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Pathogenicity of modified bat influenza virus with different M genes and its reassortment potential with swine

Jianmei Yang1,2, Jinhwa Lee1, Jingjiao Ma1

  • 1Department of Diagnostic Medicine/Pathobiology, Kansas State University, Manhattan, KS, USA.

The Journal of General Virology
|January 20, 2017
PubMed

Insights

Researchers created novel influenza viruses using reverse genetics. While some M genes from swine influenza did not increase virulence, the PR8 M gene did, highlighting its mouse adaptation and potential for pathogenicity studies.

Area of Science:

  • Virology
  • Molecular Biology
  • Infectious Diseases

Background:

  • Previous studies successfully generated reassortant influenza viruses using the PR8 H1N1 matrix (M) gene in a modified bat influenza virus (Bat09:mH1mN1).
  • The ability to rescue M genes from diverse origins and assess the resulting virus's virulence in the Bat09:mH1mN1 background remained unexplored.

Purpose of the Study:

  • To investigate the rescue and virulence of reassortant influenza viruses containing swine influenza virus M genes in the Bat09:mH1mN1 background.
  • To assess the reassortment potential between the modified bat influenza virus and swine influenza viruses through co-infection.

Main Methods:

  • Generation of reassortant viruses using reverse genetics with North American and Eurasian swine influenza M genes in the Bat09:mH1mN1 background.
  • In vitro replication assessment of generated reassortant viruses and control Bat09:mH1mN1 in cultured cells.
  • In vivo virulence studies in mice to evaluate pathogenicity of reassortant viruses.
  • In vitro co-infection experiments between Bat09:mH1mN1 and an H3N2 swine influenza virus.

Main Results:

  • Reassortant viruses with North American and Eurasian swine M genes did not enhance virulence in mice compared to the control Bat09:mH1mN1 virus.
  • The reassortant virus containing the PR8 H1N1 M gene exhibited increased pathogenicity in mice, likely due to PR8's mouse adaptation.
  • Efficient replication of all generated reassortant viruses and the control in cultured cells was observed, with the PR8 M reassortant showing higher titers.
  • No reassortant viruses were detected in co-infection experiments between Bat09:mH1mN1 and an H3N2 swine influenza virus.

Conclusions:

  • The modified bat influenza virus (Bat09:mH1mN1) can be engineered to incorporate M genes from various influenza A virus origins via reverse genetics.
  • While swine M genes did not increase virulence, the PR8 M gene conferred enhanced pathogenicity, underscoring the impact of M gene source and host adaptation.
  • The Bat09:mH1mN1 virus appears incapable of reassortment with other influenza A viruses under in vitro co-infection conditions.

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