Evidence for Subclinical Influenza A(H1N1)pdm09 Virus Infection among Dogs in Guangdong Province, China

Su, Shuo; Chen, Jidang; Jia, Kun; Khan, Salah Ud‐Din; He, Shuilin; Fu, Xinliang; Hong, Malin; Sun, Li; Qi, Wenbao; Gray, Gregory C.; Li, Shoujun

doi:10.1128/jcm.03522-13

Cited by 21 publications

(11 citation statements)

References 21 publications

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“…The continued interspecies transmission of IAVs to humans and other mammals is a constant threat (4,(39)(40)(41). As dogs are popular companion animals and can support the replication of multiple IAV subtypes such as H3N8, H3N1, H3N2, H5N1, H5N2, and H1N1 (10,11,(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53), they could act as intermediate hosts for IAV reassortment or human exposure (7). Various human IAVs, such as PR8, A/Udorn/307/72 H3N2, and pH1N1, replicate in the respiratory tract of the dog, and viable reassortant viruses between H3N8 CIV and pH1N1 IAV have been reported (54).…”

Section: Discussionmentioning

confidence: 99%

The K186E Amino Acid Substitution in the Canine Influenza Virus H3N8 NS1 Protein Restores Its Ability To Inhibit Host Gene Expression

Nogales

Chauché

DeDiego

et al. 2017

J Virol

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Canine influenza viruses (CIVs) are the causative agents of canine influenza, a contagious respiratory disease in dogs, and include the equine-origin H3N8 and the avian-origin H3N2 viruses. Influenza A virus (IAV) nonstructural protein 1 (NS1) is a virulence factor essential for counteracting the innate immune response. Here, we evaluated the ability of H3N8 CIV NS1 to inhibit host innate immune responses. We found that H3N8 CIV NS1 was able to efficiently counteract interferon (IFN) responses but was unable to block general gene expression in human or canine cells. Such ability was restored by a single amino acid substitution in position 186 (K186E) that resulted in NS1 binding to the 30-kDa subunit of the cleavage and polyadenylation specificity factor (CPSF30), a cellular protein involved in pre-mRNA processing. We also examined the frequency distribution of K186 and E186 among H3N8 CIVs and equine influenza viruses (EIVs), the ancestors of H3N8 CIV, and experimentally determined the impact of amino acid 186 in the ability of different CIV and EIV NS1s to inhibit general gene expression. In all cases, the presence of E186 was responsible for the control of host gene expression. In contrast, the NS1 protein of H3N2 CIV harbors E186 and blocks general gene expression in canine cells. Altogether, our results confirm previous studies on the strain-dependent ability of NS1 to block general gene expression. Moreover, the observed polymorphism on amino acid 186 between H3N8 and H3N2 CIVs might be the result of adaptive changes acquired during long-term circulation of avian-origin IAVs in mammals. Canine influenza is a respiratory disease of dogs caused by two CIV subtypes, the H3N8 and H3N2 viruses, of equine and avian origins, respectively. Influenza NS1 is the main viral factor responsible for the control of host innate immune responses, and changes in NS1 can play an important role in host adaptation. Here we assessed the ability of H3N8 CIV NS1 to inhibit host innate immune responses and gene expression. The H3N8 CIV NS1 did not block host gene expression, but this activity was restored by a single amino acid substitution (K186E), which was responsible for NS1 binding to the host factor CPSF30. In contrast, the H3N2 CIV NS1, which contains E186, blocks general gene expression. Our results suggest that the ability to block host gene expression is not required for influenza virus replication in mammals but might be important in the long-term adaptation of avian-origin influenza viruses to mammals.

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Section: Discussionmentioning

confidence: 99%

The K186E Amino Acid Substitution in the Canine Influenza Virus H3N8 NS1 Protein Restores Its Ability To Inhibit Host Gene Expression

Nogales

Chauché

DeDiego

et al. 2017

J Virol

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“…Interspecies transmission from human to dog or from avian to dog has been repeatedly observed. Historically, dogs have been reported to be infected with human seasonal H3N2, pandemic 2009 H1N1 viruses, equine H3N8, highly pathogenic avian influenza virus (HPAI) H5N1, lowly pathogenic avian influenza virus (LPAI) H9N2, and more recently, AIV H10N8 (Crawford et al, 2005 ; Songserm et al, 2006 ; Sun et al, 2013 , 2014 ; Su et al, 2014b , d ; Yin et al, 2014 ). Most of these belong to sporadic infections and the viruses could not become efficiently transmitted among dogs.…”

Section: Introductionmentioning

confidence: 99%

Global and quantitative proteomic analysis of dogs infected by avian-like H3N2 canine influenza virus

Jin

Hong

et al. 2015

Front. Microbiol.

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Canine influenza virus A (H3N2) is a newly emerged etiological agent for respiratory infections in dogs. The mechanism of interspecies transmission from avian to canine species and the development of diseases in this new host remain to be explored. To investigate this, we conducted a differential proteomics study in 2-month-old beagles inoculated intranasally with 106 TCID50 of A/canine/Guangdong/01/2006 (H3N2) virus. Lung sections excised at 12 h post-inoculation (hpi), 4 days, and 7 days post-inoculation (dpi) were processed for global and quantitative analysis of differentially expressed proteins. A total of 17,796 proteins were identified at different time points. About 1.6% was differentially expressed between normal and infected samples. Of these, 23, 27, and 136 polypeptides were up-regulated, and 14, 18, and 123 polypeptides were down-regulated, at 12 hpi, 4 dpi, and 7 dpi, respectively. Vann diagram analysis indicated that 17 proteins were up-regulated and one was down-regulated at all three time points. Selected proteins were validated by real-time PCR and by Western blot. Our results show that apoptosis and cytoskeleton-associated proteins expression was suppressed, whereas interferon-induced proteins plus other innate immunity proteins were induced after the infection. Understanding of the interactions between virus and the host will provide insights into the basis of interspecies transmission, adaptation, and virus pathogenicity.

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“…Further evidence that dogs can be infected with human influenza viruses comes from serological analyses [11, 12], as well as experimental infections [13, 14]. Influenza viruses have a segmented genome, which allows for reassortment in coinfected hosts and emergence of novel influenza virus strains.…”

mentioning

confidence: 99%

Assessment of Molecular, Antigenic, and Pathological Features of Canine Influenza A(H3N2) Viruses That Emerged in the United States

Pulit-Penaloza

Simpson

Yang

et al. 2017

The Journal of Infectious Diseases

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Background A single subtype of canine influenza virus (CIV), A(H3N8), was circulating in the United States until a new subtype, A(H3N2), was detected in Illinois in spring 2015. Since then, this CIV has caused thousands of infections in dogs in multiple states. Methods In this study, genetic and antigenic properties of the new CIV were evaluated. In addition, structural and glycan array binding features of the recombinant hemagglutinin were determined. Replication kinetics in human airway cells and pathogenesis and transmissibility in animal models were also assessed. Results A(H3N2) CIVs maintained molecular and antigenic features related to low pathogenicity avian influenza A(H3N2) viruses and were distinct from A(H3N8) CIVs. The structural and glycan array binding profile confirmed these findings and revealed avian-like receptor-binding specificity. While replication kinetics in human airway epithelial cells was on par with that of seasonal influenza viruses, mild-to-moderate disease was observed in infected mice and ferrets, and the virus was inefficiently transmitted among cohoused ferrets. Conclusions Further adaptation is needed for A(H3N2) CIVs to present a likely threat to humans. However, the potential for coinfection of dogs and possible reassortment of human and other animal influenza A viruses presents an ongoing risk to public health.

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Evidence for Subclinical Influenza A(H1N1)pdm09 Virus Infection among Dogs in Guangdong Province, China

Cited by 21 publications

References 21 publications

The K186E Amino Acid Substitution in the Canine Influenza Virus H3N8 NS1 Protein Restores Its Ability To Inhibit Host Gene Expression

The K186E Amino Acid Substitution in the Canine Influenza Virus H3N8 NS1 Protein Restores Its Ability To Inhibit Host Gene Expression

Global and quantitative proteomic analysis of dogs infected by avian-like H3N2 canine influenza virus

Assessment of Molecular, Antigenic, and Pathological Features of Canine Influenza A(H3N2) Viruses That Emerged in the United States

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