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Enterovirus 71 contains a type I IRES element that functions when eukaryotic initiation factor eIF4G is cleaved
Sunnie R Thompson1, Peter Sarnow
1Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Virology
|November 1, 2003
Summary
Human enterovirus 71 (EV71) utilizes an internal ribosome entry site (IRES) for translation initiation. This EV71 IRES functions similarly to other enterovirus IRES elements, even when cap-dependent translation is inhibited.
Area of Science:
- Virology
- Molecular Biology
- Biochemistry
Background:
- Human enterovirus 71 (EV71) belongs to the Enterovirus genus within the Picornaviridae family.
- Many enteroviruses employ an internal ribosome entry site (IRES) for translation initiation, bypassing the typical cap-dependent mechanism.
Purpose of the Study:
- To investigate the translation initiation mechanism of EV71.
- To characterize the function of the 5' noncoding region (5' NCR) of EV71 as an IRES.
Main Methods:
- Utilized dicistronic reporter constructs to assess IRES activity in vitro and in cultured cells.
- Examined the effect of coxsackievirus 2A protease cleavage of eIF4G on EV71 IRES function.
- Investigated the impact of an upstream out-of-frame start codon on IRES activity.
Main Results:
- Demonstrated that the 5' NCRs of EV71 strains function as an IRES.
- Showed that EV71 IRES activity is enhanced when cap-binding complex components are cleaved, similar to other enteroviruses.
- Identified EV71 as a type I IRES, dependent on scanning from an upstream position.
Conclusions:
- EV71 employs an IRES-dependent translation initiation mechanism.
- The EV71 IRES exhibits characteristics of a type I IRES, functioning independently of cap-dependent translation initiation.