Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5505345 | Biochemical and Biophysical Research Communications | 2017 | 26 Pages |
Abstract
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 full-length cDNA clone of RV-C (LZ651) from a clinical sample. IFN-β 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-β activation was ascribed to 3Cpro of RV-C, and the 40-His site of 3Cpro played an important role. Furthermore, RIG-I was degraded by 3Cpro in a caspase-dependent manner and 3Cpro 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.
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Authors
Li-li Pang, Xin-hui Yuan, Chang-sheng Shao, Mao-zhong Li, Ying Wang, Hui-min Wang, Guang-cheng Xie, Zhi-ping Xie, Yue Yuan, Dong-mei Zhou, Xiao-man Sun, Qing Zhang, Yan Xin, Dan-di Li, Zhao-jun Duan,