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Journal of Virology, February 2007, p. 2083-2086, Vol. 81, No. 4
0022-538X/07/$08.00+0     doi:10.1128/JVI.01655-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

The Cytomegalovirus Homolog of Interleukin-10 Requires Phosphatidylinositol 3-Kinase Activity for Inhibition of Cytokine Synthesis in Monocytes

Department of Biology, University of San Francisco, San Francisco, California 94117

Received 1 August 2006/ Accepted 13 November 2006

Human cytomegalovirus (CMV) has evolved numerous strategies for evading host immune defenses, including piracy of cellular cytokines. A viral homolog of interleukin-10, designated cmvIL-10, binds to the cellular IL-10 receptor and effects potent immune suppression. The signaling pathways employed by cmvIL-10 were investigated, and the classic IL-10R/JAK1/Stat3 pathway was found to be activated in monocytes. However, inhibition of JAK1 had little effect on cmvIL-10-mediated suppression of tumor necrosis factor alpha (TNF-) production. Inhibition of the phosphatidylinositol 3-kinase/Akt pathway had a more significant impact on TNF- levels but did not completely relieve the immune suppression, demonstrating that cmvIL-10 stimulates multiple signaling pathways to modulate cell function.

Published ahead of print on 22 November 2006.

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