内部收益率3
伪狂犬病
病毒
病毒学
免疫系统
生物
干扰素
干扰素基因刺激剂
先天免疫系统
免疫学
作者
Zhenfang Yan,Jiayu Yue,Yaxin Zhang,Zhengyang Hou,Dianyu Li,Yanmei Yang,Xiangrong Li,Adi Idris,Huixia Li,Shasha Li,Jingyuan Xie,Ru Feng
标识
DOI:10.1016/j.virs.2024.05.009
摘要
Herpesviruses antagonize host antiviral responses through a myriad of molecular strategies culminating in the death of the host cells. Pseudorabies virus (PRV) is a significant veterinary pathogen in pigs, causing neurological sequalae that ultimately lead to the animal's demise. PRV is known to trigger apoptotic cell death during the late stages of infection. The virion host shutdown protein (VHS) encoded by UL41 plays a crucial role in the PRV infection process. In this study, we demonstrate that UL41 inhibits PRV-induced activation of inflammatory cytokine and negatively regulates the cGAS-STING-mediated antiviral activity by targeting IRF3, thereby inhibiting the translocation and phosphorylation of IRF3. Notably, mutating the conserved amino acid sites (E192, D194, and D195) in the RNase domain of UL41 or knocking down UL41 inhibits the immune evasion of PRV, suggesting that UL41 may play a crucial role in PRV's evasion of the host immune response during infection. These results enhance our understanding of how PRV structural proteins assist the virus in evading the host immune response.
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