The suppression of innate immune response by human rhinovirus C

作者：Pang, Li-li; Yuan, Xin-hui; Sha, Chang-sheng; Li, Mao-zhong; Wang, Ying; Wang, Hui-min; Xie, Guang-cheng; Xie, Zhi-ping; Yuan, Yue; Zhou, Dong-mei; Sun, Xiao-man; Zhang, Qing; Xin, Yan; Li, Dan-di^*; Duan, Zhao-jun^*

来源：Biochemical and Biophysical Research Communications, 2017, 490(1): 22-28.

DOI：10.1016/j.bbrc.2017.05.169

• Interferon response
• MAVS
• Rhinovirus C
• RIG-I signaling pathway
• 3C protein

Rhinovirus C (RV-C), a newly identified group of human rhinoviruses (RVs), is associated with exacerbation of severe asthma. The type I interferon (IFN) response induced by this virus and the mechanisms of evasion of IFN-mediated innate immunity for RV-C remain unclear. In this study, we constructed a fulllength cDNA clone of RV-C (12651) from a clinical sample. IFN-beta mRNA and protein levels were not elevated in differentiated Human bronchial epithelial (HBE) cells at the air-liquid interface infected with RV-C, except in the early stage of infection. The ability to attenuate IFN-beta activation was ascribed to 3C(Pro) of RV-C, and the 40-His site of 3C(Pro) played an important role. Furthermore, RIG-I was degraded by 3C(Pro) in a caspase-dependent manner and 3C(pro) cleaved MAVS at 148 Q/A, which inhibited IFN signaling. Taken together, our results demonstrate the mechanism by which RV-C circumvents the production of type I IFN in infected cells.

• 出版日期2017-8-12
• 单位内蒙古医科大学; 中国疾病预防控制中心; 中国疾病预防控制中心病毒病预防控制所; 承德医学院; 兰州大学; 中国科学技术大学