Translation of Hepatitis A Virus IRES Is Upregulated by a Hepatic Cell-Specific Factor
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- 貞廣, 暁利
- Laboratory of Infection and Prevention, Department of Virus Research, Institute for Frontier Life and Medical Sciences, Kyoto University
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- 竹内, 理
- Laboratory of Biochemistry, Graduate School of Pharmaceutical Sciences, Kindai University
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- Kosaka, Mio
- Laboratory of Biochemistry, Graduate School of Pharmaceutical Sciences, Kindai University
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- Funakami, Yoshinori
- Laboratory of Biochemistry, Graduate School of Pharmaceutical Sciences, Kindai University
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- Takizawa, Naoki
- Laboratory of Virology, Institute of Microbial Chemistry (BIKAKEN)
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- Takeuchi, Osamu
- Laboratory of Infection and Prevention, Department of Virus Research, Institute for Frontier Life and Medical Sciences, Kyoto University
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- Duncan, Kent E.
- Center for Molecular Neurobiology, University Medical Center Hamburg-Eppendorf
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- Fujiwara, Toshinobu
- Laboratory of Biochemistry, Graduate School of Pharmaceutical Sciences, Kindai University
抄録
Many viruses strongly prefer to infect certain cell types, a phenomenon known as “tropism.” Understanding tropism’s molecular basis is important for the design of vaccines and antiviral therapy. A common mechanism involves viral protein interactions with cell-specific surface receptors, but intracellular mechanisms involving translation have also been described. In this report, we focus on Hepatitis A Virus (HAV) tissue tropism from the standpoint of the translational machinery. HAV genomic RNA, like other positive stranded RNA viruses, is devoid of a cap structure and its translation is driven by highly structured RNA sequences termed internal ribosome entry site (IRES) in the 5′ untranslated region (UTR). Unlike most viral IRESs, HAV IRES-mediated translation requires eIF4E and the 3′ end of HAV RNA is polyadenylated. However, the molecular mechanism of HAV IRES-mediated translation initiation remains poorly understood. We analyzed HAV-IRES-mediated translation in a cell-free system derived from either non-hepatic cells (HeLa) or hepatoma cells (Huh-7) that enables investigation of the contribution of the cap and the poly(A) tail. This revealed that HAV IRES-mediated translation activity in hepatoma cell extracts is higher as compared to extracts derived from a non-hepatic line. Our data suggest that HAV IRES-mediated translation is upregulated by a hepatic cell-specific activator in a poly(A) tail-independent manner.
収録刊行物
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- Frontiers in genetics
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Frontiers in genetics 9 2018-08-10
Frontiers Media SA
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詳細情報 詳細情報について
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- CRID
- 1050564288161173888
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- NII論文ID
- 120006534584
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- ISSN
- 16648021
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- HANDLE
- 2433/234930
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- 本文言語コード
- en
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- 資料種別
- journal article
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- データソース種別
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- IRDB
- Crossref
- CiNii Articles
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