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Restriction of SARS-CoV-2 Replication by Targeting Programmed -1 Ribosomal Frameshifting In Vitro

Yu Sun1, Laura Abriola2, Yulia V Surovtseva2

  • 1Department of Neuroscience, Yale University School of Medicine, New Haven, CT, USA.

Biorxiv : the Preprint Server for Biology
|October 27, 2020
PubMed

Insights

Merafloxacin inhibits SARS-CoV-2 programmed ribosomal frameshifting (-1 PRF), a key step in viral replication. This discovery offers a new antiviral strategy targeting -1 PRF in coronaviruses.

Area of Science:

  • Virology
  • Molecular Biology
  • Drug Discovery

Background:

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) translation relies on programmed -1 ribosomal frameshifting (-1 PRF).
  • The RNA pseudoknot is essential for promoting -1 PRF in SARS-CoV-2.
  • The impact of altered -1 PRF efficiency on SARS-CoV-2 replication is not well understood.

Conclusions:

  • Targeting -1 PRF is a viable antiviral strategy for SARS-CoV-2.
  • Merafloxacin demonstrates potential as a therapeutic agent against SARS-CoV-2 infections.
  • Further research into -1 PRF inhibitors could lead to novel antiviral treatments.

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