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. 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. Here, 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. Although 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.

Avian reovirus (ARV) is an important poultry pathogen that can cause immunosuppression. In this study, RNA-Seq technology was applied to investigate the transcriptome-wide changes of DF-1 cells upon ARV infection at the middle stage. Total RNA of ARV-infected or mock-infected samples at 10 and 18 h post infection (hpi) was extracted to build RNA-Seq datasets. Analysis of the sequencing data revealed that the expressions of numerous genes were altered, and a panel of differentially expressed genes were confirmed with RT-qPCR. At 10 hpi, 104 genes were down-regulated and 64 were up-regulated, while the expressions of 47 genes were increased and only one was down-regulated, which may play a role in retinoic acid biosynthesis, at 18 hpi in the ARV-infected cells. The similar profiles of up-regulated genes between the two groups of infected cells suggest that ARV infection activated a prolonged antiviral response of host cells. Alternative splicing analysis found no significantly changed events altered by ARV infection. Overall, the differential expression profile presented in this study can be used to expand our understanding of the comprehensive interactions between ARV and the host cells, and may be helpful for us to reveal the pathogenic mechanism on the molecular level.

Avian reovirus (ARV) is an important pathogen that can cause serious disease in poultry. Though several in vitro studies revealed some molecular mechanisms that are responsible for ARV-induced autophagy, it is still largely unknown how ARV manipulates autophagy to promote its own propagation. In this study, we demonstrated that ARV infection triggered autophagy in chicken tissues, evident from the enhancement of LC3-I/−II conversion and the appearance of abundant autophagosomes. Moreover, viral replication and the expression of IL-1β were coupled with the process of ARV-induced autophagy in the early stage of infection. Furthermore, regulation of autophagy affected the accumulation of LC3-II, the production of ARV and the expression of IL-1β. Altogether, our data suggest that ARV induces autophagy, which benefits its replication and dissemination in chicken tissues at the early infection stage.

Caveolin-1 (Cav-1) is the basic component of caveolae, a specialized form of lipid raft that plays an essential role in endocytic viral entry. However, the evidence of direct involvement of caveolae and Cav-1 in avian reovirus (ARV) entry remains insufficient. In this study, the membrane lipid rafts were isolated as detergent-resistant microdomains (DRMs) by sucrose gradient centrifugation, and the capsid protein σB of ARV was found to associate with Cav-1 in DRMs fractions. Additionally, the interaction between ARV σB protein and Cav-1 was demonstrated by immunofluorescence co-localization and co-immunoprecipitation assays. Furthermore, we found that the internalization of ARV is sensitive to caveolae and dynamin inhibitors, while it is insensitive to clathrin inhibitors. In conclusion, these results indicate that the ARV σB protein interacts with Cav-1 during dynamin-dependent caveolae-mediated endocytosis for the entry of ARV.