The Mammalian response to virus infection is independent of small RNA silencing.
The Mammalian response to virus infection is independent of small RNA silencing.
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DOI：
10.1016/j.celrep.2014.05.038
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发表时间：
2014-07-10
期刊：
影响因子：
8.8
通讯作者：
tenOever BR
中科院分区：
文献类型：
--
作者：
Backes S;Langlois RA;Schmid S;Varble A;Shim JV;Sachs D;tenOever BR
细胞对病毒感染的成功反应对于进化生存至关重要。在植物、节肢动物和线虫中，细胞的抗病毒防御依赖于RNA干扰（RNAi）。有趣的是，哺乳动物对病毒的反应主要是通过干扰素（IFN）介导的抗病毒蛋白的诱导。尽管IFN系统具有效力，但仍不清楚哺乳动物是否也具有利用抗病毒RNAi的能力。在这里，我们通过在病毒感染的背景下禁用IFN，小RNA功能或两者的活动来研究这一点。我们发现，在体内RNA病毒感染的情况下，由于宿主抗病毒反应的转录抑制减少，小RNA的丢失降低了滴度。相反，使病毒具有抑制IFN系统的能力导致滴度增加。综上所述，我们得出结论，小RNA沉默不是IFN介导的细胞对病毒感染的反应的生理贡献者。
A successful cellular response to virus infection is essential for evolutionary survival. In plants, arthropods, and nematodes, cellular antiviral defenses rely on RNA interference (RNAi). Interestingly, the mammalian response to virus is predominantly orchestrated through interferon (IFN)-mediated induction of antiviral proteins. Despite the potency of the IFN system, it remains unclear whether mammals also have the capacity to employ antiviral RNAi. Here we investigate this by disabling either IFN, small RNA function or both activities in the context of virus infection. We find that loss of small RNAs in the context of an in vivo RNA virus infection lowers titers due to reduced transcriptional repression of the host antiviral response. In contrast, enabling a virus with the capacity to inhibit the IFN system results in increased titers. Taken together, we conclude that small RNA silencing is not a physiological contributor to the IFN-mediated cellular response to virus infection.