Isolation and Identification of Novel Highly Pathogenic Avian Influenza Virus (H5N8) Subclade 2.3.4.4b from Geese in Northeastern China

Zhu, Yicheng; Cong, Yulin; Sun, Youhong; Han, Jin-Hong; Gai, Lili; Yang, Tiantian; Liu, Chang; Zhao, Lang; Cong, Yanlong

doi:10.1128/aem.01572-22

Cited by 3 publications

(6 citation statements)

References 16 publications

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“…PMEs of the coelomic cavity revealed lesions primarily localized in the digestive and respiratory tracts, including hemorrhagic trachea, larynx, liver, and glandular gastric papillae. Additionally, a diffuse hemorrhage was observed in the intestine and pancreas [226]. Natural cases of HPAI H5N1 infections in domestic geese in the UK were associated with pancreatic lesions [144].…”

Section: Domestic Ducks and Geesementioning

confidence: 97%

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Highly Pathogenic Avian Influenza (HPAI) H5 Clade 2.3.4.4b Virus Infection in Birds and Mammals

Graziosi,

Lupini,

Catelli

et al. 2024

Animals

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Avian influenza viruses (AIVs) are highly contagious respiratory viruses of birds, leading to significant morbidity and mortality globally and causing substantial economic losses to the poultry industry and agriculture. Since their first isolation in 2013-2014, the Asian-origin H5 highly pathogenic avian influenza viruses (HPAI) of clade 2.3.4.4b have undergone unprecedented evolution and reassortment of internal gene segments. In just a few years, it supplanted other AIV clades, and now it is widespread in the wild migratory waterfowl, spreading to Asia, Europe, Africa, and the Americas. Wild waterfowl, the natural reservoir of LPAIVs and generally more resistant to the disease, also manifested high morbidity and mortality with HPAIV clade 2.3.4.4b. This clade also caused overt clinical signs and mass mortality in a variety of avian and mammalian species never reported before, such as raptors, seabirds, sealions, foxes, and others. Most notably, the recent outbreaks in dairy cattle were associated with the emergence of a few critical mutations related to mammalian adaptation, raising concerns about the possibility of jumping species and acquisition of sustained human-to-human transmission. The main clinical signs and anatomopathological findings associated with clade 2.3.4.4b virus infection in birds and non-human mammals are hereby summarized.

show abstract

Section: Domestic Ducks and Geesementioning

confidence: 97%

“…In the case of domestic geese, Zhu et al [226] documented an HPAI H5N8 outbreak in January 2021 on an egg-laying farm in Northeastern China. The overall mortality rate reached 50%, with affected individuals displaying cyanosis in the head, sarcoma, oral mucosa, tongue, and hemorrhagic conjunctiva and nostrils.…”

Section: Domestic Ducks and Geesementioning

confidence: 99%

Highly Pathogenic Avian Influenza (HPAI) H5 Clade 2.3.4.4b Virus Infection in Birds and Mammals

Graziosi,

Lupini,

Catelli

et al. 2024

Animals

View full text Add to dashboard Cite

show abstract

“…PMEs of the coelomic cavity revealed lesions primarily localized in the digestive and respiratory tracts, including hemorrhagic trachea, larynx, liver, and glandular gastric papillae. Additionally, a diffuse hemorrhage was observed in the intestine and pancreas [231]. Natural cases of HPAI H5N1 infections in domestic geese in the UK were associated with pancreatic lesions [145].…”

Section: Domestic Ducks and Geesementioning

confidence: 97%

“…In the case of domestic geese, Zhu, et al [231] documented an HPAI H5N8 outbreak in January 2021 on an egg-laying farm in Northeastern China. The overall mortality rate reached 50%, with affected individuals displaying cyanosis in the head, sarcoma, oral mucosa, tongue, and hemorrhagic conjunctiva and nostrils.…”

Section: Domestic Ducks and Geesementioning

confidence: 99%

Highly Pathogenic Avian Influenza (HPAI) H5 Clade 2.3.4.4b Virus Infection in Birds and Mammals

Graziosi,

Lupini,

Catelli

et al. 2024

Preprint

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Avian influenza viruses (AIVs) are highly contagious respiratory viruses of birds, lead-ing to significant morbidity and mortality globally and causing substantial economic losses to the poultry industry. Since their first isolation in 2013, the Asian-origin H5N1 highly pathogenic avian influenza viruses (HPAI) of clade 2.3.4.4b have undergone unprecedented evolution and re-assortment of internal gene segments and have spread to Asia, Europe, Africa, and America, caus-ing outbreaks in all the poultry categories. Novel epidemiological and pathobiological character-istics, distinct from other clades, are specific of clade 2.3.4.4b viruses. Wild waterfowl, the natu-ral reservoir of AIVs, are frequently found infected with clade 2.3.4.4b viruses, which can also cause high morbidity and mortality in these birds. The sustained clade 2.3.4.4b virus circulation in waterfowl has also led to virus infection in other wild bird species, with implications for the conservation of endangered species. Furthermore, clade 2.3.4.4b viruses have been isolated in var-ious wild and domestic mammals worldwide, and critical mutations related to virus adaptation to mammalian species have been identified, raising concerns about virus spillover to humans. The main clinical signs, and anatomopathological findings associated to clade 2.3.4.4b virus infection in birds and non-human mammals are hereby summarized.

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“…Migratory birds are important vectors for the transmission of viruses, such as avian influenza virus, West Nile virus, and duck plague virus (DPV, a member of alphaherpesviridae) [ 25 – 30 ]. Therefore purporting to illustrate how migratory birds resist viruses and viruses evade antiviral innate immunity is pivotal but still enigmatic.…”

Section: Introductionmentioning

confidence: 99%

Duck STING mediates antiviral autophagy directing the interferon signaling pathway to inhibit duck plague virus infection

Tian,

Wang

et al. 2024

Vet Res

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Migratory birds are important vectors for virus transmission, how migratory birds recognize viruses and viruses are sustained in birds is still enigmatic. As an animal model for waterfowl among migratory birds, studying and dissecting the antiviral immunity and viral evasion in duck cells may pave a path to deciphering these puzzles. Here, we studied the mechanism of antiviral autophagy mediated by duck STING in DEF cells. The results collaborated that duck STING could significantly enhance LC3B-II/I turnover, LC3B-EGFP puncta formation, and mCherry/EGFP ratio, indicating that duck STING could induce autophagy. The autophagy induced by duck STING is not affected by shRNA knockdown of ATG5 expression, deletion of the C-terminal tail of STING, or TBK1 inhibitor BX795 treatment, indicating that duck STING activated non-classical selective autophagy is independent of interaction with TBK1, TBK1 phosphorylation, and interferon (IFN) signaling. The STING R235A mutant and Sar1A/B kinase mutant abolished duck STING induced autophagy, suggesting binding with cGAMP and COPII complex mediated transport are the critical prerequisite. Duck STING interacted with LC3B through LIR motifs to induce autophagy, the LIR 4/7 motif mutants of duck STING abolished the interaction with LC3B, and neither activated autophagy nor IFN expression, indicating that duck STING associates with LC3B directed autophagy and dictated innate immunity activation. Finally, we found that duck STING mediated autophagy significantly inhibited duck plague virus (DPV) infection via ubiquitously degraded viral proteins. Our study may shed light on one scenario about the control and evasion of diseases transmitted by migratory birds.

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Isolation and Identification of Novel Highly Pathogenic Avian Influenza Virus (H5N8) Subclade 2.3.4.4b from Geese in Northeastern China

Cited by 3 publications

References 16 publications

Highly Pathogenic Avian Influenza (HPAI) H5 Clade 2.3.4.4b Virus Infection in Birds and Mammals

Highly Pathogenic Avian Influenza (HPAI) H5 Clade 2.3.4.4b Virus Infection in Birds and Mammals

Highly Pathogenic Avian Influenza (HPAI) H5 Clade 2.3.4.4b Virus Infection in Birds and Mammals

Duck STING mediates antiviral autophagy directing the interferon signaling pathway to inhibit duck plague virus infection

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