Huang Fen, Yang Chenchen, Yu Wenhai, Bi Yanhong, Long Feiyan, Wang Jue, Li Yunlong, Jing Shenrong
Immunol Res. 2016 Feb;64(1):115-22. doi: 10.1007/s12026-015-8729-y.
Hepatitis E virus (HEV) is a major cause of enterically transmitted acute hepatitis worldwide. However, the mechanism of HEV replication is unclear. Type I interferon is the first defense line of host against viral infection. Signal regulator protein α (SIRP-α) plays an important role in negative regulation of innate immunity. In the present study, HEV infection significantly activated the expression of SIRP-α and down-regulated phosphorylation of IRF3, consequently resulted in suppression of type I interferon (IFN-β). In conclusion, HEV exploited SIRP-α to negative regulated IFN-β of the host innate immune system to promote viral infection. It suggested that interfering with the functions of SIRP-α should be considered as a potential therapeutic approach to the prevention and treatment of HEV infection.
戊型肝炎病毒(HEV)是全球肠道传播急性肝炎的主要病因。然而,HEV复制机制尚不清楚。I型干扰素是宿主抵御病毒感染的第一道防线。信号调节蛋白α(SIRP-α)在先天免疫的负调控中起重要作用。在本研究中,HEV感染显著激活了SIRP-α的表达并下调了IRF3的磷酸化,从而导致I型干扰素(IFN-β)的抑制。总之,HEV利用SIRP-α对宿主先天免疫系统的IFN-β进行负调控以促进病毒感染。这表明干扰SIRP-α的功能应被视为预防和治疗HEV感染的一种潜在治疗方法。