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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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The human fatty acid synthase: a new therapeutic target for coxsackievirus B3-induced diseases?

Alexander Rassmann1, Andreas Henke, Nadine Jarasch

  • 1Leibniz Institute for Natural Product Research and Infection Biology, Hans-Knoell-Institute, Department of Cell and Molecular Biology, Beutenbergstrasse 11a, D-07745 Jena, Germany.

Antiviral Research
|July 31, 2007
PubMed

Insights

Fatty acid synthase (FAS) is upregulated in coxsackievirus B3 (CVB3) infected cells and blocking FAS significantly inhibits viral replication. This suggests FAS is a potential therapeutic target for CVB3-induced diseases.

Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • Coxsackievirus infections cause severe human and animal diseases, including myocarditis.
  • Host-virus interactions are critical in determining disease outcomes.
  • Host proteins involved in coxsackievirus pathogenesis are not well understood.

Purpose of the Study:

  • To identify host proteins upregulated during coxsackievirus B3 (CVB3) infection.
  • To investigate the role of identified host proteins in CVB3 replication and pathogenesis.
  • To evaluate fatty acid synthase (FAS) as a potential therapeutic target for CVB3 infections.

Main Methods:

  • Two-dimensional gel electrophoresis of protein extracts from CVB3-infected and uninfected HeLa or HepG2 cells.
  • Spot analysis to identify differentially expressed proteins.
  • Inhibition of fatty acid synthase (FAS) using cerulenin and C75 to assess impact on CVB3 replication.

Main Results:

  • Several proteins were found to be exclusively upregulated in CVB3-infected cells.
  • Fatty acid synthase (FAS) was identified as one of the upregulated proteins.
  • Inhibition of FAS with cerulenin and C75 significantly blocked CVB3 replication.

Conclusions:

  • Fatty acid synthase (FAS) plays a direct role in coxsackievirus B3 (CVB3) pathogenesis.
  • FAS is a suitable therapeutic target for treating CVB3-induced diseases.

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