Literature detail

Rapid Evolution of H7N9 Highly Pathogenic Viruses that Emerged in China in 2017.

Jianzhong Shi¹ Guohua Deng¹ Shujie Ma¹ Xianying Zeng¹ Xin Yin¹ Mei Li¹ Bo Zhang¹ Pengfei Cui¹ Yan Chen¹ Huanliang Yang¹ Xiaopeng Wan¹ Liling Liu¹ Pucheng Chen¹ Yongping Jiang¹ Yuntao Guan¹ Jinxiong Liu¹ Wenli Gu¹ Shuyu Han¹ Yangming Song¹ Libin Liang¹ Zhiyuan Qu¹ Yujie Hou¹ Xiurong Wang¹ Hongmei Bao¹ Guobin Tian¹ Yanbing Li¹ Li Jiang¹ Chengjun Li¹ Hualan Chen²

Affiliations 2 institutions

State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, Heilongjiang 150069, People's Republic of China.
State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, Heilongjiang 150069, People's Republic of China. Electronic address: [email protected].

PMID 30269969 2018 Cell Host Microbe eng ppublish

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Article

Publication summary

H7N9 low pathogenic influenza viruses emerged in China in 2013 and mutated to highly pathogenic strains in 2017, resulting in human infections and disease in chickens. To control spread, a bivalent H5/H7 inactivated vaccine was introduced in poultry in September 2017. To monitor virus evolution and vaccine efficacy, we collected 53,884 poultry samples across China from February 2017 to January 2018. We isolated 252 H7N9 low pathogenic viruses, 69 H7N9 highly pathogenic viruses, and one H7N2 highly pathogenic virus, of which two low pathogenic and 14 highly pathogenic strains were collected after vaccine introduction. Genetic analysis of highly pathogenic strains revealed nine genotypes, one of which is predominant and widespread and contains strains exhibiting high virulence in mice. Additionally, some H7N9 and H7N2 viruses carrying duck virus genes are lethal in ducks. Thus, although vaccination reduced H7N9 infections, the increased virulence and expanded host range to ducks pose new challenges.

chickens ducks evolution H7N9 highly pathogenic influenza viruses mice vaccine virulence Evolution, Molecular Animals Chickens China Communicable Diseases, Emerging Ducks Female Humans Influenza A Virus, H7N9 Subtype Influenza in Birds Influenza Vaccines

Structured evidence records

Evidence records

11 total

Host Range Experiment 3 records

Host Range Experiment Extraction confidence 0.90

Key finding

H7N9 highly pathogenic influenza virus strains caused high virulence in experimentally infected mice.

Virus

Host

Location

Supporting text

Genetic analysis of highly pathogenic strains revealed nine genotypes, one of which is predominant and widespread and contains strains exhibiting high virulence in mice.

Method: experimental infection; virulence assay
Experimental system: in vivo animal experiment

Host Range Experiment Extraction confidence 0.90

Key finding

Some H7N9 and H7N2 influenza viruses were lethal to ducks, demonstrating susceptibility and mortality upon experimental infection.

Virus

Host

Location

Supporting text

Additionally, some H7N9 and H7N2 viruses carrying duck virus genes are lethal in ducks.

Method: experimental infection; virulence assay
Experimental system: in vivo animal experiment

Host Range Experiment Extraction confidence 0.90

Key finding

Some H7N2 influenza viruses containing duck virus genes were lethal in ducks, indicating host susceptibility and pathogenicity.

Virus

Host

Location

Supporting text

Additionally, some H7N9 and H7N2 viruses carrying duck virus genes are lethal in ducks.

Method: experimental infection; virulence assay
Experimental system: in vivo animal experiment

Molecular Adaptation 3 records

Molecular Adaptation Extraction confidence 0.95

Key finding

H7N9 and H7N2 influenza viruses acquired duck virus genes, producing genotypes with high virulence in mice and lethality in ducks, indicating molecular adaptation affecting virulence and host range.

Virus

Host

Location

Supporting text

Genetic analysis of highly pathogenic strains revealed nine genotypes, one of which is predominant and widespread and contains strains exhibiting high virulence in mice. Additionally, some H7N9 and H7N2 viruses carrying duck virus genes are lethal in ducks.

Mechanism types: pathogenicity; host_range

Molecular Adaptation Extraction confidence 0.90

Key finding

A predominant genotype of highly pathogenic H7N9 influenza virus exhibited increased virulence in mice, representing molecular adaptation linked to pathogenicity.

Virus

Host

Location

Supporting text

Genetic analysis of highly pathogenic strains revealed nine genotypes, one of which is predominant and widespread and contains strains exhibiting high virulence in mice.

Mechanism types: pathogenicity

Molecular Adaptation Extraction confidence 0.90

Key finding

H7N9 and H7N2 influenza viruses carrying duck virus genes acquired lethality in ducks, showing molecular adaptation associated with expanded host range and increased virulence.

Virus

Host

Location

Supporting text

Additionally, some H7N9 and H7N2 viruses carrying duck virus genes are lethal in ducks.

Mechanism types: host_range; pathogenicity

Zoonotic Surveillance 2 records

Zoonotic Surveillance Extraction confidence 0.90

Key finding

Extensive surveillance of poultry in China identified both low and highly pathogenic H7N9 and H7N2 influenza viruses following vaccine introduction.

Virus

Host

Location

Supporting text

To monitor virus evolution and vaccine efficacy, we collected 53,884 poultry samples across China from February 2017 to January 2018. We isolated 252 H7N9 low pathogenic viruses, 69 H7N9 highly pathogenic viruses, and one H7N2 highly pathogenic virus.

Method: virus isolation
Geographic raw: China

Zoonotic Surveillance Extraction confidence 0.90

Key finding

The surveillance detected one highly pathogenic H7N2 influenza virus among poultry samples collected across China.

Virus

Host

Location

Supporting text

Method: virus isolation
Geographic raw: China

Cross Species Transmission 1 records

Cross Species Transmission Extraction confidence 0.80

Key finding

H7N9 and H7N2 influenza viruses acquired duck virus genetic components and became lethal in ducks, demonstrating animal-to-animal host jump from chicken-associated viruses to ducks in China.

Virus

Host

Location

Supporting text

Additionally, some H7N9 and H7N2 viruses carrying duck virus genes are lethal in ducks. Thus, although vaccination reduced H7N9 infections, the increased virulence and expanded host range to ducks pose new challenges.

Method: virus isolation; genetic analysis
Study design: field surveillance
Transmission direction: animal-to-animal
Geographic raw: China
Country inferred: China

Genomic Evolution 1 records

Genomic Evolution Extraction confidence 0.90

Key finding

Genetic analyses revealed nine genotypes of H7N9 highly pathogenic influenza viruses with one dominant lineage showing increased virulence.

Virus

Host

Location

Supporting text

Genetic analysis of highly pathogenic strains revealed nine genotypes, one of which is predominant and widespread and contains strains exhibiting high virulence in mice.

Analysis methods: genetic analysis

Spillover Event 1 records

Spillover Event Extraction confidence 0.75

Key finding

H7N9 influenza viruses that originated in poultry caused human infections in China, representing an animal-to-human spillover event.

Virus

Host

Location

Supporting text

H7N9 low pathogenic influenza viruses emerged in China in 2013 and mutated to highly pathogenic strains in 2017, resulting in human infections and disease in chickens.

Transmission direction: animal-to-human
Geographic raw: China
Country inferred: China

Citation context

References

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Evidence overview

Evidence 11

Types 6

Virus 2

Host 5

Evidence types

Host Range Experiment 3 Molecular Adaptation 3 Zoonotic Surveillance 2 Cross Species Transmission 1 Genomic Evolution 1 Spillover Event 1

Linked entities

Viruses

Hosts

Locations

Publication metadata

Journal: Cell host & microbe
Volume / Issue / Pages: 24 / 4 / 558-568.e7
ISSN: 1934-6069
Journal country: United States
DOI: 10.1016/j.chom.2018.08.006