Kajaste-Rudnitski Anna, Mashimo Tomoji, Frenkiel Marie-Pascale, Guénet Jean-Louis, Lucas Marianne, Desprès Philippe
Interactions Moléculaires Flavivirus-Hôtes and Génétique des Mammifères, Institut Pasteur, 25 Rue du Dr. Roux, 75724 Paris, Cedex 15, France.
J Biol Chem. 2006 Feb 24;281(8):4624-37. doi: 10.1074/jbc.M508649200. Epub 2005 Dec 21.
The 2',5'-oligoadenylate synthetase (OAS) proteins associated with endoribonuclease RNase L are components of the interferon-regulated OAS/RNase L system, which is an RNA decay pathway known to play an important role in the innate antiviral immunity. A large body of evidence suggests a critical role for the 1b isoform of the mouse Oas gene (Oas1b) in resistance to West Nile virus (WNV) infection in vivo. WNV is a positive, single-stranded RNA virus responsible for severe encephalitis in a large range of animal species and humans. To investigate the molecular basis for the sensitivity of WNV to the Oas1b antiviral pathway, we established a stable mouse fibroblastic cell clone that up-regulates Oas1b protein expression under the control of the Tet-Off expression system. We showed that murine cells respond to Oas1b expression by efficiently inhibiting WNV replication. The antiviral action of Oas1b was essentially restricted to the early stages in virus life cycle. We found that the inability of WNV to productively infect the Oas1b-expressing cells was attributable to a dramatic reduction in positive-stranded viral RNA level. Thus, Oas1b represents an antiviral pathway that exerts its inhibitory effect on WNV replication by preventing viral RNA accumulation inside infected cells.
与核糖核酸酶RNase L相关的2',5'-寡腺苷酸合成酶(OAS)蛋白是干扰素调节的OAS/RNase L系统的组成部分,该系统是一种RNA降解途径,已知在先天性抗病毒免疫中起重要作用。大量证据表明,小鼠Oas基因的1b亚型(Oas1b)在体内抵抗西尼罗河病毒(WNV)感染中起关键作用。WNV是一种正链单链RNA病毒,可在多种动物物种和人类中引起严重脑炎。为了研究WNV对Oas1b抗病毒途径敏感性的分子基础,我们建立了一个稳定的小鼠成纤维细胞克隆,该克隆在Tet-Off表达系统的控制下上调Oas1b蛋白表达。我们表明,鼠细胞通过有效抑制WNV复制对Oas1b表达作出反应。Oas1b的抗病毒作用基本上局限于病毒生命周期的早期阶段。我们发现,WNV无法有效感染表达Oas1b的细胞是由于正链病毒RNA水平急剧下降所致。因此,Oas1b代表了一种抗病毒途径,它通过阻止病毒RNA在受感染细胞内积累来对WNV复制发挥抑制作用。