Abstract
BackgroundMelanoma differentiation associated gene 5 (MDA5) and retinoic acid-inducible gene-I (RIG-I) selectively sense cytoplasmic viral RNA to induce an antiviral immune response. Infectious bronchitis virus (IBV) is one of the most important infectious agents in chickens, and in chicken cells, it can be recognized by MDA5 to activate interferon production. RIG-I is considered to be absent in chickens. However, the absence of RIG-I in chickens raises the question of whether this protein influences the antiviral immune response against IBV infection.ResultsHere, we showed that chicken cells transfected with domestic goose RIG-I (dgRIG-I) exhibited increased IFN-β activity after IBV infection. We also found that IBV can cleave MAVS, an adaptor protein downstream of RIG-I and MDA5 that acts as a platform for antiviral innate immunity at an early stage of infection.ConclusionsAlthough chicken MDA5 (chMDA5) is functionally active during IBV infection, the absence of RIG-I may increase the susceptibility of chickens to IBV infection, and IBV may disrupt the activation of the host antiviral response through the cleavage of MAVS.
Highlights
Melanoma differentiation associated gene 5 (MDA5) and retinoic acid-inducible gene-I (RIG-I) selectively sense cytoplasmic viral RNA to induce an antiviral immune response
The replication of Infectious bronchitis virus (IBV) was quantified by RT-qPCR to detect the IBV genome load in cell culture supernatants, and N protein was detected by a Western blot assay
We observed a significant increase in the IBV genome load in cell culture supernatants, with the highest level occurring at 60 h post-infection for the IBV-infected cells compared to the other time points (Fig. 1a)
Summary
Melanoma differentiation associated gene 5 (MDA5) and retinoic acid-inducible gene-I (RIG-I) selectively sense cytoplasmic viral RNA to induce an antiviral immune response. ΚB) [13], leading to the rapid production of type I IFNs and proinflammatory cytokines [11, 14, 15] 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. It has 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]. The absence of RIG-I in chickens may contribute to the susceptibility of only chickens to IBV
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
