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Inhibition of influenza virus replication by targeting broad host cell pathways

Isabelle Marois1, Alexandre Cloutier1, Isabelle Meunier1

  • 1Department of Medicine, Pulmonary Division, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Québec, Canada; Centre de Recherche du CHUS, Sherbrooke, Québec, Canada.

Plos One
|October 22, 2014
PubMed

Insights

Lysosomotropic alkalinizing agents (LAAs) and calcium modulators (CMs) effectively inhibit influenza virus replication by targeting host cell pathways. These antivirals show promise for reducing drug resistance in influenza treatment.

Area of Science:

  • Virology
  • Cell Biology
  • Drug Discovery

Background:

  • Current influenza antivirals target rapidly mutating viral components, leading to increased drug resistance.
  • Emergence of resistant influenza strains necessitates the development of novel therapeutic strategies.

Purpose of the Study:

  • To compare the antiviral efficacy of lysosomotropic alkalinizing agents (LAAs) and calcium modulators (CMs) against diverse influenza virus subtypes.
  • To investigate the potential of targeting host cellular pathways as an alternative strategy for influenza treatment.

Main Methods:

  • In vitro assessment of LAAs and CMs against avian, swine, and human influenza viruses in MDCK cells.
  • Evaluation of drug efficacy at different time points post-infection.
  • Analysis of viral acidic polymerase (PA) expression to understand the mechanism of action.

Main Results:

  • LAAs and CMs, individually or in combination, significantly inhibited influenza viral replication.
  • Antiviral effects were observed even when treatment was initiated 8 hours post-infection.
  • Both drug classes were found to interfere with early stages of the viral replication cycle.

Conclusions:

  • Targeting broad host cellular pathways is an effective strategy for inhibiting influenza virus replication.
  • LAAs and CMs offer a promising therapeutic avenue with potentially reduced risk of viral resistance due to targeting host factors rather than viral proteins.

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