Nat.Immu：STING调节病毒衣壳与宿主细胞的膜融合

病毒的外壳与宿主的细胞膜融合是病毒感染细胞的第一步。那机体的免疫系统又是如何检测到发生了膜融合呢？最近《自然-免疫》上发表的文章给出了一些线索。

研究人员发现，无论是体内实验还是体外实验，当细胞暴露在病毒状粒子或人工合成的脂质体以及一些其它刺激的条件下时，也能够产生免疫应答，这种应答虽然不能触发传统的病原体识别途径，但能导致膜融合。融合作用依赖于STING, 该蛋白是一种干扰素刺激因子，以往的研究认为它能够对病毒DNA产生应答。

本文中，研究人员指出，膜融合可诱导干扰素受激基因的产生，从而诱导1型干扰素受激应答。这种融合依赖的应答需要STING参与，但并不需要病毒DNA、RNA或者蛋白质外壳的参与。研究人员认为，膜融合可能作为一种危险信号，提示细胞防御机制有病毒将要入侵等潜在威胁。

doi:10.1038/ni.2350

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Virus-cell fusion as a trigger of innate immunity dependent on the adaptor STING

Christian K Holm, Søren B Jensen, Martin R Jakobsen, Natalia Cheshenko, Kristy A Horan, Hanne B Moeller, Regina Gonzalez-Dosal, Simon B Rasmussen, Maria H Christensen, Timur O Yarovinsky, Frazer J Rixon, Betsy C Herold, Katherine A Fitzgerald,  & Søren R Paludan

The innate immune system senses infection by detecting either evolutionarily conserved molecules essential for the survival of microbes or the abnormal location of molecules. Here we demonstrate the existence of a previously unknown innate detection mechanism induced by fusion between viral envelopes and target cells. Virus-cell fusion specifically stimulated a type I interferon response with expression of interferon-stimulated genes, in vivo recruitment of leukocytes and potentiation of signaling via Toll-like receptor 7 (TLR7) and TLR9. The fusion-dependent response was dependent on the stimulator of interferon genes STING but was independent of DNA, RNA and viral capsid. We suggest that membrane fusion is sensed as a danger signal with potential implications for defense against enveloped viruses and various conditions of giant-cell formation.