Avian infectious bronchitis virus disrupts the melanoma differentiation associated gene 5 (MDA5) signaling pathway by cleavage of the adaptor protein MAVS

Yu, Liping; Zhang, Xiaorong; Wu, Tianqi; Su, Jin; Wang, Yuyang; Wang, Yuexin; Ruan, Baoyang; Niu, Xiaosai; Wu, Yantao

RIG-I and MDA5 interact with MAVS via CARD-CARD domains at their N-terminal, which is essential for the activation of the NF-κB and IRF3/7 , chIFN-λ (c) and chMx (d) was determined by RT-qPCR. All gene expression was calculated as the fold change relative to mock cells uninfected in parallel and normalized against a housekeeping gene (β-actin). Data are presented as the mean ± SD (n = 3, 3 wells on same plate) (* P ≤ 0.05; ** P ≤ 0.01) downstream signaling pathway. MAVS plays a critical role in antiviral activity. To determine whether chMAVS is involved in the antiviral immune response to IBV infection, the expression level of chMAVS in IBV-infected CEK cells was investigated. We found that the cleavage of MAVS was induced by IBV at 8 h and 12 h post-infection but was not cleaved after 24 h (Fig. 6) . We inferred that at the early stage of IBV infection, IBV-induced cleavage of MAVS allows IBV to evade the MDA5-mediated innate immunity signaling pathway.