Molecular characterization, receptor binding property, and replication in chickens and mice of H9N2 avian influenza viruses isolated from chickens, peafowls, and wild birds in eastern China

Guo, Jing; Wang, Yanwen; Zhao, Conghui; Gao, Xinxin; Zhang, Yaping; Li, Jiqing; Wang, Mengjing; Zhang, Hong; Liu, Wenqiang; Wang, Chao; Xia, Yingju; Xu, Lu; He, Guimei; Shen, Jinyan; Sun, Xiaohong; Wang, Wenting; Han, Xinyu; Zhang, Xiaoxuan; Hou, Zhengyang; Jin, Xinlin; Peng, Na; Li, Yubao; Deng, Guohua; Cui, Pengfei; Zhang, Qianyi; Li, Xuyong; Chen, Hualan

doi:10.1080/22221751.2021.1999778

Cited by 34 publications

(26 citation statements)

References 53 publications

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“…In particular, the wild-bird H9N2-like viruses that circulated in Shandong Province in 2019 contributed to the emergence of the reassortant H10N4 and H10N8 viruses as gene donors (Fig. S1 and S2) ( 4 ). Accordingly, SW/W3875/20 is a novel H10N8 reassortant of H10Nx, H5N8, H9N2-like, and other wild-bird viruses.…”

Section: Resultsmentioning

confidence: 99%

“…These replication and transmission studies in chickens and ducks indicated that circulating novel H10 viruses in migratory birds have a high potential risk of transmission to domestic poultry introduced by fecal droppings or the contaminated environment. The silent replication of H10 viruses in birds without clinical symptoms contributes to the generation of novel reassortant progeny viruses with other predominant subtypes, such as the widely prevalent H9N2 viruses in wild birds and poultry ( 4 , 57 ). In summary, active surveillance in both wild birds and poultry will contribute to the monitoring of the invasion and prevalence of the H10N4 and H10N8 viruses in migratory waterfowl and poultry, especially for reducing the potential transmission risk of these H10 reassortants from birds to humans.…”

Section: Discussionmentioning

confidence: 99%

“…AIVs in different wild birds pose an increasing threat to poultry and public health due to their worldwide prevalence and occasional cross-species infection ( 2 ). In the past 2 decades, the avian-origin H5N1, H5N6, H7N9, and H9N2 viruses have acquired the ability to infect mammals without prior adaptation and have led to more than 2,000 human infections in total ( 3 – 8 ). The H5Nx (H5N1, H5N2, H5N3, H5N5, H5N6, H5N8) viruses have evolved to form 10 clades and more than 20 subclades and subbranches and have continually reassorted with other subtypes of AIVs to generate different novel subtypes and genotypes ( 9 – 16 ).…”

Section: Introductionmentioning

confidence: 99%

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Emergence, Evolution, and Biological Characteristics of H10N4 and H10N8 Avian Influenza Viruses in Migratory Wild Birds Detected in Eastern China in 2020

Wang

Zhang

et al. 2022

Microbiol Spectr

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Emergence, Evolution, and Biological Characteristics of H10N4 and H10N8 Avian Influenza Viruses in Migratory Wild Birds Detected in Eastern China in 2020

Wang

Zhang

et al. 2022

Microbiol Spectr

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“…H9N2 AIV has gradually become the most prevalent subtype of AIVs in mainland China since 1994 [ 5 , 6 ]. Available evidence has demonstrated that H9N2 viruses isolated naturally from poultry have acquired the ability to preferentially bind to the human-type receptor [ 7 , 8 ]. Due to sporadic cases of human infection, and by providing reassortant internal genes to human-infecting subtypes such as H5N1, H5N6, H7N9, and H10N8 [ 9 – 12 ], H9N2 AIV is posing a significant threat to public health with potential pandemic risk.…”

Section: Introductionmentioning

confidence: 99%

The molecular determinants of antigenic drift in a novel avian influenza A (H9N2) variant virus

Zheng

Guo

et al. 2022

Virol J

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Background In early 2020, a novel H9N2 AIV immune escape variant emerged in South China and rapidly spread throughout mainland China. The effectiveness of the current H9N2 vaccine is being challenged by emerging immune escape strains. Assessing key amino acid substitutions that contribute to antigenic drift and immune escape in the HA gene of circulating strains is critical for understanding virus evolution and in selecting more effective vaccine components. Methods In this study, a representative immune escape strain, A/chicken/Fujian/11/2020 (FJ/20), differed from current H9N2 vaccine strain, A/chicken/Anhui/LH99/2017 (AH/17) by 18 amino acids in the head domain in HA protein. To investigate the molecular determinants of antigenic drift of FJ/20, a panel of mutants were generated by reverse genetics including specific amino acids changes in the HA genes of FJ/20 and AH/17. The antigenic effect of the substitutions was evaluated by hemagglutination inhibition (HI) assay and antigenic cartography. Results Fujian-like H9N2 viruses had changed antigenicity significantly, having mutated into an antigenically distinct sub-clade. Relative to the titers of the vaccine virus AH/17, the escape strain FJ/20 saw a 16-fold reduction in HI titer against antiserum elicited by AH/17. Our results showed that seven residue substitutions (D127S, G135D, N145T, R146Q, D179T, R182T and T183N) near the HA receptor binding sites were critical for converting the antigenicity of both AH/17 and FJ/20. Especially, the combined mutations 127D, 135G, 145N, and 146R could be a major factor of antigenic drift in the current immune escape variant FJ/20. The avian influenza A (H9N2) variant virus need further ongoing epidemiological surveillance. Conclusions In this study, we evaluated the relative contributions of different combinations of amino acid substitutions in the HA globular head domain of the immune escape strain FJ/20 and the vaccine strain AH/17. Our study provides more insights into the molecular mechanism of the antigenic drift of the H9N2 AIV immune escape strain. This work identified important markers for understanding H9N2 AIV evolution as well as for improving vaccine development and control strategies in poultry.

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“…The H7N9 influenza virus that emerged in China in 2013 mutated to a highly pathogenic virus in chickens and posed an increasing threat to human public health ( 8 – 12 ). Moreover, the widespread H9N2 viruses that circulate in poultry have undergone mammalian adaptation and acquired increased transmissibility in ferrets ( 13 , 14 ). In addition, the cocirculation of different subtypes in migratory waterfowl and domestic birds promotes the emergence of novel influenza reassortants, which threaten the poultry industry and human health ( 8 , 15 , 16 ).…”

Section: Introductionmentioning

confidence: 99%

SUMOylation of Matrix Protein M1 and Filamentous Morphology Collectively Contribute to the Replication and Virulence of Highly Pathogenic H5N1 Avian Influenza Viruses in Mammals

Guo

Chen

et al. 2022

J Virol

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The matrix protein (M1) of influenza A virus plays an important role in replication, assembly, and budding. A previous study found that aspartic acid (D) at position 30 and alanine (A) at position 215 of M1 contribute to the high pathogenicity of H5N1 viruses in mice, and double mutations of D to asparagine (N) at position 30 (D30N) and A to threonine (T) at position 215 (A215T) in M1 dramatically attenuate H5N1 viruses in mice. However, the underlying mechanisms by which these M1 mutations attenuate the virulence of H5N1 viruses are unknown. Here, we found that the amino acid mutation A215T eliminates the SUMOylation of M1 by reducing its interaction with the host SUMO1 protein, significantly reducing the stability of M1, slowing the export of the M1-vRNP complex from the nucleus to the cytoplasm, and reducing viral replication in MDCK cells. We further found that the D30N mutation in M1 alters the shape of progeny viruses from filamentous to spherical virions. Our findings reveal an essential role for M1 215A SUMOylation and M1 30D-related filamentous morphology in the pathogenesis of avian influenza viruses, which could be targeted in novel antiviral drug designs. Importance Identification of the pathogenic mechanism of highly pathogenic avian influenza viruses in mammals is helpful to develop novel anti-influenza virus strategies. Two amino acid mutations (D30N and A215T) in M1 were found to collectively attenuate H5N1 influenza viruses in mice, but the underlying mechanism remained unknown. This study found that the A215T mutation significantly decreases the SUMOylation of M1, which in turn attenuates the replication of H5N1 virus in mammalian cells. The D30N mutation in M1 was found to change the virion shape from filamentous to spherical. These findings are important for understanding the molecular mechanism of virulence of highly pathogenic avian influenza viruses in mammals.

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Molecular characterization, receptor binding property, and replication in chickens and mice of H9N2 avian influenza viruses isolated from chickens, peafowls, and wild birds in eastern China

Cited by 34 publications

References 53 publications

Emergence, Evolution, and Biological Characteristics of H10N4 and H10N8 Avian Influenza Viruses in Migratory Wild Birds Detected in Eastern China in 2020

Emergence, Evolution, and Biological Characteristics of H10N4 and H10N8 Avian Influenza Viruses in Migratory Wild Birds Detected in Eastern China in 2020

The molecular determinants of antigenic drift in a novel avian influenza A (H9N2) variant virus

SUMOylation of Matrix Protein M1 and Filamentous Morphology Collectively Contribute to the Replication and Virulence of Highly Pathogenic H5N1 Avian Influenza Viruses in Mammals

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