The Key Laboratory of Plant Cell Engineering and Germplasm Innovation of Ministry of Education/Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Jinan, Shandong, People's Republic of China.
J Virol. 2013 Jan;87(1):636-47. doi: 10.1128/JVI.01671-12. Epub 2012 Oct 24.
Successful viruses have evolved superior strategies to escape host defenses or exploit host biological pathways. Most of the viral immediate-early (ie) genes are essential for viral infection and depend solely on host proteins; however, the molecular mechanisms are poorly understood. In this study, we focused on the modification of viral IE proteins by the crayfish small ubiquitin-related modifier (SUMO) and investigated the role of SUMOylation during the viral life cycle. SUMO and SUMO ubiquitin-conjugating enzyme 9 (UBC9) involved in SUMOylation were identified in red swamp crayfish (Procambarus clarkii). Both SUMO and UBC9 were upregulated in crayfish challenged with white spot syndrome virus (WSSV). Replication of WSSV genes increased in crayfish injected with recombinant SUMO or UBC9, but injection of mutant SUMO or UBC9 protein had no effect. Subsequently, we analyzed the mechanism by which crayfish SUMOylation facilitates WSSV replication. Crayfish UBC9 bound to all three WSSV IE proteins tested, and one of these IE proteins (WSV051) was covalently modified by SUMO in vitro. The expression of viral ie genes was affected and that of late genes was significantly inhibited in UBC9-silenced or SUMO-silenced crayfish, and the inhibition effect was rescued by injection of recombinant SUMO or UBC9. The results of this study demonstrate that viral IE proteins can be modified by crayfish SUMOylation, prompt the expression of viral genes, and ultimately benefit WSSV replication. Understanding of the mechanisms by which viruses exploit host components will greatly improve our knowledge of the virus-host "arms race" and contribute to the development of novel methods against virulent viruses.
成功的病毒已经进化出了优越的策略来逃避宿主防御或利用宿主的生物途径。大多数病毒的即刻早期(IE)基因对于病毒感染是必不可少的,并且完全依赖于宿主蛋白;然而,其分子机制尚不清楚。在这项研究中,我们专注于甲壳类动物小泛素相关修饰物(SUMO)对病毒 IE 蛋白的修饰,并研究了 SUMO 化在病毒生命周期中的作用。在克氏原螯虾(Procambarus clarkii)中鉴定到参与 SUMO 化的 SUMO 和 SUMO 泛素连接酶 9(UBC9)。在受到白斑综合征病毒(WSSV)挑战的克氏原螯虾中,SUMO 和 UBC9 均上调。在注射重组 SUMO 或 UBC9 的克氏原螯虾中,WSSV 基因的复制增加,但注射突变 SUMO 或 UBC9 蛋白则没有影响。随后,我们分析了克氏原螯虾 SUMO 化促进 WSSV 复制的机制。克氏原螯虾 UBC9 与所有三种测试的 WSSV IE 蛋白结合,其中一种 IE 蛋白(WSV051)在体外被 SUMO 共价修饰。IE 基因的表达受到影响,在 UBC9 沉默或 SUMO 沉默的克氏原螯虾中晚期基因的表达受到显著抑制,并且通过注射重组 SUMO 或 UBC9 可以挽救抑制作用。本研究的结果表明,病毒 IE 蛋白可以被克氏原螯虾 SUMO 化修饰,从而促进病毒基因的表达,并最终有益于 WSSV 复制。对病毒利用宿主成分的机制的理解将极大地提高我们对病毒-宿主“军备竞赛”的认识,并有助于开发针对毒力病毒的新方法。