神经肽激素Kiss1及其受体GPR54在生殖系统发育、青春期控制，以及抑制肿瘤转移等过程中发挥重要作用，但其对免疫功能和在抗病毒感染中的作用及机制尚待阐明。我们发现：Kiss1在青春期大量表达并参与性腺发育，而病毒感染也能诱导其在小鼠下丘脑和垂体大量表达；当GPR54缺失时可显著降低小鼠体内病毒感染数量，明显提高小鼠I型干扰素的分泌及对VSV病毒感染的耐受；反之过表达GPR54，这种细胞则更容易被病毒感染，I型干扰素分泌显著下降，提示GPR54负调控I型干扰素从而影响机体的抗病毒免疫。本课题拟重点探讨：病毒诱导表达的Kiss1与机体抗病毒免疫有怎样的联系？GPR54调控的信号通路如何影响抗病毒免疫功能？神经内分泌系统如何通过GPR54调节机体的免疫平衡？即从动物整体、细胞和分子三个层面探讨和阐明GPR54在病毒感染过程中的重要调控功能和分子机制，为病毒性疾病的防治及新药研发提供理论依据。

G protein-coupled receptor 54 (GPR54), a key neuropeptide hormone receptor for Kiss1, plays essential roles in regulating puberty development and cancer metastasis. However, its role in the antiviral innate immune response is unknown. We demonstrated that the neuropeptide hormone kisspeptin was highly increased in mouse serum during viral infection as well as in puberty development. Furthermore, both RNA and DNA virus replication and infection was significantly reduced in Gpr54-deficient mice. Whereas, the virus-induced IFN-I production was increased obviously in Gpr54-deficient mice. Accordingly, overexpression of GPR54 facilitated virus infection and reduced IFN-I production suggested that Gpr54 plays key roles in negatively regulating innate antiviral immune responses. Thus, in this study we want to explore the correlation between virus-induced kiss1 expression and innate antiviral immune responses. How the innate antiviral immune responses are regulated by Gpr54? And how the balance is kept by neuroendocrine system through Gpr54. Finally, we will reveal the function and mechanism of Gpr54 in regulation of virus infection which will lay a theoretical basis for prevention and drug discovery of viral diseases.