Archives of Virology

, Volume 157, Issue 2, pp 259–269

Inhibition of fatty acid synthase by amentoflavone reduces coxsackievirus B3 replication

Authors

  • Steffi Wilsky
    • Department of Virology and Antiviral TherapyUniversity Hospital Jena, Friedrich Schiller University
  • Katharina Sobotta
    • Department of Virology and Antiviral TherapyUniversity Hospital Jena, Friedrich Schiller University
  • Nadine Wiesener
    • Department of Virology and Antiviral TherapyUniversity Hospital Jena, Friedrich Schiller University
  • Johanna Pilas
    • Department of Medical Engineering and BiotechnologyUniversity of Applied Sciences Jena
  • Nadine Althof
    • Department of Virology and Antiviral TherapyUniversity Hospital Jena, Friedrich Schiller University
  • Thomas Munder
    • Department of Medical Engineering and BiotechnologyUniversity of Applied Sciences Jena
  • Peter Wutzler
    • Department of Virology and Antiviral TherapyUniversity Hospital Jena, Friedrich Schiller University
    • Department of Virology and Antiviral TherapyUniversity Hospital Jena, Friedrich Schiller University
Original Article

DOI: 10.1007/s00705-011-1164-z

Cite this article as:
Wilsky, S., Sobotta, K., Wiesener, N. et al. Arch Virol (2012) 157: 259. doi:10.1007/s00705-011-1164-z

Abstract

Coxsackievirus B3 (CVB3) is a human pathogen that causes acute and chronic infections, but an antiviral drug to treat these diseases has not yet been developed for clinical use. Several intracellular pathways are altered to assist viral transcription, RNA replication, and progeny release. Among these, fatty acid synthase (FAS) expression is increased. In order to test the potential of FAS inhibition as an anti-CVB3 strategy, several experiments were performed, including studies on the correlation of CVB3 replication and FAS expression in human Raji cells and an analysis of the time and dose dependence of the antiviral effect of FAS inhibition due to treatment with amentoflavone. The results demonstrate that CVB3 infection induces an up-regulation of FAS expression already at 1 h postinfection (p.i.). Incubation with increasing concentrations of amentoflavone inhibited CVB3 replication significantly up to 8 h p.i. In addition, suppression of p38 MAP kinase activity by treatment with SB239063 decreased FAS expression as well as viral replication. These data provide evidence that FAS inhibition via amentoflavone administration might present a target for anti-CVB3 therapy.

Supplementary material

705_2011_1164_MOESM1_ESM.doc (2.8 mb)
Supplementary material 1 (DOC 2833 kb)

Copyright information

© Springer-Verlag 2011