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Compound FC-10696 Inhibits Egress of Marburg Virus.

Ziying Han1, Hong Ye2, Jingjing Liang1

  • 1University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Antimicrobial Agents and Chemotherapy
|April 13, 2021
PubMed
Summary

A novel compound, FC-10696, effectively inhibits Marburg virus (MARV) replication by targeting the virus-host interaction essential for viral spread. This host-oriented inhibitor shows promise in preclinical models, offering a new therapeutic strategy against MARV.

Keywords:
L domainMarburg virusNedd4PPxY motifWW domainantiviral therapeuticbuddingfilovirushost-orientedvirus-host interaction

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Area of Science:

  • Virology
  • Drug Discovery
  • Molecular Biology

Background:

  • Marburg virus (MARV) VP40 protein (mVP40) is crucial for viral egress and spread.
  • mVP40 utilizes a PPxY late (L) domain motif to interact with host WW domain proteins, facilitating virus-cell separation.
  • Previous studies identified small-molecule inhibitors targeting this viral PPxY/host WW domain interaction.

Purpose of the Study:

  • To evaluate the antiviral potency of a novel compound, FC-10696, derived from structure-activity relationship (SAR) studies of PPxY inhibitors.
  • To assess FC-10696's efficacy in inhibiting MARV VP40-mediated egress and authentic MARV replication in vitro and in vivo.

Main Methods:

  • Structure-activity relationship (SAR) analysis to develop FC-10696.
  • In vitro assays using Marburg virus-like particles (VLPs) and authentic MARV in HeLa cells and primary human macrophages to assess viral egress inhibition.
  • In vivo studies using a lethal MARV challenge model in mice to evaluate FC-10696's therapeutic effect on clinical signs, viral load, and survival.

Main Results:

  • FC-10696 demonstrated significant inhibition of mVP40 VLP egress and authentic MARV egress from infected cells.
  • Mice treated with FC-10696 exhibited delayed onset of MARV-induced weight loss and clinical symptoms.
  • FC-10696 treatment resulted in significantly lower viral loads and improved survival rates (14%) in mice challenged with a lethal MARV dose.

Conclusions:

  • FC-10696 is a potent, first-in-class, host-oriented inhibitor targeting late-stage MARV replication.
  • The compound effectively inhibits MARV egress and spread by disrupting the PPxY/WW domain interaction.
  • FC-10696 shows therapeutic potential for treating Marburg virus infections.