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Viruses 2016, 8(4), 104; doi:10.3390/v8040104

Translational Control during Calicivirus Infection

Faculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford GU2 7HX, UK
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Author to whom correspondence should be addressed.
Academic Editor: Craig McCormick
Received: 29 February 2016 / Revised: 14 April 2016 / Accepted: 15 April 2016 / Published: 20 April 2016
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Abstract

In this review, we provide an overview of the strategies developed by caliciviruses to subvert or regulate the host protein synthesis machinery to their advantage. As intracellular obligate parasites, viruses strictly depend on the host cell resources to produce viral proteins. Thus, many viruses have developed strategies that regulate the function of the host protein synthesis machinery, often leading to preferential translation of viral mRNAs. Caliciviruses lack a 5′ cap structure but instead have a virus-encoded VPg protein covalently linked to the 5′ end of their mRNAs. Furthermore, they encode 2–4 open reading frames within their genomic and subgenomic RNAs. Therefore, they use alternative mechanisms for translation whereby VPg interacts with eukaryotic initiation factors (eIFs) to act as a proteinaceous cap-substitute, and some structural proteins are produced by reinitiation of translation events. This review discusses our understanding of these key mechanisms during caliciviruses infection as well as recent insights into the global regulation of eIF4E activity. View Full-Text
Keywords: calicivirus; VPg; reinitiation calicivirus; VPg; reinitiation
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Royall, E.; Locker, N. Translational Control during Calicivirus Infection. Viruses 2016, 8, 104.

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