Abstract
The stimulator of interferon genes (STING) protein has been shown to play a pivotal role in response to both cytosolic RNA and dsDNA to elicit interferon (IFN) production in mammals. However, the role of duck STING (DuSTING) in antiviral innate immunity, especially in anti-RNA virus infection, has yet to be elucidated. In this study, the function of DuSTING in IFN induction and its role in anti-RNA virus infections were studied. DuSTING was amplified via reverse transcription-polymerase chain reaction (RT-PCR) from Pekin duck, showing that its cDNA sequence contains an open reading frame (ORF) of 1,149 bp and encodes 382 amino acids (aa). Sequence alignment showed that DuSTING protein shares 71.1, 43.4, and 33.3% identity with chickens, humans, and zebra fish, respectively. Overexpression of DuSTING in duck embryo fibroblasts (DEFs) strongly activated IFN-β promotor activity. Deletion mutant analysis revealed that the first 42 aa containing the first transmembrane (TM) domains and the last 32 aa containing a part of the C-terminal tail (CTT) are essential for its IFN-β activation. In vitro experiments showed that the mRNA levels of DuSTING and IFNs were all upregulated when the DEFs were infected with H9N2 avian influenza virus (AIV) SH010, while overexpression of DuSTING inhibited the replication of this virus. In vivo studies showed that DuSTING mRNA was widely expressed in different tissues, and was up-regulated in the spleen and lung of ducks challenged with SH010. In conclusion, our results indicate that DuSTING is an essential IFN mediator and plays a role in anti-RNA virus innate immunity.
Highlights
Type I interferons (IFNs) play an essential role in innate immune responses against viral infection [1]
Phylogenetic analysis showed that the duck, chicken and zebra finch stimulator of the IFN gene (STING) protein sequences were in the same subgroup
It has been discovered that ducks have an intact retinoic acid-inducible gene I (RIG-I) gene, while chickens lack this gene [15], highlighting the importance of functional research on RLR in birds
Summary
Type I interferons (IFNs) play an essential role in innate immune responses against viral infection [1]. The production of IFNs was elicited by a series of recognition molecules called cellular pattern recognition receptors (PRRs), such as the family of retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), the family of toll-like receptors (TLRs), and numerous DNA receptors [2, 3]. Each PRR family includes many members, PRRs from the same family converge on the activation of one or two common junction adaptor proteins, which are essential for the subsequent signaling transduction [4, 5]. Stimulator of the IFN gene (STING) was discovered as a multifaceted junction adaptor protein in the innate immune response that is involved in both DNA and RNA recognition signaling in mammals [10]. For RNA recognition, STING utilizes RIG-I to recognize the RNA stimulus to trigger IFN signaling for inducing IFNs production; melanoma differentiation– associated gene 5 (MDA5), which belongs to the same family and shares a similar IFN pathway to RIG-I, cannot activate the IFNs via STING [10,11,12]
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.
