, including type I interferon signaling and microRNAs. These interactions eventually promote efficient viral replication and increased susceptibility to the disease. In this review we discuss the functions of EV71 viral proteins in the modulation of host innate immune responses to facilitate viral replication.
引用
收藏
页码:6613 / 6630
页数:18
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