Ricci Emiliano P, Soto Rifo Ricardo, Herbreteau Cécile H, Decimo Didier, Ohlmann Théophile
Unité de Virologie Humaine, Ecole Normale Supérieure de Lyon, IFR 128, Lyon, F-69364, France.
Biochem Soc Trans. 2008 Aug;36(Pt 4):690-3. doi: 10.1042/BST0360690.
The full-length genomic RNA of lentiviruses can be translated to produce proteins and incorporated as genomic RNA in the viral particle. Interestingly, both functions are driven by the genomic 5'-UTR (5'-untranslated region), which harbours structural RNA motifs for the replication cycle of the virus. Recent work has shown that this RNA architecture also functions as an IRES (internal ribosome entry site) in HIV-1 and -2, and in SIV (simian immunodeficiency virus). In addition, the IRES extends to the gag coding region for all these viruses and this leads to the synthesis of shorter isoforms of the Gag polyprotein from downstream initiation codons. In the present study, we have investigated how different members of the lentivirus family (namely HIV-1 and -2, and SIV) can initiate protein synthesis by distinct mechanisms. For this, we have used the competitive reticulocyte lysate that we have recently described. Our results show that HIV-1 is able to drive the synthesis of the Gag polyprotein both by a classical cap-dependent mechanism and an IRES, whereas HIV-2 and SIV appear to use exclusively an IRES mechanism.
慢病毒的全长基因组RNA可被翻译以产生蛋白质，并作为基因组RNA整合到病毒颗粒中。有趣的是，这两种功能均由基因组5'-UTR（5'-非翻译区）驱动，该区域含有病毒复制周期的结构性RNA基序。最近的研究表明，这种RNA结构在HIV-1、HIV-2和猴免疫缺陷病毒（SIV）中也作为内部核糖体进入位点（IRES）发挥作用。此外，所有这些病毒的IRES延伸至gag编码区，这导致从下游起始密码子合成较短的Gag多蛋白异构体。在本研究中，我们研究了慢病毒家族的不同成员（即HIV-1、HIV-2和SIV）如何通过不同机制启动蛋白质合成。为此，我们使用了我们最近描述的竞争性网织红细胞裂解物。我们的结果表明，HIV-1能够通过经典的帽依赖性机制和IRES驱动Gag多蛋白的合成，而HIV-2和SIV似乎仅使用IRES机制。
