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].

Abstract

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.

Supporting text Virus Host Location
Cross-species transmission 75 Genetic Evolution 12 H7N9 avian influenza virus 2 Host origin 1 Pathogenicity 54 Chickens 146 Influenza A Virus, H7N9 Subtype 87 Influenza in Birds 341 Orthomyxoviridae Infections 228 Poultry Diseases 74 Animals 1948 China 229 Hemagglutinin Glycoproteins, Influenza Virus 180 Mice 253 Mice, Inbred BALB C 73 Phylogeny 805 Virulence 108

Evidence records

8 total
Zoonotic Surveillance
3 records · 1 evidence types
Evidence type
3 records
OVE10623
Key finding

A highly pathogenic H7N9 avian influenza virus isolate, 229-4, was obtained from chicken in China in 2022.

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).

Sample type
not specified
OVE10624
Key finding

A highly pathogenic H7N9 avian influenza virus isolate, 782-2, was obtained from quail in China in 2022.

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).

Sample type
not specified
OVE10625
Key finding

A highly pathogenic H7N9 avian influenza virus isolate, 621, was obtained from quail in China in 2022.

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).

Sample type
not specified
Experimental Infection
3 records · 2 evidence types
Evidence type
2 records
OVE10626
Key finding

Group.y.2.3 H7N9 avian influenza virus isolates showed stronger replication and pathogenicity in chickens than other lineages.

Virus
Host
Location
Not specified
Supporting text

Group.y.2.3 isolates displayed stronger replication and pathogenicity in chickens and mice, with isolate 782‑2 being the most virulent.

Method
experimental infection | comparison of replication and pathogenicity
Experimental system
controlled infection of chickens
OVE10627
Key finding

Group.y.2.3 H7N9 avian influenza virus isolates showed stronger replication and pathogenicity in mice, with isolate 782‑2 being the most virulent.

Virus
Host
Location
Not specified
Supporting text

Group.y.2.3 isolates displayed stronger replication and pathogenicity in chickens and mice, with isolate 782‑2 being the most virulent.

Method
experimental infection | comparison of replication and pathogenicity
Experimental system
controlled infection of mice
Evidence type
1 records
OVE10628
Key finding

A chicken-origin H7N9 isolate (229-4) infected mice experimentally, showing avian-to-mammalian cross-species transmission potential.

Virus
Host
Location
Not specified
Supporting text

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.

Method
infection experiment | pathogenicity assessment | viral load measurement
Experimental system
experimental infection
Functional Mechanism
1 records · 1 evidence types
Evidence type
1 records
OVE10629
Key finding

H7N9 avian influenza virus isolates contained multiple basic HA cleavage sites and an HA 186V substitution linked to mammalian adaptation.

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.

Genes or proteins
HA
Mutations
HA 186 V
Mechanism types
host-range expansion | virulence adaptation
Genomic Evolution
1 records · 1 evidence types
Evidence type
1 records
OVE10631
Key finding

Phylogenetic analysis of the HA gene identified two evolutionary lineages of H7N9 avian influenza virus, Group.y.2.3 and Group.y.2.4, represented by isolates from chicken and quail.

Virus
Host
Location
Not specified
Supporting text

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.

Genes or proteins
HA gene | hemagglutinin
Analysis methods
phylogenetic analysis