伪狂犬病病毒(PRV)属于疱疹病毒科中的α疱疹病毒亚科，是引起猪伪狂犬病的病原体。伪狂犬病是危害养猪业的主要传染病之一，每年造成巨大的经济损失。控制和消灭伪狂犬病所面临的主要困难是PRV的潜伏感染问题。虽然目前关于潜伏感染的建立、维持及激活机制尚不明确，但是大多数病毒已被发现会产生抗凋亡因子，进而促进感染早期的宿主细胞存活。PRV US3的两个异构体（US3a和US3b）已被证实能够产生抗凋亡因子，且US3a的抗凋亡活性大于US3b。本项目将以鼠和猪的三叉神经节细胞（TG)为体外模型，以鼠和猪为体内模型，通过PI3K/Akt和NF-кB两条信号通路激活的PRV US3蛋白出发，研究并揭示PRV感染引起三叉神经节细胞激活的分子机制。该研究将为阐明PRV致病与免疫机理奠定基础，而且还可为其它疱疹科病毒感染问题的揭示提供借鉴。

The pseudorabies virus (PRV), a member of the Alphaherpesvirus subfamily, is the causative agent of pseudorabies in pigs. Pseudorabies is one of the primary contagious diseases which impacts the pig industry with substantial economic losses each year. The main difficulty in control and eradicate Pseudorabies is due to the PRV latent infections. Although the underlying mechanisms responsible for the establishment, maintenance and reactivation of the latency infections are still unclear at the moment, most viruses have been shown to promote host cell survival during the early stages of infection by producing anti-apoptotic factors. Two isoforms of PRV US3, namely US3a and US3b, have been shown to produce anti-apoptotic factors, and the anti-apoptosis effect of US3a is greater than that of US3a has a greater anti-apoptotic effect than US3b. This project will use the rat and swine trigeminal ganglion (TG) in vitro model and use rat and swine in vivo model. It will proceed from the two signaling pathways that activate the PRV US3 proteins, i.e., NF-кB and PI3/AKT, to study and reveal the molecular mechanism of TG cell activation induced by JEV infections. This study will not only lay the foundation for the elucidation of the pathogenesis and immune of PRV but also provide a reference for the studies on the viral infections due to other members of family Herpesviridae.