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Identifying Caspases and their Motifs that Cleave Proteins During Influenza A Virus Infection
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Cellular Protein Phosphatase 2A Regulates Cell Survival Mechanisms in Influenza A Virus Infection

Vanessa Gerlt1, Juliane Mayr1, Juliana Del Sarto1,2

  • 1Institute of Virology Muenster, University of Muenster, 48149 Muenster, Germany.

International Journal of Molecular Sciences
|October 23, 2021
PubMed

Insights

Protein phosphatase 2A (PP2A) is crucial for efficient influenza A virus (IAV) replication. Reduced PP2A activity impairs viral replication but also leads to increased cell death during IAV infection.

Area of Science:

  • Virology
  • Cellular Biology
  • Immunology

Background:

  • Influenza A viruses (IAVs) are significant respiratory pathogens.
  • IAV replication involves hijacking host cell machinery and posttranslational modifications like phosphorylation.
  • Protein phosphatase 2A (PP2A) is a key enzyme in eukaryotic dephosphorylation, but its role in IAV infection is poorly understood.

Purpose of the Study:

  • To investigate the role of the catalytic subunit of PP2A (PP2Ac) in influenza A virus replication.
  • To elucidate the mechanisms by which PP2A influences IAV infection and host cell fate.

Main Methods:

  • Knockdown and inhibition of the PP2Ac catalytic subunit.
  • Analysis of viral replication efficiency across different IAV subtypes.
  • Assessment of host cell viability and immune response.
  • Kinase activity profiling to identify affected signaling pathways.

Main Results:

  • PP2Ac is essential for efficient replication of multiple IAV subtypes.
  • Reduced PP2Ac levels did not affect antiviral immune response, viral gene transcription, or translation.
  • Lower PP2Ac levels significantly decreased host cell viability post-IAV infection.
  • Kinase activity profiling revealed hyper-activation of PI3K/Akt, MAPK/JAK-STAT, and NF-kB pathways, promoting apoptosis.

Conclusions:

  • IAV utilizes host PP2A activity for efficient replication.
  • Depletion of PP2Ac hinders viral replication but compromises host cell survival mechanisms, leading to premature cell death.
  • The interplay between PP2A, viral replication, and host cell signaling pathways is critical during IAV infection.
Keywords:
apoptosisinfluenza A virus (IAV)phosphorylationprotein phosphatase 2A (PP2A)

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