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Three amino acid changes in PB1-F2 of highly pathogenic H5N1 avian influenza virus affect pathogenicity in mallard

Henju Marjuki1, Christoph Scholtissek, John Franks

  • 1Division of Virology, Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, 262 Danny Thomas Place, Memphis, TN 38105-3678, USA.

Archives of Virology
|April 13, 2010
PubMed

Insights

Synonymous mutations in the PB1-F2 protein of avian influenza A (H5N1) virus significantly reduced its lethality in mallard ducks. Repairing these mutations restored pathogenicity, highlighting PB1-F2

Area of Science:

  • Virology
  • Molecular Biology
  • Avian Pathogenesis

Background:

  • The PB1-F2 protein's role in influenza virus pathogenicity is established in mice but less understood in avian hosts.
  • Previous studies showed wild-type H5N1 virus was more lethal to mallard ducks than a reverse genetics-derived strain.
  • Investigating viral factors responsible for pathogenicity differences in avian models is crucial.

Purpose of the Study:

  • To identify viral factors contributing to the observed pathogenicity discrepancy of H5N1 influenza virus in mallard ducks.
  • To elucidate the role of the PB1-F2 protein and associated mutations in avian influenza virus virulence.

Main Methods:

  • Comparative analysis of wild-type (wtVN1203) and reverse genetics (rgVN1203) H5N1 influenza viruses in mallard ducks.
  • Introduction of synonymous mutations (SMs) into rgVN1203, specifically within the PB1-F2 open reading frame.
  • Construction of recombinant viruses with repaired mutations to assess their impact on pathogenicity and viral replication.

Main Results:

  • Synonymous mutations in the PB1 gene of rgVN1203 (rgVN1203/SM-3) led to amino acid substitutions in PB1-F2 and reduced virus lethality in mallard ducks.
  • Recombinant viruses with repaired PB1-F2 mutations (rgVN1203/R-PB1-F2) or all SMs (rgVN1203/R-PB1) exhibited significantly higher pathogenicity than rgVN1203/SM-3.
  • Repairing three key mutations in PB1-F2 in cultured cells enhanced viral polymerase activity and viral RNA expression.

Conclusions:

  • Specific amino acid changes in the PB1-F2 protein, resulting from synonymous mutations, are critical for H5N1 influenza virus pathogenicity in mallard ducks.
  • The PB1-F2 protein plays a significant role in avian influenza virus virulence, influencing viral replication and host lethality.
  • Understanding these viral factors can inform strategies for controlling avian influenza outbreaks.

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