State key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China.
Virus Res. 2009 Dec;146(1-2):135-9. doi: 10.1016/j.virusres.2009.09.011. Epub 2009 Sep 24.
Host cells sense double-stranded RNA (dsRNA) produced during viral replication and initiate type I interferon (IFN-alpha/beta) production, leading to subsequent antiviral responses. Many viruses, including classical swine fever virus (CSFV), have developed strategies for counteracting the IFN-alpha/beta response. In this study, we explored the role of the CSFV E(rns) glycoprotein in the inhibition of IFN-beta production induced by dsRNA [poly(IC)]. Our results demonstrated that CSFV E(rns) could bind to exogenous dsRNA and inhibit dsRNA-induced IFN-beta production but failed to inhibit TRIF-triggered IFN-beta production. Our data suggest that the inhibition of IFN-beta induction occurred at the initial step of the TLR3 signaling pathway. We also showed that deglycosylation of E(rns) rendered it unable to bind to dsRNA, and thus unable to inhibit dsRNA-induced IFN-beta production. Taken together, these results indicated that N-glycan of CSFV E(rns) is essential for E(rns) blocking of IFN-beta induction.
宿主细胞感知病毒复制过程中产生的双链 RNA(dsRNA)，并启动 I 型干扰素(IFN-α/β)的产生，从而引发后续的抗病毒反应。许多病毒，包括经典猪瘟病毒(CSFV)，已经开发出了对抗 IFN-α/β反应的策略。在本研究中，我们探讨了 CSFV E(rns)糖蛋白在抑制 dsRNA[poly(IC)]诱导的 IFN-β产生中的作用。结果表明，CSFV E(rns)可以与外源性 dsRNA 结合，并抑制 dsRNA 诱导的 IFN-β产生，但不能抑制 TRIF 触发的 IFN-β产生。我们的数据表明，IFN-β诱导的抑制发生在 TLR3 信号通路的初始步骤。我们还表明，E(rns)的糖基化缺失使其无法与 dsRNA 结合，从而无法抑制 dsRNA 诱导的 IFN-β产生。综上所述，这些结果表明 CSFV E(rns)的 N-聚糖对于 E(rns)阻断 IFN-β诱导是必不可少的。
