Abstract
RIG-I functions as a virus sensor that induces a cellular antiviral response. Although it has been investigated in other species, there have been no further studies to date on canine RIG-I against canine influenza virus (CIV). In the present study, we cloned the RIG-I gene of beagle dogs and characterized its expression, subcellular localization, antiviral response, and interactions with CIV proteins. RIG-I was highly expressed and mainly localized in the cytoplasm, with low levels detected in the nucleus. The results revealed that overexpression of the CARD domain of RIG-I and knockdown of RIG-I showed its ability to activate the RLR pathway and induced the expression of downstream interferon-stimulated genes. Moreover, overexpression of canine RIG-I suppressed the replication of CIV. The association between RIG-I and CIV was evaluated with the luciferase assay and by indirect immunofluorescence and bimolecular fluorescence complementation analyses. The results showed that CIV nonstructural protein 1 (NS1) can strongly suppress the RIG-I–mediated innate immune response, and the novel interactions between CIV matrix proteins (M1 and M2) and canine RIG-I were disclosed. These findings provide a basis for investigating the antiviral mechanism of canine RIG-I against CIV, which can lead to effective strategies for preventing CIV infection in dogs.
Highlights
Canine influenza virus (CIV) is an eight segments single stranded virus of the Orthomyxovirus type A influenza virus family
By performing a BLAST search, we found that 1 nucleobase in canine Retinoic acid-inducible gene I (RIG-I) was a variant of the predicted sequence at amino acid po
These results suggest that canine RIG-I is required for activation of the antiviral innate immune response in dogs
Summary
Canine influenza virus (CIV) is an eight segments single stranded virus of the Orthomyxovirus type A influenza virus family. After binding to the viral ligand, a conformational change exposes the N-terminal caspase activation and recruitment domain (CARD) of the receptor This triggers adapter mitochondrial antiviral signaling (MAVS) [7,8] and induces the transcription of interferon (IFN) regulatory factor 3 (IRF-3) and IRF-7, which are involved in the type I IFN-mediated antiviral response. RIG-I has been characterized in many species, but little is known about the role of canine RIG-I in canine influenza virus (CIV) infection This was investigated in the present study by cloning canine RIG-I and examining its tissue distribution and subcellular localization; its interaction with viral proteins; and the antiviral response triggered by RIG-I. We demonstrate that activated RIG-I induces RLRs pathway signaling and the activation of ISGs as part of the host antiviral innate immune response. RIG-I is available to interact with various CIV proteins, including CIV RNA polymerase subunits (PB2, PB1, and PA), nucleoprotein, NS1, and matrix proteins (M1 and M2), but further influenced mechanism needs to be clarified
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