This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Camerini, V.
Right arrow Articles by Ohlmann, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Camerini, V.
Right arrow Articles by Ohlmann, T.

 Previous Article  |  Next Article 

Journal of Virology, April 2008, p. 3574-3583, Vol. 82, No. 7
0022-538X/08/$08.00+0     doi:10.1128/JVI.02038-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

A Dormant Internal Ribosome Entry Site Controls Translation of Feline Immunodeficiency Virus{triangledown}

Valentina Camerini,1,2,3 Didier Decimo,1,2 Laurent Balvay,1,2 Mauro Pistello,3 Mauro Bendinelli,3 Jean-Luc Darlix,1,2 and Théophile Ohlmann1,2*

Ecole Normale Supérieure de Lyon, Unité de Virologie Humaine, IFR 128, Lyon F-69364, France,1 INSERM, U758, Lyon F-69364, France,2 Retrovirus Center and Virology Section, Department of Experimental Pathology, University of Pisa, Via San Zeno, 35, I-56127 Pisa, Italy3

Received 14 September 2007/ Accepted 21 January 2008

The characterization of internal ribosome entry sites (IRESs) in virtually all lentiviruses prompted us to investigate the mechanism used by the feline immunodeficiency virus (FIV) to produce viral proteins. Various in vitro translation assays with mono- and bicistronic constructs revealed that translation of the FIV genomic RNA occurred both by a cap-dependent mechanism and by weak internal entry of the ribosomes. This weak IRES activity was confirmed in feline cells expressing bicistronic RNAs containing the FIV 5' untranslated region (UTR). Surprisingly, infection of feline cells with FIV, but not human immunodeficiency virus type 1, resulted in a great increase in FIV translation. Moreover, a change in the cellular physiological condition provoked by heat stress resulted in the specific stimulation of expression driven by the FIV 5' UTR while cap-dependent initiation was severely repressed. These results reveal the presence of a "dormant" IRES that becomes activated by viral infection and cellular stress.


* Corresponding author. Mailing address: INSERM, U758, Lyon F-69364, France. Phone: (33) 4 72 72 89 53. Fax: (33) 4 72 72 81 37. E-mail: tohlmann{at}ens-lyon.fr

{triangledown} Published ahead of print on 30 January 2008.


Journal of Virology, April 2008, p. 3574-3583, Vol. 82, No. 7
0022-538X/08/$08.00+0     doi:10.1128/JVI.02038-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Kenyon, J. C., Ghazawi, A., Cheung, W. K.S., Phillip, P. S., Rizvi, T. A., Lever, A. M.L. (2008). The secondary structure of the 5' end of the FIV genome reveals a long-range interaction between R/U5 and gag sequences, and a large, stable stem-loop. RNA 14: 2597-2608 [Abstract] [Full Text]  
  • Ricci, E. P., Herbreteau, C. H., Decimo, D., Schaupp, A., Datta, S. A.K., Rein, A., Darlix, J.-L., Ohlmann, T. (2008). In vitro expression of the HIV-2 genomic RNA is controlled by three distinct internal ribosome entry segments that are regulated by the HIV protease and the Gag polyprotein. RNA 14: 1443-1455 [Abstract] [Full Text]