Strong interferon-inducing capacity of a highly virulent variant of influenza A virus strain PR8 with deletions in the NS1 gene
Strong interferon-inducing capacity of a highly virulent variant of influenza A virus strain PR8 with deletions in the NS1 gene
复制标题
DOI：
10.1099/vir.0.015727-0
复制
发表时间：
2009-12-01
影响因子：
3.8
通讯作者：
Staeheli, Peter
中科院分区：
文献类型：
--
作者：
Kochs, Georg;Martinez-Sobrido, Luis;Staeheli, Peter
缺乏干扰素（IFN）拮抗性非结构NS 1蛋白的流感病毒被强烈减毒。在这里，我们表明，携带NS 1完全缺失或C末端截短的A/PR/8/34（H1N1）高毒力变体的突变体在感染小鼠中比源自标准A/PR/8/34的NS 1突变体更有效地诱导IFN。IFN的有效诱导与小鼠肺中成功的初始病毒复制相关，表明IFN应答通过增强的病毒活性而增强。由于新的NS 1突变体可以在标准的生物安全实验室中处理，它们代表了用于研究病毒诱导的体内IFN表达的方便的新工具。
Influenza viruses lacking the interferon (IFN)-antagonistic non-structural NS1 protein are strongly attenuated. Here, we show that mutants of a highly virulent variant of A/PR/8/34 (H1N1) carrying either a complete deletion or C-terminal truncations of NS1 were far more potent inducers of IFN in infected mice than NS1 mutants derived from standard A/PR/8/34. Efficient induction of IFN correlated with successful initial virus replication in mouse lungs, indicating that the IFN response is boosted by enhanced viral activity. As the new NS1 mutants can be handled in standard biosafety laboratories, they represent convenient novel tools for studying virus-induced IFN expression in vivo.