HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Shin, Y.-K. Articles by Zhou, Y. Search for Related Content PubMed PubMed Citation Articles by Shin, Y.-K. Articles by Zhou, Y. Agricola Articles by Shin, Y.-K. Articles by Zhou, Y.

Effect of the phosphatidylinositol 3-kinase/Akt pathway on influenza A virus propagation

Vaccine and Infectious Disease Organization, University of Saskatchewan, Saskatoon, SK S7N 5E3, Canada

Correspondence
Yan Zhou
yan.zhou{at}usask.ca

The phosphatidylinositol 3-kinase (PI3K)/Akt signalling pathway has attracted much recent interest due to its central role in modulating diverse downstream signalling pathways associated with cell survival, proliferation, differentiation, morphology and apoptosis. An increasing amount of information has demonstrated that many viruses activate the PI3K/Akt pathway to augment their efficient replication. In this study, the effect of the PI3K/Akt signalling pathway on influenza virus propagation was investigated. It was found that Akt phosphorylation was elevated in the late phase of influenza A/PR/8/34 infection in human lung carcinoma cells (A549). The PI3K-specific inhibitor LY294002 could suppress Akt phosphorylation, suggesting that influenza A virus-induced Akt phosphorylation is PI3K-dependent. UV-irradiated influenza virus failed to induce Akt phosphorylation, indicating that viral attachment and entry were not sufficient to trigger PI3K/Akt pathway activation. Blockage of PI3K/Akt activation by LY294002 and overexpression of the general receptor for phosphoinositides-1 PH domain (Grp1-PH) led to a reduction in virus yield. Moreover, in the presence of LY294002, viral RNA synthesis and viral protein expression were suppressed and, possibly as a consequence of low NP and M1 protein level, viral RNP nuclear export was also suppressed. These data suggest that the PI3K/Akt signalling pathway plays a role in influenza virus propagation.

This article has been cited by other articles:

				Y. Li, D. H. Anderson, Q. Liu, and Y. Zhou Mechanism of Influenza A Virus NS1 Protein Interaction with the p85{beta}, but Not the p85{alpha}, Subunit of Phosphatidylinositol 3-Kinase (PI3K) and Up-regulation of PI3K Activity J. Biol. Chem., August 22, 2008; 283(34): 23397 - 23409. [Abstract] [Full Text] [PDF]

				L. S. Heikkinen, A. Kazlauskas, K. Melen, R. Wagner, T. Ziegler, I. Julkunen, and K. Saksela Avian and 1918 Spanish Influenza A Virus NS1 Proteins Bind to Crk/CrkL Src Homology 3 Domains to Activate Host Cell Signaling J. Biol. Chem., February 29, 2008; 283(9): 5719 - 5727. [Abstract] [Full Text] [PDF]

				B. G. Hale, I. H. Batty, C. P. Downes, and R. E. Randall Binding of Influenza A Virus NS1 Protein to the Inter-SH2 Domain of p85 Suggests a Novel Mechanism for Phosphoinositide 3-Kinase Activation J. Biol. Chem., January 18, 2008; 283(3): 1372 - 1380. [Abstract] [Full Text] [PDF]

				Y.-K. Shin, Y. Li, Q. Liu, D. H. Anderson, L. A. Babiuk, and Y. Zhou SH3 Binding Motif 1 in Influenza A Virus NS1 Protein Is Essential for PI3K/Akt Signaling Pathway Activation J. Virol., December 1, 2007; 81(23): 12730 - 12739. [Abstract] [Full Text] [PDF]