ArticleVirus genes2018
Genetic characterization of H9N2 avian influenza viruses isolated from poultry in Poland during 2013/2014.
Article in Virus genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Mutual antagonism of mouse-adaptation mutations in HA and PA proteins on H9N2 virus replication.Virologica Sinica · 2024Article
- Review
- Non-basic amino acids in the hemagglutinin proteolytic cleavage site of a European H9N2 avian influenza virus modulate virulence in turkeys.Scientific reports · 2020Article
- Assessing the efficacy of a recombinant H9N2 avian influenza virus-inactivated vaccine.Poultry science · 2020Article
- Article
- A Global Perspective on H9N2 Avian Influenza Virus.Viruses · 2019Review
- Effect of experimental infectious bursal disease virus on clinical signs and pathogenesis of avian influenza virus HVeterinary research forum : an international quarterly journal · 2019Article
- Avian influenza overview November 2017 - February 2018.EFSA journal. European Food Safety Authority · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The study presents molecular characterization of H9N2 avian influenza (AI) isolates from field outbreaks in turkeys that occurred in Poland in 2013-2014. Sequences of all gene segments of one isolate from 2013 (A/turkey/Poland/14/2013(H9N2)) and two isolates from 2014 (A/turkey/Poland/08/2014(H9N2), A/turkey/Poland/09/2014(H9N2)) were obtained and analyzed in search of the phylogenetic relationship and molecular markers of zoonotic potential or increased pathogenicity. All gene segments were shown to originate from the wild bird reservoir and the close relationship of the analyzed isolates proved the link between the outbreaks in 2013 and 2014. However, remarkable molecular differences between isolates from 2013 to 2014 were identified, including mutation in the HA cleavage site (CS) leading to conversion from the PAASNR*GLF to the PAASKR*GLF motif and truncation of the PB1-F2 protein. Additionally, T97I substitution in the PA protein in A/turkey/Poland/08/2014 was detected which can be responsible for enhanced activity of viral polymerase in mammalian cells. However, experimental infection of mice with both isolates from 2014 showed their low pathogenicity, and no statistically significant differences in virus replication were observed between the viruses. Nevertheless, these findings indicate the dynamic evolution of H9N2 in the field emphasizing the need for monitoring of the situation in terms of H9N2 AI in Europe.
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