ArticleVirology journal2013
The PB2, PA, HA, NP, and NS genes of a highly pathogenic avian influenza virus A/whooper swan/Mongolia/3/2005 (H5N1) are responsible for pathogenicity in ducks.
Article in Virology journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- The Highly Interrelated Morbidity Respiratory Viruses Cause Among Humans and Animals in Mongolia.Viruses · 2025Review
- Long-term efficacy of an inactivated H5N1 whole-particle influenza vaccine in nonhuman primates.NPJ vaccines · 2025Article
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- Susceptibility of common dabbling and diving duck species to clade 2.3.2.1 H5N1 high pathogenicity avian influenza virus: an experimental infection study.The Journal of veterinary medical science · 2023Article
- Development of an Inactivated Avian Influenza Virus Vaccine against Circulating H9N2 in Chickens and Ducks.Vaccines · 2023Article
- Phylogenetic analysis, molecular changes, and adaptation to chickens of Mexican lineage H5N2 low-pathogenic avian influenza viruses from 1994 to 2019.Transboundary and emerging diseases · 2022Article
- Susceptibility of common family Anatidae bird species to clade 2.3.4.4e H5N6 high pathogenicity avian influenza virus: an experimental infection study.BMC veterinary research · 2022Article
- Prior infection with antigenically heterologous low pathogenic avian influenza viruses interferes with the lethality of the H5 highly pathogenic strain in domestic ducks.The Journal of veterinary medical science · 2021Article
- Amino acid substitutions in the H5N1 avian influenza haemagglutinin alter pH of fusion and receptor binding to promote a highly pathogenic phenotype in chickens.The Journal of general virology · 2021Article
- The pathogenicity and transmission of live bird market H2N2 avian influenza viruses in chickens, Pekin ducks, and guinea fowl.Veterinary microbiology · 2021Article
- Multiple Gene Segments Are Associated with Enhanced Virulence of Clade 2.3.4.4 H5N8 Highly Pathogenic Avian Influenza Virus in Mallards.Journal of virology · 2021Article
- Mutations in PB1, NP, HA, and NA Contribute to Increased Virus Fitness of H5N2 Highly Pathogenic Avian Influenza Virus Clade 2.3.4.4 in Chickens.Journal of virology · 2021Article
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- Loss of Fitness of Mexican H7N3 Highly Pathogenic Avian Influenza Virus in Mallards after Circulating in Chickens.Journal of virology · 2019Article
- A novel European H5N8 influenza A virus has increased virulence in ducks but low zoonotic potential.Emerging microbes & infections · 2018Article
- Comparison of the virulence and transmissibility of canine H3N2 influenza viruses and characterization of their canine adaptation factors.Emerging microbes & infections · 2018Article
- Infectivity, transmission and pathogenicity of H5 highly pathogenic avian influenza clade 2.3.4.4 (H5N8 and H5N2) United States index viruses in Pekin ducks and Chinese geese.Veterinary research · 2017Article
- Article
- PA-X decreases the pathogenicity of highly pathogenic H5N1 influenza A virus in avian species by inhibiting virus replication and host response.Journal of virology · 2015Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWild ducks are the natural hosts of influenza A viruses. Duck influenza, therefore, has been believed inapparent infection with influenza A viruses, including highly pathogenic avian influenza viruses (HPAIVs) in chickens. In fact, ducks experimentally infected with an HPAIV strain, A/Hong Kong/483/1997 (H5N1) (HK483), did not show any clinical signs. Another HPAIV strain, A/whooper swan/Mongolia/3/2005 (H5N1) (MON3) isolated from a dead swan, however, caused neurological dysfunction and death in ducks.
methodTo understand the mechanism whereby MON3 shows high pathogenicity in ducks, HK483, MON3, and twenty-four reassortants generated between these two H5N1 viruses were compared for their pathogenicity in domestic ducks.
resultsNone of the ducks infected with MON3-based single-gene reassortants bearing the PB2, NP, or NS gene segment of HK483 died, and HK483-based single-gene reassortants bearing PB2, NP, or NS genes of MON3 were not pathogenic in ducks, suggesting that multiple gene segments contribute to the pathogenicity of MON3 in ducks. All the ducks infected with the reassortant bearing PB2, PA, HA, NP, and NS gene segments of MON3 died within five days post-inoculation, as did those infected with MON3. Each of the viruses was assessed for replication in ducks three days post-inoculation. MON3 and multi-gene reassortants pathogenic in ducks were recovered from all of the tissues examined and replicated with high titers in the brains and lungs.
conclusionThe present results indicate that multigenic factors are responsible for efficient replication of MON3 in ducks. In particular, virus growth in the brain might correlate with neurological dysfunction and the disease severity.
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