A dormant internal ribosome entry site controls translation of feline immunodeficiency virus
A dormant internal ribosome entry site controls translation of feline immunodeficiency virus
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DOI：
10.1128/jvi.02038-07
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发表时间：
2008-04-01
影响因子：
5.4
通讯作者：
Ohlmann, Thophile
中科院分区：
文献类型：
--
作者：
Camerini, Valentina;Decimo, Didier;Ohlmann, Thophile
几乎所有慢病毒的内部核糖体进入位点（IRES）的特征促使我们研究猫免疫缺陷病毒（FIV）产生病毒蛋白的机制。单顺反子和双顺反子构建体的各种体外翻译测定显示，FIV基因组RNA的翻译通过帽依赖性机制和核糖体的弱内部进入发生。在表达含有FIV 5'非翻译区（UTR）的双顺反子RNA的猫细胞中证实了这种弱IRES活性。令人惊讶的是，用FIV感染猫细胞，而不是人类免疫缺陷病毒1型，导致FIN翻译大大增加。此外，由热应激引起的细胞生理条件的变化导致由FIV 5' UTR驱动的表达的特异性刺激，而帽依赖性起始被严重抑制。这些结果揭示了存在一个“休眠”的IRES，它被病毒感染和细胞应激激活。
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 FIN 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.