scholarly journals Experimental Infection of Dogs with Avian-Origin Canine Influenza A Virus (H3N2)

2009 ◽  
Vol 15 (1) ◽  
pp. 56-58 ◽  
Author(s):  
Daesub Song ◽  
Chulseung Lee ◽  
Bokyu Kang ◽  
Kwonil Jung ◽  
Taehoon Oh ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Experimental Infection ◽  
Influenza A ◽  
Avian Origin ◽  
Canine Influenza ◽  
Canine Influenza A Virus

scholarly journals Complete Genome Sequence of an Avian-Origin H3N2 Canine Influenza A Virus Isolated in Farmed Dogs in Southern China

2012 ◽  
Vol 86 (18) ◽  
pp. 10238-10238 ◽  
Author(s):  
Shuo Su ◽  
Nan Cao ◽  
Jidang Chen ◽  
Furong Zhao ◽  
Huatao Li ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Genomic Sequence ◽  
Southern China ◽  
Phylogenetic Analyses ◽  
Influenza Viruses ◽  
Interspecies Transmission ◽  
Avian Origin ◽  
Canine Influenza ◽  
Canine Influenza A Virus

We report here the complete genomic sequence of an avian-origin H3N2 canine influenza A virus containing multiple mutations in farmed dogs in southern China. Phylogenetic analyses of the sequences of all eight viral RNA segments demonstrated that these are wholly avian influenza viruses of the Asia lineage. To our knowledge, this is the first report of interspecies transmission of an avian H3N2 influenza virus to domestic farm dogs under natural conditions in Southern China. The amino acid information provided herein suggests that continued study is required to determine if this virus could be established in the farm dog population and pose potential threats to public health.

scholarly journals No evidence of horizontal infection in horses kept in close contact with dogs experimentally infected with canine influenza A virus (H3N8)

2012 ◽  
Vol 54 (1) ◽  
Author(s):  
Takashi Yamanaka ◽  
Manabu Nemoto ◽  
Hiroshi Bannai ◽  
Koji Tsujimura ◽  
Takashi Kondo ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Close Contact ◽  
Canine Influenza ◽  
Canine Influenza A Virus

Genetic characterization of canine influenza A virus (H3N2) in Thailand

Virus Genes ◽  
2013 ◽  
Vol 48 (1) ◽  
pp. 56-63 ◽  
Author(s):  
Napawan Bunpapong ◽  
Nutthawan Nonthabenjawan ◽  
Supassama Chaiwong ◽  
Ratanaporn Tangwangvivat ◽  
Supanat Boonyapisitsopa ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Genetic Characterization ◽  
Canine Influenza ◽  
Canine Influenza A Virus

scholarly journals Multiple Incursions and Recurrent Epidemic Fade-Out of H3N2 Canine Influenza A Virus in the United States

2018 ◽  
Vol 92 (16) ◽  
Author(s):  
Ian E. H. Voorhees ◽  
Benjamin D. Dalziel ◽  
Amy Glaser ◽  
Edward J. Dubovi ◽  
Pablo R. Murcia ◽  
...  
Keyword(s):  
United States ◽  
Influenza A ◽  
The United States ◽  
Whole Genome Sequence ◽  
Whole Genome ◽  
Canine Influenza Virus ◽  
Emerging Virus ◽  
Avian Origin ◽  
Canine Influenza ◽  
Comprehensive Surveillance

ABSTRACT Avian-origin H3N2 canine influenza virus (CIV) transferred to dogs in Asia around 2005, becoming enzootic throughout China and South Korea before reaching the United States in early 2015. To understand the posttransfer evolution and epidemiology of this virus, particularly the cause of recent and ongoing increases in incidence in the United States, we performed an integrated analysis of whole-genome sequence data from 64 newly sequenced viruses and comprehensive surveillance data. This revealed that the circulation of H3N2 CIV within the United States is typified by recurrent epidemic burst–fade-out dynamics driven by multiple introductions of virus from Asia. Although all major viral lineages displayed similar rates of genomic sequence evolution, H3N2 CIV consistently exhibited proportionally more nonsynonymous substitutions per site than those in avian reservoir viruses, which is indicative of a large-scale change in selection pressures. Despite these genotypic differences, we found no evidence of adaptive evolution or increased viral transmission, with epidemiological models indicating a basic reproductive number, R0, of between 1 and 1.5 across nearly all U.S. outbreaks, consistent with maintained but heterogeneous circulation. We propose that CIV's mode of viral circulation may have resulted in evolutionary cul-de-sacs, in which there is little opportunity for the selection of the more transmissible H3N2 CIV phenotypes necessary to enable circulation through a general dog population characterized by widespread contact heterogeneity. CIV must therefore rely on metapopulations of high host density (such as animal shelters and kennels) within the greater dog population and reintroduction from other populations or face complete epidemic extinction. IMPORTANCE The relatively recent appearance of influenza A virus (IAV) epidemics in dogs expands our understanding of IAV host range and ecology, providing useful and relevant models for understanding critical factors involved in viral emergence. Here we integrate viral whole-genome sequence analysis and comprehensive surveillance data to examine the evolution of the emerging avian-origin H3N2 canine influenza virus (CIV), particularly the factors driving ongoing circulation and recent increases in incidence of the virus within the United States. Our results provide a detailed understanding of how H3N2 CIV achieves sustained circulation within the United States despite widespread host contact heterogeneity and recurrent epidemic fade-out. Moreover, our findings suggest that the types and intensities of selection pressures an emerging virus experiences are highly dependent on host population structure and ecology and may inhibit an emerging virus from acquiring sustained epidemic or pandemic circulation.

scholarly journals H5N1 Influenza A Virus PB1-F2 Relieves HAX-1-Mediated Restriction of Avian Virus Polymerase PA in Human Lung Cells

2018 ◽  
Vol 92 (11) ◽  
pp. e00425-18 ◽  
Author(s):  
B. Mazel-Sanchez ◽  
I. Boal-Carvalho ◽  
F. Silva ◽  
R. Dijkman ◽  
M. Schmolke
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Influenza Viruses ◽  
Zoonotic Transmission ◽  
Restriction Factor ◽  
Influenza A Viruses ◽  
Human Lung Cells ◽  
Enzymatic Function ◽  
H5n1 Influenza ◽  
Avian Origin

ABSTRACTHighly pathogenic influenza A viruses (IAV) from avian hosts were first reported to directly infect humans 20 years ago. However, such infections are rare events, and our understanding of factors promoting or restricting zoonotic transmission is still limited. One accessory protein of IAV, PB1-F2, was associated with pathogenicity of pandemic and zoonotic IAV. This short (90-amino-acid) peptide does not harbor an enzymatic function. We thus identified host factors interacting with H5N1 PB1-F2, which could explain its importance for virulence. PB1-F2 binds to HCLS1-associated protein X1 (HAX-1), a recently identified host restriction factor of the PA subunit of IAV polymerase complexes. We demonstrate that the PA of a mammal-adapted H1N1 IAV is resistant to HAX-1 imposed restriction, while the PA of an avian-origin H5N1 IAV remains sensitive. We also showed HAX-1 sensitivity for PAs of A/Brevig Mission/1/1918 (H1N1) and A/Shanghai/1/2013 (H7N9), two avian-origin zoonotic IAV. Inhibition of H5N1 polymerase by HAX-1 can be alleviated by its PB1-F2 through direct competition. Accordingly, replication of PB1-F2-deficient H5N1 IAV is attenuated in the presence of large amounts of HAX-1. Mammal-adapted H1N1 and H3N2 viruses do not display this dependence on PB1-F2 for efficient replication in the presence of HAX-1. We propose that PB1-F2 plays a key role in zoonotic transmission of avian H5N1 IAV into humans.IMPORTANCEAquatic and shore birds are the natural reservoir of influenza A viruses from which the virus can jump into a variety of bird and mammal host species, including humans. H5N1 influenza viruses are a good model for this process. They pose an ongoing threat to human and animal health due to their high mortality rates. However, it is currently unclear what restricts these interspecies jumps on the host side or what promotes them on the virus side. Here we show that a short viral peptide, PB1-F2, helps H5N1 bird influenza viruses to overcome a human restriction factor of the viral polymerase complex HAX-1. Interestingly, we found that human influenza A virus polymerase complexes are already adapted to HAX-1 and do not require this function of PB1-F2. We thus propose that a functional full-length PB1-F2 supports direct transmission of bird viruses into humans.

scholarly journals Genetic and serologic surveillance of canine (CIV) and equine (EIV) influenza virus in Nuevo León State, México

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e8239
Author(s):  
Claudia B. Plata-Hipólito ◽  
Sibilina Cedillo-Rosales ◽  
Nelson Obregón-Macías ◽  
Carlos E. Hernández-Luna ◽  
Cristina Rodríguez-Padilla ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Influenza A Virus ◽  
Influenza A ◽  
Companion Animals ◽  
Enzyme Linked Immunosorbent Assay ◽  
Nuevo Leon ◽  
Stray Dogs ◽  
Matrix Gene ◽  
Nuevo León ◽  
Canine Influenza

Background Despite the uncontrolled distribution of the Influenza A virus through wild birds, the detection of canine influenza virus and equine influenza virus in Mexico was absent until now. Recently, outbreaks of equine and canine influenza have been reported around the world; the virus spreads quickly among animals and there is potential for zoonotic transmission. Methods Amplification of the Influenza A virus matrix gene from necropsies, nasal and conjunctival swabs from trash service horses and pets/stray dogs was performed through RT-PCR. The seroprevalence was carried out through Sandwich enzyme-linked immunosorbent assay system using the M1 recombinant protein and polyclonal antibodies anti-M1. Results The matrix gene was amplified from 13 (19.11%) nasal swabs, two (2.94%) conjunctival swabs and five (7.35%) lung necropsies, giving a total of 20 (29.41%) positive samples in a pet dog population. A total of six (75%) positive samples of equine nasal swab were amplified. Sequence analysis showed 96–99% identity with sequences of Influenza A virus matrix gene present in H1N1, H1N2 and H3N2 subtypes. The phylogenetic analysis of the sequences revealed higher identity with matrix gene sequences detected from zoonotic isolates of subtype H1N1/2009. The detection of anti-M1 antibodies in stray dogs showed a prevalence of 123 (100%) of the sampled population, whereas in horses, 114 (92.68%) positivity was obtained. Conclusion The results unveil the prevalence of Influenza A virus in the population of horses and dogs in the state of Nuevo Leon, which could indicate a possible outbreak of equine and Canine Influenza in Mexico. We suggest that the prevalence of Influenza virus in companion animals be monitored to investigate its epizootic and zoonotic potential, in addition to encouraging the regulation of vaccination in these animal species in order to improve their quality of life.

scholarly journals Avian-origin H3N2 canine influenza A viruses in Southern China

2010 ◽  
Vol 10 (8) ◽  
pp. 1286-1288 ◽  
Author(s):  
Shoujun Li ◽  
Zhihai Shi ◽  
Peirong Jiao ◽  
Guihong Zhang ◽  
Zhiwen Zhong ◽  
...  
Keyword(s):  
Influenza A ◽  
Southern China ◽  
Influenza A Viruses ◽  
Avian Origin ◽  
Canine Influenza

scholarly journals Influenza Viruses in Mice: Deep Sequencing Analysis of Serial Passage and Effects of Sialic Acid Structural Variation

2019 ◽  
Vol 93 (23) ◽  
Author(s):  
Brian R. Wasik ◽  
Ian E. H. Voorhees ◽  
Karen N. Barnard ◽  
Brynn K. Alford-Lawrence ◽  
Wendy S. Weichert ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Sialic Acid ◽  
Influenza A Virus ◽  
Deep Sequencing ◽  
Influenza A ◽  
Natural Host ◽  
H1n1 Pandemic ◽  
Influenza A Viruses ◽  
Canine Influenza Virus ◽  
Canine Influenza

ABSTRACT Influenza A viruses have regularly jumped to new host species to cause epidemics or pandemics, an evolutionary process that involves variation in the viral traits necessary to overcome host barriers and facilitate transmission. Mice are not a natural host for influenza virus but are frequently used as models in studies of pathogenesis, often after multiple passages to achieve higher viral titers that result in clinical disease such as weight loss or death. Here, we examine the processes of influenza A virus infection and evolution in mice by comparing single nucleotide variations of a human H1N1 pandemic virus, a seasonal H3N2 virus, and an H3N2 canine influenza virus during experimental passage. We also compared replication and sequence variation in wild-type mice expressing N-glycolylneuraminic acid (Neu5Gc) with those seen in mice expressing only N-acetylneuraminic acid (Neu5Ac). Viruses derived from plasmids were propagated in MDCK cells and then passaged in mice up to four times. Full-genome deep sequencing of the plasmids, cultured viruses, and viruses from mice at various passages revealed only small numbers of mutational changes. The H3N2 canine influenza virus showed increases in frequency of sporadic mutations in the PB2, PA, and NA segments. The H1N1 pandemic virus grew well in mice, and while it exhibited the maintenance of some minority mutations, there was no clear evidence for adaptive evolution. The H3N2 seasonal virus did not establish in the mice. Finally, there were no clear sequence differences associated with the presence or absence of Neu5Gc. IMPORTANCE Mice are commonly used as a model to study the growth and virulence of influenza A viruses in mammals but are not a natural host and have distinct sialic acid receptor profiles compared to humans. Using experimental infections with different subtypes of influenza A virus derived from different hosts, we found that evolution of influenza A virus in mice did not necessarily proceed through the linear accumulation of host-adaptive mutations, that there was variation in the patterns of mutations detected in each repetition, and that the mutation dynamics depended on the virus examined. In addition, variation in the viral receptor, sialic acid, did not affect influenza virus evolution in this model. Overall, our results show that while mice provide a useful animal model for influenza virus pathology, host passage evolution will vary depending on the specific virus tested.

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