ISG15被痘苗病毒E3蛋白所抑制，并控制针对病毒感染的促炎反应。
ISG15 is counteracted by vaccinia virus E3 protein and controls the proinflammatory response against viral infection.
作者信息
Eduardo-Correia Benedito, Martínez-Romero Carles, García-Sastre Adolfo, Guerra Susana
机构信息
Department of Preventive Medicine and Public Health and Microbiology, Universidad Autónoma, Madrid, Spain.
出版信息
J Virol. 2014 Feb;88(4):2312-8. doi: 10.1128/JVI.03293-13. Epub 2013 Nov 20.
Abstract
Conjugation of ISG15 inhibits replication of several viruses. Here, using an expression system for assaying human and mouse ISG15 conjugations (ISGylations), we have demonstrated that vaccinia virus E3 protein binds and antagonizes human and mouse ISG15 modification. To study ISGylation importance in poxvirus infection, we used a mouse model that expresses deconjugating proteases. Our results indicate that ISGylation restricts in vitro replication of the vaccinia virus VVΔE3L mutant but unconjugated ISG15 is crucial to counteract the inflammatory response produced after VVΔE3L infection.
摘要
ISG15的缀合作用可抑制多种病毒的复制。在此，我们利用一种用于检测人和小鼠ISG15缀合（ISGylation）的表达系统，证明了痘苗病毒E3蛋白可结合并拮抗人和小鼠的ISG15修饰。为了研究ISGylation在痘病毒感染中的重要性，我们使用了一种表达去缀合蛋白酶的小鼠模型。我们的结果表明，ISGylation可限制痘苗病毒VVΔE3L突变体的体外复制，但未缀合的ISG15对于对抗VVΔE3L感染后产生的炎症反应至关重要。
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