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  • Oral presentation
  • Open Access

Ritonavir Inhibits NF-AT Activation Through Effects on the PI-3 Kinase/Akt Pathway

  • 1,
  • 2,
  • 1,
  • 3 and
  • 1Email author
Retrovirology20052 (Suppl 1) :S44

  • Published:


  • Protease Inhibitor
  • Ritonavir
  • Multiple Signaling
  • Lipodystrophy
  • NFkB Activation

The HIV protease inhibitor ritonavir has been reported to have activities unrelated to inhibition of HIV protease, including anti-tumor activity in vivo and in vitro, induction of lipodystrophy in vivo, inhibition of the 20S proteasome, and inhibition of NFkB activation. Here we show that ritonavir also inhibits activation of NF-AT by PMA plus ionomycin and by the HHV-8 vGPCR. Inhibition of NF-AT activation occurs through the PI-3 kinase/Akt/GSK-3 pathway, since ritonavir treatment leads to decreased Akt phosphorylation and a resultant decrease in GSK-3 phosphorylation. Treatment with ritonavir also inhibits the expression of NF-AT-dependent pro-inflammatory factors. Inhibition of multiple signaling pathways may help to explain the anti-tumor and other effects of ritonavir that are unrelated to its anti-retroviral activity.


Authors’ Affiliations

Institute of Human Virology, University of Maryland Biotechnology Institute, 725 W. Lombard St., Baltimore, MD 21201, USA
University of Maryland, Baltimore County, Baltimore, MD 21259, USA
Morgan State University, 1700 East Cold Spring Lane, Baltimore, MD 21251, USA


© The Author(s) 2005