由于昆虫缺乏获得性免疫，昆虫的抗病毒防御机制完全依赖于天然免疫。我们先前的研究表明，多种昆虫RNA病毒可以激发Toll天然免疫通路并且显著的受到RNAi通路关键蛋白Dicer-2(Dcr-2)的调控。我们还发现Dcr-2能够直接结合于Toll mRNA的3’-UTR区域，导致Toll蛋白水平的提高，进而调控Toll通路。考虑到这些RNA病毒并不具备典型的激发昆虫Toll通路的病原体相关分子模式，我们拟在此前研究的基础上探索Dcr-2在调控Toll通路中的作用机制，及Dcr-2是否能够作为模式识别受体识别病毒并将该病毒感染信号传递给Toll通路和其中具体分子机制，进而研究昆虫中Dcr-2调控Toll通路的工作模式是否适用于哺乳动物或其他物种。本项目将推进昆虫病毒及昆虫抗病毒天然免疫方面的研究，也对哺乳动物RNAi及TLR通路的研究具有借鉴意义。

Insects lack acquired immune responses, and completely relies on various innate immune pathways to defend against viruses. Our previous studies have find that several insect RNA viruses have the ablilty to induce Toll immune signaling under the control of Dicer-2(Dcr-2), which is the key protein in RNAi pathway. We further found that Dcr-2 can binds to the 3’-UTR of Toll mRNA directly and regulates the translation of Toll and the induction of Toll immune signaling. Considering that these RNA viruses have no classical pathogen-associated molecular patterns to induce Toll pathway, we planed to study whether Dcr-2 workes as a pattern recognition receptor in virus induced Toll immune pathway and the acting mechanism of Dcr-2 in regulating Toll immune pathway. After that, we will study whether this mechanism of Dcr-2 in Toll pathway is conservative in mammalian or other species. The accomplishment of this project will promote the research of insect virus and insect antiviral innate immunity and have reference values for the research of RNAi and TLR pathway in mammals.