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PSPC1 Binds to HCV IRES and Prevents Ribosomal Protein S5 Binding, Inhibiting Viral RNA Translation.

Sachin Kumar Tripathi1, Ashish Aneja1, Teji Borgaonkar1

  • 1Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore 560012, Karnataka, India.

Viruses
|May 25, 2024
PubMed
Summary

Host protein PSPC1 (Paraspeckle Component 1) prevents Hepatitis C virus (HCV) RNA translation by binding to the viral IRES. Silencing PSPC1 enhances viral replication, revealing a host defense mechanism against HCV.

Keywords:
IRESPSPC1hepatitis C virusparaspecklesribosomal protein S5

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Area of Science:

  • Virology
  • Molecular Biology
  • Hepatology

Background:

  • Hepatitis C virus (HCV) infection is a leading cause of liver cancer.
  • HCV RNA translation relies on an Internal Ribosome Entry Site (IRES).
  • Host RNA-binding proteins modulate HCV IRES activity.

Purpose of the Study:

  • To investigate the role of PSPC1 (Paraspeckle Component 1) in HCV infection.
  • To determine how PSPC1 interacts with the HCV IRES and affects viral translation.
  • To elucidate the host's cellular strategy against HCV.

Main Methods:

  • Demonstration of PSPC1 relocalization upon HCV infection.
  • Competition UV-crosslinking to identify PSPC1 binding sites on HCV IRES.
  • Partial silencing of PSPC1 and assessment of viral RNA translation and replication.
  • Analysis of RPS5 interaction with HCV IRES in PSPC1-silenced cells.

Main Results:

  • PSPC1 relocalizes to the cytoplasm and binds the SLIV region of the HCV IRES, inhibiting translation.
  • PSPC1 interaction with the IRES prevents ribosomal protein S5 (RPS5) binding.
  • Partial PSPC1 silencing increases HCV RNA translation and replication.
  • PSPC1 depletion enhances RPS5 interaction with the IRES, increasing viral RNA in polysomes.

Conclusions:

  • PSPC1 acts as a host antiviral factor by inhibiting HCV IRES-mediated translation.
  • Relocalization of nuclear PSPC1 to the cytoplasm is a host survival strategy against HCV.
  • PSPC1 negatively regulates HCV replication through direct interaction with the viral IRES.