Takeover of host ribosomes by divergent IRES elements

被引:39
|
作者
Sarnow, P [1 ]
Cevallos, RC [1 ]
Jan, E [1 ]
机构
[1] Stanford Univ, Sch Med, Dept Immunol & Microbiol, Stanford, CA 94305 USA
关键词
eukaryotic initiation factof 4E (eIF4E); eukaryotic initiation factor 4E-binding protein (4E-BP); hepatitis C virus (HCV); insect virus; internal ribosome entry site (IRES); translation; PICORNA-LIKE VIRUS; ENTRY SITE; TRANSLATION INITIATION; HEPATITIS-C; INTERNAL INITIATION; TAURA-SYNDROME; 80S RIBOSOME; RNA; ELONGATION; PROTEIN;
D O I
10.1042/BST0331479
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The ribosome is the macromolecular machinery in the host cell for which all viruses have to compete. Early in infection, the viral mRNAs have to compete with the host for both the ribosomes and for the limited pool of eukaryotic initiation factors that are needed to facilitate the recruitment of ribosomes to both viral and cellular mRNAs. To circumvent this competition, certain viruses have evolved to recruit ribosomes to IRESs (internal ribosome entry sites), highly specialized RNA elements that are located at the 5'-end of the viral genomes. Here, we discuss how divergent IRES elements can recruit ribosomes and start protein synthesis with only a minimal set of eukaryotic translation initiation factors, and how this mode of translation initiation aids viral gene amplification during early onset of innate immune responses.
引用
收藏
页码:1479 / 1482
页数:4
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