BmCPV dsRNA基因组S5节段负链编码病毒小肽vSP27抑制BmCPV感染，然而vSP27调控病毒感染的分子机制目前尚不清楚。我们前期研究发现vSP27能够促进细胞内活性氧(ROS)产生以及激活NF-κB信号通路，因此推测vSP27通过ROS-NF-κB信号通路抑制BmCPV感染。本项目拟通过vSP27调控细胞内ROS产生途径、vSP27激活NF-κB信号通路的方式、vSP27调节抗病毒效应分子的表达，筛选和鉴定vSP27互作蛋白、vSP27互作蛋白调节ROS产生途径、vSP27互作蛋白调节NF-κB信号通路方式，研究其与BmCPV感染的相关性，探讨vSP27调控细胞内ROS的水平激活NF-κB信号通路抑制BmCPV感染的分子机制。本项目不仅能进一步揭示vSP-27的功能和调控机制，也能为开发新型抗病毒小肽防治家蚕细胞质型多角体病提供新的策略。

BmCPV infection was inhibited by the viral small peptide vSP27 encoded by the negative (−) strand of BmCPV dsRNA segment S5, however, the molecular mechanism of vSP27 regulating BmCPV infection is still unclear. In our previous study, vSP27 induced the reactive oxygen species (ROS) generation and activated the NF-κB signal pathway. Here, it is reasonable to hypothesize that vSP27 activates the NF-κB signal pathway via ROS burst to inhibit BmCPV infection. In this project, we intend to explore the intracellular ROS generation pathway, to validate the activation modes of NF-κB signal pathway, to investigate the expression of antiviral effecter molecules regulated by vSP27, to screen and identify of vSP27 interacted proteins, to understand the effect of vSP27 interacted proteins on ROS generation pathway, to investigate the effect of vSP27 interacted proteins on NF-κB signal pathway. These results will uncover the molecular mechanism of BmCPV infection inhibited by vSP27 via NF-κB signal pathway that is activated by ROS burst. Taken together, this project will not only uncover the function of vSP27 and regulation mechanism, but also provide the novel strategy for developing new antiviral peptides to prevention of silkworm cytoplasmic polyhedrosis.