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Journal of Virology, April 2009, p. 3988-3992, Vol. 83, No. 8
0022-538X/09/$08.00+0     doi:10.1128/JVI.02284-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

PI3K Signaling Regulates Rapamycin-Insensitive Translation Initiation Complex Formation in Vaccinia Virus-Infected Cells{triangledown}

Izabela Zaborowska and Derek Walsh*

National Institute for Cellular Biotechnology, Dublin City University, Dublin 9, Ireland

Received 31 October 2008/ Accepted 1 February 2009

How vaccinia virus (VV) regulates assembly of the host translation initiation complex eIF4F remains unclear. Here, we show that VV activated host PI3K to stimulate downstream mammalian target of rapamycin (mTOR), a kinase that inactivates the translational repressor 4E-BP1. However, although the mTOR inhibitor rapamycin suppressed VV-induced inactivation of 4E-BP1, it failed to inhibit eIF4F assembly. In contrast, PI3K inhibition in VV-infected cells increased the abundance of hypophosphorylated 4E-BP1 and disrupted eIF4F complex formation. PI3K signaling, therefore, plays a critical role in regulating protein production during VV infection, at least in part by controlling the abundance and activity of 4E-BP1.

* Corresponding author. Mailing address: National Institute for Cellular Biotechnology, Dublin City University, Dublin 9, Ireland. Phone: 353-1-7006260. Fax: 353-1-7005484. E-mail: derek.walsh{at}dcu.ie

{triangledown} Published ahead of print on 11 February 2009.

Journal of Virology, April 2009, p. 3988-3992, Vol. 83, No. 8
0022-538X/09/$08.00+0     doi:10.1128/JVI.02284-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



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