Detection of reassortant avian influenza A (H11N9) virus in wild birds in China

Ge, Yuejing; Yao, Qiucheng; Wang, Xianfu; Chai, Hongliang; Chen, Hualan; Yue, Hua

doi:10.1111/tbed.13044

Cited by 4 publications

(6 citation statements)

References 20 publications

(33 reference statements)

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“…This observation suggested that cocirculation of these viruses may predispose toward reassortment events to produce further genotypes with unknown disease risks to both poultry and humans. The continued circulation of H7N9 and H9N2 viruses with other AIV subtypes, enzootic in farmed and wild bird populations, has resulted in emergence of novel reassortant viruses with variable pathogenesis, along with the potential for mammalian adaptation and zoonotic transmission ( 17 – 23 ).…”

Section: Introductionmentioning

confidence: 99%

Coinfection of Chickens with H9N2 and H7N9 Avian Influenza Viruses Leads to Emergence of Reassortant H9N9 Virus with Increased Fitness for Poultry and a Zoonotic Potential

Bhat

James

Sadeyen

et al. 2022

J Virol

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An H7N9 low pathogenicity avian influenza virus (LPAIV) emerged in 2013 through genetic reassortment between H9N2 and other LPAIVs circulating in birds in China. This virus causes inapparent clinical disease in chickens, but zoonotic transmission results in severe and fatal disease in humans. To examine a natural reassortment scenario between H7N9 and G1 lineage H9N2 viruses predominant in the Indian sub-continent, we performed an experimental co-infection of chickens with A/Anhui/1/2013/H7N9 (Anhui/13) virus and A/Chicken/Pakistan/UDL-01/2008/H9N2 (UDL/08) virus. Plaque purification and genotyping of the reassortant viruses shed via oropharynx of contact chickens showed H9N2 and H9N9 as predominant subtypes. The reassortant viruses shed by contact chickens also showed selective enrichment of polymerase genes from H9N2 virus. The viable ‘6+2’ reassortant H9N9 (having NP, NA from H7N9 and remaining genes from H9N2) was successfully shed from the oropharynx of contact chickens, plus it showed an increased replication rate in human A549 cells and a significantly higher receptor binding to α2,6 and α2,3 sialoglycans compared to H9N2. The reassortant H9N9 virus also had a lower fusion pH, replicated in directly infected ferrets at similar levels compared to H7N9 and transmitted via direct contact. Ferrets exposed to H9N9 via aerosol contact were also found to be seropositive, compared to H7N9 aerosol contact ferrets. To the best of our knowledge, this is the first study demonstrating that co-circulation of H7N9 and G1 lineage H9N2 viruses could represent a threat for the generation of novel reassortant H9N9 viruses with greater virulence in poultry and a zoonotic potential. Importance We evaluated the consequences of reassortment between the H7N9 and the contemporary H9N2 viruses of G1 lineage that are enzootic in poultry across the Indian sub-continent and the Middle East. Co-infection of chickens with these viruses resulted in emergence of novel reassortant H9N9 viruses with genes derived from both H9N2 and H7N9 viruses. The ‘6+2’ reassortant H9N9 (having NP and NA from H7N9) virus was shed from contact chickens in a significantly higher proportion compared to most of the reassortant viruses, showed significantly increased replication fitness in human A549 cells, receptor binding towards human (α2,6) and avian (α2,3) sialic acid receptor analogues and the potential to transmit via contact among ferrets. This study demonstrated the ability of viruses that already exist in nature to exchange genetic material, highlighting the potential emergence of viruses from these subtypes with zoonotic potential.

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Section: Introductionmentioning

confidence: 99%

Coinfection of Chickens with H9N2 and H7N9 Avian Influenza Viruses Leads to Emergence of Reassortant H9N9 Virus with Increased Fitness for Poultry and a Zoonotic Potential

Bhat

James

Sadeyen

et al. 2022

J Virol

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“…Notably, the H11 HA and N9 NA genes showed high sequence similarity to the corresponding genes of isolates from wild birds in South Africa and Spain, respectively, and did not cluster in the major groups with recent wild-bird isolates from East Asia, suggesting that dynamic movements of wild birds in Japan occur in the Izumi plain. Previously, H11N9 in China was detected from avian birds in 2006-2015 and in environmental samples from live poultry markets in China in 2016 [69]. This indicates that Chinese H11N9 obtained the potential for transmission from avians to poultry.…”

Section: Discussionmentioning

confidence: 96%

“…H11N9 has been found in wild birds in Brazil, Europe, and Japan [14,17,19,21,22,69,70]. Japan is an overwintering site of endangered cranes (hooded cranes and white-naped cranes) and many other migratory birds (including wild ducks), which are considered as carriers of AIVs [70].…”

Section: Discussionmentioning

confidence: 99%

Genetic Characterization of Avian Influenza A (H11N9) Virus Isolated from Mandarin Ducks in South Korea in 2018

Tuong

Nguyen

Sung

et al. 2020

Viruses

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In July 2018, a novel avian influenza virus (A/Mandarin duck/South Korea/KNU18-12/2018(H11N9)) was isolated from Mandarin ducks in South Korea. Phylogenetic and molecular analyses were conducted to characterize the genetic origins of the H11N9 strain. Phylogenetic analysis indicated that eight gene segments of strain H11N9 belonged to the Eurasian lineages. Analysis of nucleotide sequence similarity of both the hemagglutinin (HA) and neuraminidase (NA) genes revealed the highest homology with A/duck/Kagoshima/KU57/2014 (H11N9), showing 97.70% and 98.00% nucleotide identities, respectively. Additionally, internal genes showed homology higher than 98% compared to those of other isolates derived from duck and wild birds. Both the polymerase acidic (PA) and polymerase basic 1 (PB1) genes were close to the H5N3 strain isolated in China; whereas, other internal genes were closely related to that of avian influenza virus in Japan. A single basic amino acid at the HA cleavage site (PAIASR↓GLF), the lack of a five-amino acid deletion (residue 69–73) in the stalk region of the NA gene, and E627 in the polymerase basic 2 (PB2) gene indicated that the A/Mandarin duck/South Korea/KNU18-12/2018(H11N9) isolate was a typical low-pathogenicity avian influenza. In vitro viral replication of H11N9 showed a lower titer than H1N1 and higher than H9N2. In mice, H11N9 showed lower adaptation than H1N1. The novel A/Mandarin duck/South Korea/KNU18-12/2018(H11N9) isolate may have resulted from an unknown reassortment through the import of multiple wild birds in Japan and Korea in approximately 2016–2017, evolving to produce a different H11N9 compared to the previous H11N9 in Korea (2016). Further reassortment events of this virus occurred in PB1 and PA in China-derived strains. These results indicate that Japanese- and Chinese-derived avian influenza contributes to the genetic diversity of A/Mandarin duck/South Korea/KNU18-12/2018(H11N9) in Korea.

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“…First, poultry infected with H9N2 AIV will display clinical symptoms such as egg reduction. Typically, a substantial amount of poultry is kept in large and intensive environments on farms, and due to the high transmissibility of low-pathogenicity avian influenza virus, the economic impact of an outbreak of AIV can be incredibly damaging [3][4][5]. In addition, chickens infected with AIV are more likely to be coinfected with other pathogens due to the low resistance of the immune system, resulting in a high fatality rate [6,7].…”

Section: Introductionmentioning

confidence: 99%

Effects of the Glycosylation of the HA Protein of H9N2 Subtype Avian Influenza Virus on the Pathogenicity in Mice and Antigenicity

Liang,

Fan,

Meng

et al. 2024

Transboundary and Emerging Diseases

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As the H9N2 subtype avian influenza virus (H9N2 AIV) evolves naturally, mutations in the hemagglutinin (HA) protein still occur, which involves some sites with glycosylations. It is widely established that glycosylation of the H9N2 AIV HA protein has a major impact on the antigenicity and pathogenicity of the virus. However, the biological implications of a particular glycosylation modification site (GMS) have not been well investigated. In this study, we generated viruses with different GMSs based on wild-type (WT) viruses. Antigenicity studies revealed that the presence of viruses with a 200G+/295G− mutation (with glycosylation at position 200 and deletion of glycosylation at position 295 in the HA protein) combined with a single GMS, such as 87G+, 127G+, 148G+, 178G+, or 265G+, could significantly affect the antigenicity of the virus. Pathogenicity assays revealed that the addition of GMS, such as 127G+, 188G+, 148G+, 178G+, or 54G+, decreased the virulence of the virus in mice, except for 87G+. The removal of GMS, such as 280G− or 295G−, increased the pathogenicity of the virus in mice. Further studies on pathogenicity revealed that 87G+/295G− could also enhance the pathogenicity of the virus. Finally, we selected the WT, WT-87G+, WT-295G−, and WT-87G+/295G− strains as our further research targets to investigate the detailed biological properties of the viruses. GMS, which can enhance viral pathogenicity, did not significantly affect replication or viral stability in vitro but significantly promoted the expression of proinflammatory factors to enhance inflammatory responses in mouse lungs. These findings further deepen our understanding of the influence of the glycosylation of the HA protein of H9N2 AIV on the pathogenicity and antigenicity of the virus in mice.

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Detection of reassortant avian influenza A (H11N9) virus in wild birds in China

Cited by 4 publications

References 20 publications

Coinfection of Chickens with H9N2 and H7N9 Avian Influenza Viruses Leads to Emergence of Reassortant H9N9 Virus with Increased Fitness for Poultry and a Zoonotic Potential

Coinfection of Chickens with H9N2 and H7N9 Avian Influenza Viruses Leads to Emergence of Reassortant H9N9 Virus with Increased Fitness for Poultry and a Zoonotic Potential

Genetic Characterization of Avian Influenza A (H11N9) Virus Isolated from Mandarin Ducks in South Korea in 2018

Effects of the Glycosylation of the HA Protein of H9N2 Subtype Avian Influenza Virus on the Pathogenicity in Mice and Antigenicity

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