Adenovirus infection inactivates the translational inhibitors 4E-BP1 and 4E-BP2.
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| Abstract |
Infection with many viruses results in the selective shutoff of host protein synthesis. A common target for virus interference with host protein synthesis is the cap-binding protein complex, eIF4F. The large subunit of the complex, eIF4G, is cleaved upon picornavirus (except cardiovirus) infection. Infection with adenovirus and influenza virus causes dephosphorylation of the cap-binding subunit, eIF4E. Recently, it has been shown that infection with poliovirus or encephalomyocarditis virus activates 4E-BP1, which is a specific inhibitor of eIF4E. Here we show that early in adenovirus infection, 4E-BP1 and its related protein 4E-BP2 are phosphorylated and hence inactivated. This is not consistent with a role of 4E-BPs in adenovirus-induced shutoff, but could explain the increase in protein synthesis reported early in infection. Phosphorylation of 4E-BP1 and 4E-BP2 is consistent with earlier findings in adenovirus-infected cells on the activation of the protein kinase p70(S6k), whose phosphorylation lies on the same pathway as 4E-BPs, by E1A. Findings similar to those described here were reported for 4E-BP1 by D. Feigenblum and R. J. Schneider (1996, Mol. Cell. Biol. 16, 5450-5457).
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| Authors | A C Gingras, N Sonenberg |
| Journal | Virology (Virology) Vol. 237 Issue 1 Pg. 182-6 (Oct 13 1997) ISSN: 0042-6822 [Print] United States |
| PMID | 9344920 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't) |
| Copyright | Copyright 1997 Academic Press. |
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