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The Upf1 protein restricts EV-A71 viral replication.

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Enterovirus A71 (EV-A71) down-regulates Upf1 (Up-frameshift protein 1), a key factor in nonsense-mediated decay (NMD). Suppressing NMD enhances EV-A71 replication, suggesting NMD/Upf1 as a therapeutic target.

Keywords:
Enterovirus A71Nonsense-mediated decayUp-frameshift protein 1Viral replication

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Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Enterovirus A71 (EV-A71) causes hand, foot, and mouth disease and vesicular sore throat.
  • Upf1 (Up-frameshift protein 1) is crucial for nonsense-mediated decay (NMD), a cellular process degrading aberrant mRNAs.
  • Upf1 acts as a host factor that can inhibit viral replication.

Purpose of the Study:

  • To investigate the role of Upf1 in EV-A71 infected cells.
  • To determine if Upf1 influences EV-A71 replication.
  • To explore the impact of EV-A71 infection on the NMD pathway.

Main Methods:

  • Analyzing Upf1 expression levels in EV-A71 infected RD, Hela, and 293T cells.
  • Performing Upf1 knockdown and overexpression experiments.
  • Measuring viral RNA and progeny virus production.
  • Assessing the expression of asparagine synthetase (ASNS) as an NMD indicator.

Main Results:

  • Upf1 expression was significantly down-regulated in EV-A71 infected cells.
  • Knockdown of Upf1 increased EV-A71 RNA and progeny virus production.
  • Overexpression of Upf1 decreased EV-A71 RNA and progeny virus production.
  • EV-A71 infection led to increased ASNS RNA levels, indicating suppressed NMD activity.

Conclusions:

  • Upf1 is unfavorable for EV-A71 replication, and its down-regulation by the virus facilitates viral proliferation.
  • EV-A71 infection suppresses host cell NMD activity.
  • The NMD/Upf1 pathway represents a potential target for developing anti-picornavirus therapeutics.