威斯腾促销
伯豪生物转化医学服务平台
年终盘点

中华鳖虹彩病毒引起宿主细胞出现类凋亡

2011/11/26 来源:科学网
分享: 
导读
虹彩病毒是一类大DNA病毒,能够感染野生或养殖的鱼类、两栖类或爬行类等低等脊椎动物。但是,对该类病毒的致病机理,特别是感染引起的细胞死亡机制了解甚少。

虹彩病毒是一类大DNA病毒,能够感染野生或养殖的鱼类、两栖类或爬行类等低等脊椎动物。但是,对该类病毒的致病机理,特别是感染引起的细胞死亡机制了解甚少。最近,依托于中科院南海海洋研究所的中科院海洋生物资源可持续利用重点实验室(LMB)秦启伟研究员带领的团队,在虹彩病毒感染致病机理及参与的信号通路等研究方面取得了一系列突破性进展,团队成员黄晓红博士等人发现一种新的由病毒感染引起的宿主细胞死亡机制。

石斑鱼虹彩病毒(SGIV)和中华鳖虹彩病毒(STIV)是分离于鱼类和爬行类动物不同株的虹彩病毒,对两株病毒死亡机制的研究能够为深入了解虹彩病毒的致病机理提供重要的信息。通过一系列的分子生物学及生化特征分析,研究结果表明,STIV感染细胞后能够引起经典的细胞凋亡,而SGIV感染宿主细胞引起的是一种非凋亡形式的死亡——类凋亡(paraptosis),这是大DNA病毒引起类凋亡的首次报道。STIV和SGIV感染均能激活丝裂原活化蛋白激酶(MAPK)信号通路,ERK和p38MAPK信号通路对STIV复制及病毒诱导的凋亡是必需,而ERK和JNK对SGIV复制及病毒诱导的类凋亡是必需的。

研究成果为阐释鱼类病毒性疾病的致病机制及研发有效的抗病毒对策奠定了重要理论基础。

以上研究结果以3篇论文形式分别发表在国际知名期刊《细胞凋亡》(Apoptosis,2011, 16: 831-845; 2011, 16: 581-590)和《综合病毒学期刊》(Journal of General Virology,2011, 92: 1292-1301)。研究得到国家重点基础研究计划(“973”计划)、国家杰出青年基金项目、国家自然科学基金重点项目及中科院知识创新工程项目的支持。

 

Roles of stress-activated protein kinases in the replication of Singapore grouper iridovirus and regulation of the inflammatory responses in grouper cells

Xiaohong Huang, Youhua Huang, Zhengliang OuYang, Jia Cai, Yang Yan and Qiwei Qin

Stress-activated protein kinases (SAPKs), including p38 mitogen-activated protein kinase (p38 MAPK) and c-Jun N-terminal kinase (JNK), are usually activated in response to different environmental stimuli, including virus infection. In the present study, the roles of SAPKs during Singapore grouper iridovirus (SGIV) infection were investigated in fish cells. The results showed that increased phosphorylation of JNK1/2 and p38 MAPK occurred during active replication of SGIV in grouper cell cultures. Moreover, downstream effectors (c-Jun, MAPK-activated protein kinase 2, p53, activator protein 1, Myc and nuclear factor of activated T cells) were activated after SGIV infection, suggesting that SGIV replication activated the JNK and p38 MAPK signalling pathways. Notably, using specific inhibitors, it was found that viral gene transcripts, protein expression and viral titres were not affected by inhibition of p38 MAPK but were suppressed significantly by inhibiting JNK1/2 activation. In addition, transcription of grouper immune genes including interferon regulatory factor 1, interleukin-8 and tumour necrosis factor alpha (TNF-α) were regulated by JNK, whilst only TNF-α was regulated by p38 MAPK. It is proposed that the JNK pathway is important for SGIV replication and modulates the inflammatory responses during virus infection.

文献链接:http://vir.sgmjournals.org/content/92/6/1292.abstract?sid=f89b4ebb-70d8-4dcc-a1ae-eac902eb4a67

本网站所有注明“来源:生物探索”的文字、图片和音视频资料,版权均属于生物探索所有,其他平台转载需得到授权。本网所有转载文章系出于传递更多信息之目的,且明确注明来源和作者,不希望被转载的媒体或个人可与我们联系(editor@biodiscover.com),我们将立即进行删除处理。所有文章仅代表作者观点,不代表本站立场。