A dormant internal ribosome entry site controls translation of feline immunodeficiency virus |
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Authors: | Camerini Valentina Decimo Didier Balvay Laurent Pistello Mauro Bendinelli Mauro Darlix Jean-Luc Ohlmann Théophile |
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Institution: | 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 |
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Abstract: | 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. |
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