Identification of the IFN-β response in H3N2 canine influenza virus infection

Su, Shuo; San, Huang; Fu, Cheng; Wang, Lifang; Zheng, Yun; Zhou, Pei

doi:10.1099/jgv.0.000322

Cited by 9 publications

(5 citation statements)

References 41 publications

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“…Previous studies have demonstrated that protein degradation, inhibited phosphorylation and ubiquitination in RLRs pathway results from the accumulation of multi-functional IAV NS1 [15,16,32]. In present study, the results of the luciferase assay and western blotting in MDCK cells showed that CIV NS1 protein suppressed the activation of the RLRs pathway, including down-regulating canine RIG-I and decreasing phosphorylation of IRF-3, which is in accordance with our previous finding that CIV NS1 inhibited the production of type I IFN induced by SEV [33]. Taken together, CIV NS1 does not directly down-regulate the expression of IRF-3, but it decreases the ratio of phosphorylated IRF-3 to inhibit the signaling transduction of RLRs pathway.…”

Section: Discussionsupporting

confidence: 92%

Antiviral Activity of Canine RIG-I against Canine Influenza Virus and Interactions between Canine RIG-I and CIV

Wang

Yao

et al. 2021

Viruses

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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.

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Section: Discussionsupporting

confidence: 92%

Antiviral Activity of Canine RIG-I against Canine Influenza Virus and Interactions between Canine RIG-I and CIV

Wang

Yao

et al. 2021

Viruses

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“…Previously, Stephan found that NS1 could inhibit activation of the AP-1 transcription factor. Activation of AP-1 plays an important role in the immune response to viral infection since the factor can transcribe and activate genes encoding various antiviral factors [ 43 ]. Su found that CIV H3N2 can inhibit the IFN-β promoter by inhibiting activation of the NF-κB and IRF3 recognition elements, and NS1 is the key gene that inhibits IFNs [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Canine Influenza Virus is Mildly Restricted by Canine Tetherin Protein

Zheng

Hao

Zheng

et al. 2018

Viruses

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Tetherin (BST2/CD317/HM1.24) has emerged as a key host-cell ·defence molecule that acts by inhibiting the release and spread of diverse enveloped virions from infected cells. We analysed the biological features of canine tetherin and found it to be an unstable hydrophilic type I transmembrane protein with one transmembrane domain, no signal peptide, and multiple glycosylation and phosphorylation sites. Furthermore, the tissue expression profile of canine tetherin revealed that it was particularly abundant in immune organs. The canine tetherin gene contains an interferon response element sequence that can be regulated and expressed by canine IFN-α. A CCK-8 assay showed that canine tetherin was effective in helping mitigate cellular damage caused by canine influenza virus (CIV) infection. Additionally, we found that the overexpression of canine tetherin inhibited replication of the CIV and that interference with the canine tetherin gene enhanced CIV replication in cells. The impact of canine tetherin on CIV replication was mild. However, these results elucidate the role of the innate immune factor, canine tetherin, during CIV infection for the first time.

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“…The canine promoter reporter plasmid pIFNβ-Luc was constructed according to a previous study [25]; a pISRE-Luc and pRL-TK were purchased from Beyotime (Shanghai, China) and Promega (USA), respectively. Poly(I:C) (Sigma, USA) at a final concentration of 2 g/mL was the control for promoter activation experiments.…”

Section: Plasmids and Reagentsmentioning

confidence: 99%

Molecular characterization and antiviral effects of canine interferon regulatory factor 1 (CaIRF1)

Hao

Chen

et al. 2022

BMC Vet Res

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Background Interferon regulatory factor 1 (IRF1) is an important transcription factor that activates the type I interferon (IFN-I) response and plays a vital role in the antiviral immune response. Although IRF1 has been identified in several mammals, little information related to its function in canines has been described. Results In this study, canine IRF1 (CaIRF1) was cloned. After a series of bioinformatics analyses, we found that the CaIRF1 protein structure was similar to that of other animal IRF1 proteins, including a conserved DNA-binding domain (DBD), an IRF-association domain 2 (IAD2) domain and two nuclear localization signals (NLSs). An indirect immunofluorescence assay (IFA) revealed that CaIRF1 was mainly distributed in the nucleus. Overexpression of CaIRF1 in Madin-Darby canine kidney cells (MDCK) induced high levels of interferon β (IFNβ) and IFN-stimulated response element (ISRE) promoter activation and induced interferon-stimulated gene (ISG) expression. Subsequently, we assayed the antiviral activity of CaIRF1 against vesicular stomatitis virus (VSV) and canine parvovirus type-2 (CPV-2) in MDCK cells. Overexpression of CaIRF1 effectively inhibited the viral yields of VSV and CPV-2, while knocking down of CaIRF1 expression mildly increased viral gene copies. Conclusions CaIRF1 is involved in the cellular IFN-I signaling pathway and plays an important role in the antiviral response.

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Identification of the IFN-β response in H3N2 canine influenza virus infection

Cited by 9 publications

References 41 publications

Antiviral Activity of Canine RIG-I against Canine Influenza Virus and Interactions between Canine RIG-I and CIV

Antiviral Activity of Canine RIG-I against Canine Influenza Virus and Interactions between Canine RIG-I and CIV

Canine Influenza Virus is Mildly Restricted by Canine Tetherin Protein

Molecular characterization and antiviral effects of canine interferon regulatory factor 1 (CaIRF1)

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