Polypyrimidine Tract-Binding Protein Regulates Enterovirus 71 Translation Through Interaction with the Internal

Juemin Xi1, Fei Ye2, Guanzhou Wang2

  • 1Institute of Medical Biology, Chinese Academy of Medical Sciences, and Peking Union Medical College, Kunming, 650118, China.

Virologica Sinica
|February 24, 2019
PubMed

Insights

Polypyrimidine tract-binding protein 1 (PTB) binds to the Enterovirus 71 (EV71) internal ribosomal entry site (IRES). PTB positively regulates viral protein translation, offering insights into EV71 replication mechanisms.

Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • Enterovirus 71 (EV71) causes hand, foot, and mouth disease outbreaks.
  • Understanding EV71's life cycle requires knowledge of virus-host interactions.
  • The EV71 5' untranslated region, including the IRES, is crucial for viral protein synthesis.

Purpose of the Study:

  • To elucidate the molecular mechanisms of EV71-host interactions.
  • To identify host factors involved in EV71 replication.
  • To determine the role of polypyrimidine tract-binding protein 1 (PTB) in EV71 infection.

Main Methods:

  • Investigated PTB binding to the EV71 IRES using biochemical assays.
  • Identified specific PTB RNA recognition motifs (RRMs) involved in binding.
  • Observed PTB subcellular localization changes upon EV71 infection.
  • Utilized PTB knockdown to assess its effect on IRES activity and viral protein production.

Main Results:

  • Polypyrimidine tract-binding protein 1 (PTB) directly binds to the EV71 internal ribosomal entry site (IRES).
  • RNA recognition motifs 1 and 2 of PTB are essential for this interaction.
  • EV71 infection induces the translocation of PTB from the nucleus to the cytoplasm.
  • PTB knockdown significantly inhibits EV71 IRES activity and viral protein synthesis.

Conclusions:

  • PTB is a host factor that interacts with the EV71 IRES.
  • PTB positively regulates viral protein translation, playing a key role in EV71 replication.
  • These findings contribute to understanding EV71 pathogenesis and potential therapeutic targets.

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