Skip to main content

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

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.

Author information

Authors and Affiliations


Corresponding author

Correspondence to Marvin Reitz.

Rights and permissions

Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Reprints and permissions

About this article

Cite this article

Pati, S., Nguyen, A., Foulke, J.S. et al. Ritonavir Inhibits NF-AT Activation Through Effects on the PI-3 Kinase/Akt Pathway. Retrovirology 2 (Suppl 1), S44 (2005).

Download citation

  • Published:

  • DOI: