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Multiple amino acid substitutions involved in enhanced pathogenicity of LPAI H9N2 in mice

Zongde Zhang1, Sishun Hu, Zili Li

  • 1State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, People's Republic of China.

Infection, Genetics and Evolution : Journal of Molecular Epidemiology and Evolutionary Genetics in Infectious Diseases
|September 8, 2011
PubMed

Insights

Avian influenza H9N2 adapted to mice (ma01) caused lethal infections due to amino acid changes and altered microRNA interactions. This mouse-adapted virus offers insights into influenza virus interspecies transmission mechanisms.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Human infections with avian influenza H9N2 underscore the need to understand interspecies transmission.
  • The mechanisms by which influenza viruses adapt to new hosts are not fully understood.

Purpose of the Study:

  • To generate a mouse-adapted H9N2 influenza virus (ma01) to study interspecies transmission.
  • To identify genetic and molecular changes responsible for increased virulence in mice.

Main Methods:

  • Serial lung-to-lung passages of wild-type H9N2 in mice to generate ma01.
  • Whole-genome sequencing to identify mutations in ma01.
  • Analysis of viral gene targets for mouse microRNAs (miRNAs).
  • Measurement of cytokine and interferon levels in infected mice.

Main Results:

  • Ma01 caused highly lethal infections in mice with severe lung pathology and broader tissue tropism.
  • Nine amino acid substitutions were identified in ma01 across five viral genes (PB2, PA, NA, M1, NS1).
  • Ma01 exhibited altered recognition of mouse miRNAs (mmu-mir-1940, mmu-mir-1904), with PB2(627) mutation being key.
  • Significantly higher levels of IL-1β, IL-6, TNF-α, and IFN-β were induced by ma01 compared to the parental strain.

Conclusions:

  • Multiple amino acid substitutions and altered microRNA recognition are crucial for lethal influenza infection and rapid viral growth.
  • The ma01 model provides insights into the genetic adaptations required for influenza virus interspecies transmission and virulence.

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