Inhibition of fatty acid synthase by amentoflavone reduces coxsackievirus B3 replication

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Use of Viral Entry Assays and Molecular Docking Analysis for the Identification of Antiviral Candidates against Coxsackievirus A16
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Use of Viral Entry Assays and Molecular Docking Analysis for the Identification of Antiviral Candidates against Coxsackievirus A16

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Steffi Wilsky1, Katharina Sobotta, Nadine Wiesener

  • 1Department of Virology and Antiviral Therapy, University Hospital Jena, Friedrich Schiller University, Hans-Knöll-Str. 2, 07745 Jena, Germany.

Archives of Virology
|November 15, 2011
PubMed

Insights

Fatty acid synthase (FAS) expression increases during Coxsackievirus B3 (CVB3) infection. Inhibiting FAS with amentoflavone significantly reduces viral replication, suggesting FAS as a potential therapeutic target for CVB3 infections.

Area of Science:

  • Virology
  • Molecular Biology
  • Drug Discovery

Background:

  • Coxsackievirus B3 (CVB3) causes significant acute and chronic human infections.
  • Current treatments lack effective antiviral drugs for CVB3.
  • Viral replication involves altering host cell pathways, including increased fatty acid synthase (FAS) expression.

Purpose of the Study:

  • To investigate fatty acid synthase (FAS) inhibition as a potential anti-CVB3 therapeutic strategy.
  • To evaluate the antiviral effects of amentoflavone, a FAS inhibitor, against CVB3.
  • To explore the role of p38 MAP kinase in CVB3 replication and FAS expression.

Main Methods:

  • Correlating CVB3 replication with FAS expression in human Raji cells.
  • Assessing the time and dose-dependent antiviral effects of amentoflavone on CVB3.
  • Investigating the impact of p38 MAP kinase inhibition (using SB239063) on FAS expression and viral replication.

Main Results:

  • CVB3 infection significantly up-regulates FAS expression as early as 1 hour post-infection.
  • Amentoflavone treatment inhibited CVB3 replication in a dose-dependent manner up to 8 hours post-infection.
  • Suppression of p38 MAP kinase activity reduced both FAS expression and CVB3 replication.

Conclusions:

  • FAS expression is an early host response to CVB3 infection.
  • FAS inhibition by amentoflavone demonstrates significant antiviral activity against CVB3.
  • Targeting FAS, potentially through p38 MAP kinase pathways, offers a promising therapeutic avenue for CVB3 infections.

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