Mouse gammaherpesvirus-68 infection acts as a rheostat to set the level of type I interferon signaling in primary macrophages.
Mouse gammaherpesvirus-68 infection acts as a rheostat to set the level of type I interferon signaling in primary macrophages.
复制标题
小鼠 gammaherpesvirus-68 感染充当变阻器来设定原代巨噬细胞中 I 型干扰素信号传导的水平。
DOI：
10.1016/j.virol.2013.04.036
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Tarakanova,VeraL
中科院分区：
文献类型：
--
作者：
Wood,BrittaniM;Mboko,WadzanaiP;Mounce,BryanC;Tarakanova,VeraL
Type I interferon (IFN) is a critical antiviral response of the host. We found that Interferon Regulatory Factor 3 (IRF-3) was responsible for induction of type I IFN following mouse gammaherpesvirus-68 (MHV68) infection of primary macrophages. Intriguingly, type I IFN signaling was maintained throughout the entire MHV68 replication cycle, in spite of several known viral IFN antagonists. However, MHV68-infected primary macrophages displayed attenuated responses to exogenous type I IFN, suggesting that MHV68 controls the level of type I IFN signaling that is allowed to occur during replication. Type I IFN receptor and IRF-3 were necessary to attenuate transcription of MHV68 RTA, an immediate early gene critical for replication. Furthermore, higher constitutive activity of RTA promoters was observed in the absence of type I IFN signaling. Our study suggests that MHV68 has preserved the ability to sense type I IFN status of the host in order to limit lytic replication.
