Literature detail

Evolutionary lineage and host origin influence virulence and mammalian adaptation of H7N9 avian influenza viruses.

Wenqi Wu1 Yang Liu1 Jiaqi Zhang1 Jiaji Zhou1 Tong Wang1 Hao Chang1 Qizhang Yang1 Xirong Huang1 Huifang Yin2 Weixin Jia3,4
Affiliations 4 institutions
  1. Guangdong Engineering Laboratory for Medicament of Zoonosis Prevention and Control, Key Laboratory of Zoonoses Prevention and Control of Guangdong Province, National Avian Influenza Para-Reference Laboratory (Guangzhou), College of Veterinary Medicine, South China Agricultural University, Guangzhou, China.
  2. Engineering Research Center for the Prevention and Control of Animal Original Zoonosis of Fujian Province University, College of Life Science, Longyan University, Longyan 364012, China.
  3. Guangdong Engineering Laboratory for Medicament of Zoonosis Prevention and Control, Key Laboratory of Zoonoses Prevention and Control of Guangdong Province, National Avian Influenza Para-Reference Laboratory (Guangzhou), College of Veterinary Medicine, South China Agricultural University, Guangzhou, China
  4. Guangzhou Danong Biotechnology Co., Ltd, Guangzhou 510665, China. Electronic address: [email protected].
PMID 41747464 2026 Poult Sci eng ppublish
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Article

Publication summary

The H7N9 avian influenza virus (AIV) has posed a major global public health concern since its first detection in China in 2013. Transmitted among wild birds and poultry, this virus has crossed the species barrier to infect humans, causing severe respiratory disease and high mortality. Although the widespread use of H7 vaccines has markedly reduced human infections, the ongoing circulation and adaptive evolution of the virus in poultry remain a serious threat. In this study, we analyzed three highly pathogenic H7N9 isolates collected in China in 2022, representing two hemagglutinin (HA) gene evolutionary lineages: Group.y.2.3 (isolate 229-4, chicken origin; isolate 782-2, quail origin) and Group.y.2.4 (isolate 621, quail origin). Pathogenicity was compared through phylogenetic analysis, molecular characterization, and infection experiments in both avian and mammalian models. Group.y.2.3 isolates displayed stronger replication and pathogenicity in chickens and mice, with isolate 782-2 being the most virulent. The chicken-origin isolate 229-4 caused more severe weight loss and higher viral loads in the lungs of mice, indicating that host origin influences cross-species transmission potential. Molecular analyses revealed that all isolates possessed multiple basic cleavage sites and mutations linked to mammalian adaptation, including HA 186 V. Some isolates also harbored newly acquired glycosylation sites associated with immune evasion. Overall, our findings demonstrate that both genetic lineage and host origin shape the biological characteristics of H7N9 isolates. Group.y.2.3 isolates warrant priority in surveillance, providing critical insights for vaccine updates and risk assessment.

Cross-species transmission Genetic Evolution H7N9 avian influenza virus Host origin Pathogenicity Chickens Influenza A Virus, H7N9 Subtype Influenza in Birds Orthomyxoviridae Infections Poultry Diseases Animals China Hemagglutinin Glycoproteins, Influenza Virus Mice Mice, Inbred BALB C Phylogeny Virulence

Structured evidence records

Evidence records

6 total
2 records
Extraction confidence 0.93
Key finding

Experimental infection of chickens and mice with H7N9 isolates showed that Group.y.2.3 viruses replicated more efficiently and were more virulent than other lineages, demonstrating differential host susceptibility and cross-species adaptation potential.

Virus
Location
Not specified
Supporting text

Pathogenicity was compared through phylogenetic analysis, molecular characterization, and infection experiments in both avian and mammalian models. Group.y.2.3 isolates displayed stronger replication and pathogenicity in chickens and mice, with isolate 782-2 being the most virulent.

Method
infection experiments; replication assay; pathogenicity assay
Sample type
lungs
Experimental system
in vivo animal experiment
Extraction confidence 0.93
Key finding

H7N9 Group.y.2.3 isolates exhibited increased replication and virulence in chickens compared to other isolates, indicating lineage-dependent host adaptation in poultry.

Virus
Location
Not specified
Supporting text

Pathogenicity was compared through phylogenetic analysis, molecular characterization, and infection experiments in both avian and mammalian models. Group.y.2.3 isolates displayed stronger replication and pathogenicity in chickens and mice.

Method
infection experiments; replication assay; pathogenicity assay
Experimental system
in vivo animal experiment
1 records
Extraction confidence 0.95
Key finding

H7N9 avian influenza virus circulates among wild birds and poultry, with isolates of chicken and quail origin demonstrating avian-to-avian cross-species transmission potential.

Virus
Host
Location
Supporting text

Transmitted among wild birds and poultry, this virus has crossed the species barrier to infect humans ... isolate 229-4, chicken origin; isolate 782-2, quail origin ... host origin influences cross-species transmission potential.

Method
phylogenetic analysis; molecular characterization; infection experiments
Study design
phylogenetic analysis
Transmission direction
animal-to-animal
Geographic raw
China
Country inferred
China
1 records
Extraction confidence 0.88
Key finding

Phylogenetic and molecular characterization of H7N9 isolates revealed two HA gene evolutionary lineages in poultry associated with differing virulence and mammalian adaptation potential.

Virus
Host
Location
Not specified
Supporting text

We analyzed three highly pathogenic H7N9 isolates collected in China in 2022, representing two hemagglutinin (HA) gene evolutionary lineages: Group.y.2.3 (isolate 229-4, chicken origin; isolate 782-2, quail origin) and Group.y.2.4 (isolate 621, quail origin). Pathogenicity was compared through phylogenetic analysis, molecular characterization, and infection experiments in both avian and mammalian models.

Genes or proteins
hemagglutinin (HA)
Analysis methods
phylogenetic analysis; molecular characterization
1 records
Extraction confidence 0.97
Key finding

H7N9 isolates showed molecular adaptations for mammalian infection, including an HA 186V mutation and new glycosylation sites linked to immune evasion.

Virus
Host
Not specified
Location
Not specified
Supporting text

Molecular analyses revealed that all isolates possessed multiple basic cleavage sites and mutations linked to mammalian adaptation, including HA 186 V. Some isolates also harbored newly acquired glycosylation sites associated with immune evasion.

Genes or proteins
HA
Mutations
HA 186V
Mechanism types
mammalian_adaptation; immune_escape
1 records
Extraction confidence 0.90
Key finding

H7N9 avian influenza virus transmitted from wild birds and poultry to humans, causing severe respiratory disease and high mortality.

Virus
Location
Supporting text

Transmitted among wild birds and poultry, this virus has crossed the species barrier to infect humans, causing severe respiratory disease and high mortality.

Method
phylogenetic analysis; molecular characterization; infection experiments
Study design
experimental infection and phylogenetic analysis
Transmission direction
animal-to-human
Geographic raw
China
Country inferred
China