Fish DDX3X exerts antiviral function against grouper nervous necrosis virus infection
Liu, JX; Huang, XH; Yu, YP; Zhang, JC; Ni, SW; Hu, Y; Huang, YH; Qin, QW; huangyh@scsio.ac.cn; qinqw@scau.edu.cn
2018
发表期刊FISH & SHELLFISH IMMUNOLOGY
卷号71页码:95-104
摘要Human DEAD box ATP-dependent RNA helicase DDX3X has been demonstrated to exert crucial functions in carcinogenesis and antiviral immune response. However, to our knowledge, few information focused on the functions of fish DDX3X. In this study, we cloned and characterized a DDX3X homolog from orange spotted grouper (Epinephelus coioides) (EcDDX3X). EcDDX3X encoded a 733-amino acid protein which shared 97% and 76% identity to spiny damselfish (Acanthochromis polyacanthus) and human (Homo sapiens), respectively. Amino acid alignment analysis showed that EcDDX3X contained conserved DExDc and Helic C domains. The transcription levels of EcDDX3X were significantly increased in poly I:C transfected cells and red-spotted grouper nervous necrosis virus (RGNNV) infected cells. Under fluorescence microscopy, the green fluorescence was observed evenly in the cytoplasm in EcDDX3X transfected cells. The ectopic expression of EcDDX3X significantly inhibited the replication of RGNNV, evidenced by the decreased numbers of the vacuoles evoked by RGNNV infection, and the reduced transcription levels of RGNNV coat protein (CP) and RNA-dependent RNA polymerase (RdRp) genes. In contrast, the replication of Singapore grouper iridovirus (SGIV) in grouper spleen (GS) cells was not significantly affected by EcDDX3X overexpression. Further studies showed that overexpression of EcDDX3X in vitro significantly increased the expression levels of several interferon associated cytokines or effectors. Moreover, the regulatory effect of EcDDX3X on interferon immune response was dependent on its N terminal region, but not the DExDc and Helic C domain. In addition, we also found that overexpression of EcDDX3X significantly increased the interferon promoter activity, and the activation of interferon immune response was regulated by both IRF3 and IRF7. Together, our results firstly showed that fish DDX3X exerted crucial roles in antiviral immunity against RNA virus infection via upregulating interferon antiviral responses. (C) 2017 Elsevier Ltd. All rights reserved.
部门归属[Liu, Jiaxin; Huang, Xiaohong; Yu, Yepin; Zhang, Jingcheng; Ni, Songwei; Hu, Yin; Huang, Youhua] Chinese Acad Sci, South China Sea Inst Oceanol, Key Lab Trop Marine Bioresources & Ecol, 164 West Xingang Rd, Guangzhou 510301, Guangdong, Peoples R China; [Huang, Xiaohong; Huang, Youhua; Qin, Qiwei] South China Agr Univ, Coll Marine Sci, Guangzhou 510642, Guangdong, Peoples R China; [Liu, Jiaxin; Zhang, Jingcheng; Ni, Songwei; Hu, Yin] Univ Chinese Acad Sci, Beijing, Peoples R China; [Liu, Jiaxin; Zhang, Jingcheng; Ni, Songwei; Hu, Yin] Chinese Acad Sci, South China Sea Inst Oceanol, Guangdong Prov Key Lab Appl Marine Biol, Guangzhou 510301, Guangdong, Peoples R China; [Qin, Qiwei] Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao 266000, Peoples R China
学科领域Fisheries ; Immunology ; Marine & Freshwater Biology ; Veterinary Sciences
关键词[WOS]Grouper ; DDX3X ; RGNNV ; Antiviral immunity ; Interferon
资助项目LMB
文献类型期刊论文
条目标识符http://ir.scsio.ac.cn/handle/344004/17040
专题中科院海洋生物资源可持续利用重点实验室
通讯作者huangyh@scsio.ac.cn; qinqw@scau.edu.cn
推荐引用方式
GB/T 7714
Liu, JX,Huang, XH,Yu, YP,et al. Fish DDX3X exerts antiviral function against grouper nervous necrosis virus infection[J]. FISH & SHELLFISH IMMUNOLOGY,2018,71:95-104.
APA Liu, JX.,Huang, XH.,Yu, YP.,Zhang, JC.,Ni, SW.,...&qinqw@scau.edu.cn.(2018).Fish DDX3X exerts antiviral function against grouper nervous necrosis virus infection.FISH & SHELLFISH IMMUNOLOGY,71,95-104.
MLA Liu, JX,et al."Fish DDX3X exerts antiviral function against grouper nervous necrosis virus infection".FISH & SHELLFISH IMMUNOLOGY 71(2018):95-104.
条目包含的文件
文件名称/大小 文献类型 版本类型 开放类型 使用许可
Fish DDX3X exerts an(4487KB)期刊论文作者接受稿开放获取CC BY-NC-SA请求全文
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。