Literature detail

Novel Polymerase Gene Mutations for Human Adaptation in Clinical Isolates of Avian H5N1 Influenza Viruses.

Yasuha Arai1,2,3 Norihito Kawashita4,5 Tomo Daidoji3 Madiha S Ibrahim3,6 Emad M El-Gendy3,6 Tatsuya Takagi4,5 Kazuo Takahashi7 Yasuo Suzuki8 Kazuyoshi Ikuta2 Takaaki Nakaya3 Tatsuo Shioda1 Yohei Watanabe1,2,3
Affiliations 8 institutions
  1. Department of Viral infection, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
  2. Department of Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
  3. Department of Infectious Diseases, Kyoto Prefectural University of Medicine, Kyoto, Japan.
  4. Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
  5. Genome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
  6. Department of Microbiology, Faculty of Veterinary Medicine, Damanhour University, Damanhour, Egypt.
  7. Department of Laboratory Examination, International University of Health and Welfare Hospital, Tochigi, Japan.
  8. Health Science Hills, College of Life and Health Sciences, Chubu University, Aichi, Japan.
PMID 27097026 2016 PLoS Pathog eng epublish
PubMed DOI Browse context

Article

Publication summary

A major determinant in the change of the avian influenza virus host range to humans is the E627K substitution in the PB2 polymerase protein. However, the polymerase activity of avian influenza viruses with a single PB2-E627K mutation is still lower than that of seasonal human influenza viruses, implying that avian viruses require polymerase mutations in addition to PB2-627K for human adaptation. Here, we used a database search of H5N1 clade 2.2.1 virus sequences with the PB2-627K mutation to identify other polymerase adaptation mutations that have been selected in infected patients. Several of the mutations identified acted cooperatively with PB2-627K to increase viral growth in human airway epithelial cells and mouse lungs. These mutations were in multiple domains of the polymerase complex other than the PB2-627 domain, highlighting a complicated avian-to-human adaptation pathway of avian influenza viruses. Thus, H5N1 viruses could rapidly acquire multiple polymerase mutations that function cooperatively with PB2-627K in infected patients for optimal human adaptation.

Adaptation, Physiological Animals Blotting, Western Disease Models, Animal DNA-Directed RNA Polymerases Female Humans Influenza A Virus, H5N1 Subtype Influenza, Human Mice Mice, Inbred BALB C Mutagenesis, Site-Directed Mutation Real-Time Polymerase Chain Reaction Transfection Viral Proteins PB2 protein, influenza virus

Structured evidence records

Evidence records

4 total
2 records
Extraction confidence 0.95
Key finding

Polymerase mutations in avian H5N1 viruses increased viral growth in human airway epithelial cells when combined with PB2-E627K.

Virus
Location
Not specified
Supporting text

Several of the mutations identified acted cooperatively with PB2-627K to increase viral growth in human airway epithelial cells and mouse lungs.

Method
polymerase activity assay; viral growth assay; transfection
Sample type
airway epithelial cells
Experimental system
in vitro cell culture
Extraction confidence 0.95
Key finding

Polymerase mutations in avian H5N1 viruses enhanced viral growth in mouse lungs in combination with PB2-E627K, indicating improved replication in mammals.

Virus
Location
Not specified
Supporting text

Several of the mutations identified acted cooperatively with PB2-627K to increase viral growth in human airway epithelial cells and mouse lungs.

Method
experimental infection; viral growth assay
Sample type
lungs
Experimental system
in vivo animal experiment
1 records
Extraction confidence 0.82
Key finding

Comparative sequence analysis of H5N1 viral genomes showed multiple polymerase mutations, including PB2-E627K and additional polymerase domain changes, associated with enhanced replication and adaptation to human hosts.

Virus
Location
Not specified
Supporting text

We used a database search of H5N1 clade 2.2.1 virus sequences with the PB2-627K mutation to identify other polymerase adaptation mutations that have been selected in infected patients.

Genes or proteins
PB2; polymerase complex
Analysis methods
database sequence search; comparative genomic analysis
1 records
Extraction confidence 0.98
Key finding

Polymerase gene mutations in addition to PB2-E627K enhance replication of avian H5N1 influenza viruses in human cells and mice, demonstrating cooperative molecular adaptation toward humans.

Virus
Host
Not specified
Location
Not specified
Supporting text

Several of the mutations identified acted cooperatively with PB2-627K to increase viral growth in human airway epithelial cells and mouse lungs, indicating polymerase adaptation facilitating avian-to-human host range expansion of H5N1 viruses.

Genes or proteins
PB2; polymerase complex
Mutations
PB2 E627K
Mechanism types
polymerase_activity; replication_efficiency; host_adaptation