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Threonine 157 of influenza virus PA polymerase subunit modulates RNA replication in infectious viruses

Maite Huarte1, Ana Falcón, Yuri Nakaya

  • 1Centro Nacional de Biotecnología, Cantoblanco, 28049 Madrid, Spain.

Journal of Virology
|April 30, 2003
PubMed

Insights

Influenza A virus PA protein residue T157 is crucial for viral polymerase function. Mutations here severely impair viral replication, cRNA synthesis, and pathogenesis, with some mutations rendering the virus non-viable.

Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • Influenza A virus PA protein possesses protease activity linked to viral replication.
  • Previous studies indicated a correlation between decreased PA protease activity and reduced viral ribonucleoprotein (RNP) replication capacity.

Purpose of the Study:

  • To investigate the in vivo phenotype of influenza A virus PA protein mutants.
  • To determine the role of specific PA protein residues (T162 and T157) in viral replication, nuclear transport, and pathogenesis.

Main Methods:

  • Generation and characterization of mutant influenza A viruses with specific PA protein mutations (T162A, T157A, T157E).
  • Assessment of viral RNP protease and replication activities in vitro.
  • Analysis of viral protein nuclear transport, virus multiplication, RNA synthesis (cRNA and mRNA), and viral pathogenesis in a mouse model.

Main Results:

  • The T162A mutation showed a wild-type phenotype with moderate effects on protease and RNP replication.
  • The T157A mutation resulted in delayed nuclear transport of PA protein, reduced virus multiplication, diminished replicative synthesis (especially cRNA), and decreased viral pathogenesis.
  • Recombinant viruses with the T157E mutation were non-viable, indicating a critical role for this residue.

Conclusions:

  • Influenza A virus PA protein residue T157 is essential for viral polymerase activity, particularly for cRNA synthesis.
  • The T157A mutation significantly impacts multiple stages of the viral life cycle and pathogenesis.
  • Severe impairment of PA protein protease and replication activities leads to non-viable influenza A viruses.

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