Open AccessA Dormant Internal Ribosome Entry Site Controls Translation of Feline Immunodeficiency Virus
Author(s) -
Valentina Camerini,
Didier Décimo,
Laurent Balvay,
Mauro Pistello,
Mauro Bendinelli,
JeanLuc Darlix,
Théophile Ohlmann
Publication year - 2008
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.02038-07
Subject(s) - internal ribosome entry site , biology , feline immunodeficiency virus , translation (biology) , ribosome , virology , five prime untranslated region , untranslated region , stress granule , rna , messenger rna , protein biosynthesis , eukaryotic initiation factor , microbiology and biotechnology , virus , lentivirus , genetics , gene , viral disease
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.