Cellular microRNAs influence replication of H3N2 canine influenza virus in infected cells

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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In VitroSusceptibility of Canine Influenza A (H3N8) Virus to Nitazoxanide and Tizoxanide

Veterinary Medicine International ◽

10.4061/2010/891010 ◽

2010 ◽

Vol 2010 ◽

pp. 1-5 ◽

Cited By ~ 8

Author(s):

Laura V. Ashton ◽

Robert L. Callan ◽

Sangeeta Rao ◽

Gabriele A. Landolt

Keyword(s):

Influenza Virus ◽

Influenza A ◽

The United States ◽

Canine Influenza Virus ◽

Valuable Adjunct ◽

Canine Influenza ◽

The Impact ◽

H3n8 Virus

Infection of dogs with canine influenza virus (CIV) is considered widespread throughout the United States following the first isolation of CIV in 2004. While vaccination against influenza A infection is a common and important practice for disease control, antiviral therapy can serve as a valuable adjunct in controlling the impact of the disease. In this study, we examined the antiviral activity of nitazoxanide (NTZ) and tizoxanide (TIZ) against three CIV isolatesin vitro. NTZ and TIZ inhibited virus replication of all CIVs with 50% and 90% inhibitory concentrations ranging from 0.17 to 0.21 μMand from 0.60 to 0.76 μM, respectively. These results suggest that NTZ and TIZ are effective against CIV and may be useful for treatment of canine influenza in dogs but further investigation of thein vivoefficacy against CIV as well as the drug's potential for toxicity in dogs is needed.

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Evolution of the hemagglutinin gene of H3N8 canine influenza virus in dogs

Virus Genes ◽

10.1007/s11262-014-1102-8 ◽

2014 ◽

Vol 49 (3) ◽

pp. 393-399 ◽

Cited By ~ 7

Author(s):

Heidi L. Pecoraro ◽

Susi Bennett ◽

Miranda E. Spindel ◽

Gabriele A. Landolt

Keyword(s):

Influenza Virus ◽

Canine Influenza Virus ◽

Hemagglutinin Gene ◽

Canine Influenza

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Role of CARD Region of MDA5 Gene in Canine Influenza Virus Infection

Viruses ◽

10.3390/v12030307 ◽

2020 ◽

Vol 12 (3) ◽

pp. 307 ◽

Cited By ~ 1

Author(s):

Cheng Fu ◽

Shaotang Ye ◽

Yongbo Liu ◽

Shoujun Li

Keyword(s):

Innate Immunity ◽

Influenza Virus ◽

Cytokine Production ◽

Influenza Virus Infection ◽

Luciferase Assay ◽

Canine Influenza Virus ◽

Card Domain ◽

Canine Influenza ◽

Receptor Family

MDA5 belongs to the RIG-I-like receptor family, which is involved in innate immunity. During viral infection, MDA5 generates an antiviral response by recognizing the ligand to activate interferon. However, the role and mechanism of MDA5 in canine influenza virus (CIV) infection are unclear. To understand the mechanism of canine MDA5-mediated innate immunity during CIV infection, we detected the distribution of MDA5 in beagles, and the structural prediction showed that MDA5 was mainly composed of a CARD domain, RD domain, and DExD/H helix structure. Moreover, we found that MDA5 inhibits CIV replication. Furthermore, in the dual luciferase assay, we revealed that the CARD region of MDA5 strongly activated the IFN-β promoter and mainly transmitted signals through the CARD region. Overexpression of the CARD region of MDA5 revealed that the MDA5-mediated signaling pathway could transmit signals by activating the IRF3/NF-κB and IRF3 promoters, promoting the expression of antiviral proteins and cytokine release, thereby inhibiting CIV replication. Upon silencing of MDA5, cytokine production decreased, while the replication ability of CIV was increased. Thus, this study revealed a novel mechanism by which MDA5 mediated CIV infection and provided new avenues for the development of antiviral strategies.

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