scholarly journals Characterization of Canine Influenza Virus A (H3N2) Circulating in Dogs in China from 2016 to 2018

Viruses ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2279
Author(s):  
Yuanguo Li ◽  
Xinghai Zhang ◽  
Yuxiu Liu ◽  
Ye Feng ◽  
Tiecheng Wang ◽  
...  

Avian H3N2 influenza virus follows cross-host transmission and has spread among dogs in Asia since 2005. After 2015–2016, a new H3N2 subtype canine influenza epidemic occurred in dogs in North America and Asia. The disease prevalence was assessed by virological and serological surveillance in dogs in China. Herein, five H3N2 canine influenza virus (CIV) strains were isolated from 1185 Chinese canine respiratory disease samples in 2017–2018; these strains were on the evolutionary branch of the North American CIVs after 2016 and genetically far from the classical canine H3N2 strain discovered in China before 2016. Serological surveillance showed an HI antibody positive rate of 6.68%. H3N2 was prevalent in the coastal areas and northeastern regions of China. In 2018, it became the primary epidemic strain in the country. The QK01 strain of H3N2 showed high efficiency in transmission among dogs through respiratory droplets. Nevertheless, the virus only replicated in the upper respiratory tract and exhibited low pathogenicity in mice. Furthermore, highly efficient transmission by direct contact other than respiratory droplet transmission was found in a guinea pig model. The low-level replication in avian species other than ducks could not facilitate contact and airborne transmission in chickens. The current results indicated that a novel H3N2 virus has become a predominant epidemic strain in dogs in China since 2016 and acquired highly efficient transmissibility but could not be replicated in avian species. Thus, further monitoring is required for designing optimal immunoprophylactic tools for dogs and estimating the zoonotic risk of CIV in China.

2013 ◽  
Vol 141 (12) ◽  
pp. 2595-2603 ◽  
Author(s):  
X. J. ZENG ◽  
Y. LIN ◽  
Y. B. ZHAO ◽  
C. P. LU ◽  
Y. J. LIU

SUMMARYCanine influenza virus (CIV) is an emerging pathogen that causes acute respiratory disease in dogs. The aim of this study was to investigate the pathogenicity of A/canine/Jiangsu/06/2010 (H3N2) virus isolated in China. Nine dogs were inoculated intranasally with 107·95 of 50% egg infectious dose (EID50) of the virus. The onset of clinical signs and virus shedding was observed on day 1 post-infection (p.i.). The peak clinical score occurred between days 4 and 6 p.i. The experimentally infected dogs were found to shed virus not only via the respiratory tract but also via the digestive tract. Viral RNA could be detected in multiple organs including the trachea, lung, liver, spleen, kidney, brain and duodenum. All the sampled organs from infected dogs showed significant lesions and viral antigen staining. The results differed from those reporting using previous CIV strains; the Chinese isolate could induce extrapulmonary infection and cause extensive lesions in dogs.


2010 ◽  
Vol 4 (4) ◽  
pp. 563-569 ◽  
Author(s):  
Nawarat Posuwan ◽  
Sunchai Payungporn ◽  
Aunyaratana Thontiravong ◽  
Pravina Kitikoon ◽  
Alongkorn Amonsin ◽  
...  

Abstract Background: A highly contagious respiratory disease in canines is infectious tracheobronchitis or kennel cough characterized by inflammation of the upper respiratory tract. The cause of kennel cough has been associated with multiple or complex agents such as canine adeno virus (CAV), canine influenza virus (CIV), canine distemper virus (CDV), and canine para influenzavirus (CPIV). Objective: Study the prevalence of canine respiratory viruses detected from in Thailand during 2008-2009. Methods: Nasal swab samples collected from 102 healthy dogs and 109 dogs with respiratory diseases. Then CAV, CIV, CDV, and CPIV were detected by in-house nested PCR and further confirmed by nucleotide sequencing. Results: Nested PCR showed that primers designed and used in this study yielded high specificity without any non-specific amplification. The prevalence of CAV, CIV, CDV and CPIV in healthy dogs was 0%, 2.94%, 2.94%, and 0.98%, whereas that found in dogs with respiratory diseases was 9.17%, 1.83%, 2.75%, and 11.93%, respectively. In healthy dogs, co-infection with CPIV + CDV was detected in only 0.98%. On the other hand, dogs with respiratory symptoms showed multiple infections with CAV + CIV in 1.83%, CIV + CPIV in 0.92%, CAV + CPIV in 1.83%, and CAV + CDV + CPIV in 0.92%. Conclusion: The prevalence data obtained from this study may be useful for outbreak preventions and to raise awareness of potential transmission of the newly emerged canine influenza virus to humans.


2018 ◽  
Vol 92 (8) ◽  
Author(s):  
Hailiang Sun ◽  
Sherry Blackmon ◽  
Guohua Yang ◽  
Kaitlyn Waters ◽  
Tao Li ◽  
...  

Viruses ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 565
Author(s):  
Yun Zheng ◽  
Xiangqi Hao ◽  
Qingxu Zheng ◽  
Xi Lin ◽  
Xin Zhang ◽  
...  

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.


2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
Laura V. Ashton ◽  
Robert L. Callan ◽  
Sangeeta Rao ◽  
Gabriele A. Landolt

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.


Virus Genes ◽  
2014 ◽  
Vol 49 (3) ◽  
pp. 393-399 ◽  
Author(s):  
Heidi L. Pecoraro ◽  
Susi Bennett ◽  
Miranda E. Spindel ◽  
Gabriele A. Landolt

Viruses ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 307 ◽  
Author(s):  
Cheng Fu ◽  
Shaotang Ye ◽  
Yongbo Liu ◽  
Shoujun Li

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.


Virus Genes ◽  
2013 ◽  
Vol 46 (3) ◽  
pp. 554-557 ◽  
Author(s):  
Shuo Su ◽  
Ziguo Yuan ◽  
Jidang Chen ◽  
Jiexiong Xie ◽  
Huatao Li ◽  
...  

2020 ◽  
Vol 7 ◽  
Author(s):  
Yongbo Liu ◽  
Cheng Fu ◽  
Shaotang Ye ◽  
Yingxin Liang ◽  
Zhonghe Qi ◽  
...  

Avian-origin H3N2 canine influenza viruses (CIVs) cause severe contagious respiratory disease in dogs, and quickly adapt to new environments. To further understand the mechanism of virus infection and host-virus interactions, we characterized the complete phosphoproteome of dogs infected with H3N2 CIV. Nine-week-old Beagle dogs were inoculated intranasally with 106 EID50 of A/canine/Guangdong/04/2014 (H3N2) virus. Lung sections were harvested at 5 days post-inoculation (dpi) and processed for global and quantitative analysis of differentially expressed phosphoproteins. A total of 1,235 differentially expressed phosphorylated proteins were identified in the dog lung after H3N2 CIV infection, and 3,016 modification sites were identified among all differentially expressed proteins. We then performed an enrichment analysis of functional annotations using Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene ontology (GO) database analyses to predict the functions of the identified differential phosphoproteins. Our data indicate that H3N2 CIV infection causes dramatic changes in the host protein phosphorylation of dog lungs. To our knowledge, this is the first study to assess the effect of H3N2 CIV infection on the phosphoproteome of beagles. These data provide novel insights into H3N2-CIV-triggered regulatory phosphorylation circuits and signaling networks and may improve our understanding of the mechanisms underlying CIV pathogenesis in dogs.


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