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

Although both RIG-I and MDA5 are closely related, exhibiting 25% and 40% identities in their N-terminal CARD and C-terminal helicase domains [16, 17] , they can recognize different types of ligands and distinct subsets of RNA viruses. RIG-I has been reported to recognize short dsRNA produced during the replication of RNA viruses and uncapped 5′-triphosphate (5′-ppp) ssRNA [18] . MDA5 can be activated by long dsRNA, including the synthetic dsRNA analogue poly I:C [16, 19] . Overexpression of MDA5 and RIG-I inhibits the growth of encephalomyocarditis virus (EMCV) and vesicular stomatitis virus (VSV) [19] , and overproduction of MDA5 but not RIG-I leads to enhanced IFN-β promoter activity in measles virus (MV)-infected A549 cells [9] . It has also been demonstrated that expression of MDA5 and RIG-I resulted in the activation of the IFN-β promoter in influenza A virus-infected epithelial cells [20] . Barber et al. suggested that the lack of RIG-I observed in chickens results in a deficiency of the antiviral innate immune response, possibly explaining the high susceptibility of chickens compared to ducks during Avian influenza virus (AIV) infection [21] . Similarly, the absence of RIG-I in chickens may contribute to the susceptibility of only chickens to IBV.