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Peroxiredoxin 1 is required for efficient transcription and replication of measles virus

Akira Watanabe1, Misako Yoneda, Fusako Ikeda

  • 1The Institute of Medical Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Tokyo 108-8639, Japan.

Journal of Virology
|December 17, 2010
PubMed

Insights

Peroxiredoxin 1 (Prdx1) binds to the measles virus (MeV) nucleoprotein, inhibiting viral RNA synthesis. Suppressing Prdx1 reduces MeV growth, highlighting its role as a host factor in MeV replication.

Area of Science:

  • Virology
  • Molecular Biology
  • Host-Pathogen Interactions

Background:

  • Measles virus (MeV) is a highly contagious pathogen causing significant global health burdens.
  • Understanding host factors involved in MeV replication is crucial for developing antiviral strategies.

Purpose of the Study:

  • To identify host factors interacting with the measles virus nucleoprotein (N).
  • To elucidate the role of identified host factors in MeV RNA synthesis and replication.

Main Methods:

  • Proteomic analysis to identify host-N protein interactions.
  • Glutathione S-transferase (GST) pulldown and surface plasmon resonance (SPR) assays to characterize binding.
  • RNA interference (RNAi) and minigenome assays to assess viral replication and transcription.
  • Quantitative real-time PCR (RT-PCR) for viral RNA quantification.

Main Results:

  • Peroxiredoxin 1 (Prdx1) was identified as a host factor binding to the C-terminal region of MeV nucleoprotein (N(TAIL)).
  • Prdx1 competes with the MeV phosphoprotein (P) for binding to N(TAIL), suggesting interference with viral polymerase complex formation.
  • Suppression of Prdx1 significantly reduced MeV replication and viral RNA synthesis, impacting transcription and replication steps.
  • Prdx1 exhibits lower binding affinity to MeV-N compared to MeV-P, suggesting a role in early infection stages.

Conclusions:

  • Prdx1 is an inherent host factor that negatively regulates measles virus RNA synthesis.
  • Prdx1's interaction with MeV nucleoprotein impacts viral transcription and replication, offering a potential target for antiviral therapies.

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