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Norovirus infection results in assembly of virus-specific G3BP1 granules and evasion of eIF2α signaling

Michèle Brocard, Valentina Iadevaia, Philipp Klein, Belinda Hall, Glenys Lewis, Jia Lu, James Burke, Roy Parker, Alessia Ruggieri, Ian G. Goodfellow, View ORCID ProfileNicolas Locker
doi: https://doi.org/10.1101/490318
Michèle Brocard
1Faculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford, United Kingdom.
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Valentina Iadevaia
1Faculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford, United Kingdom.
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Philipp Klein
3Department of Infectious Diseases, Molecular Virology, Centre for Integrative Infectious Disease Research, University of Heidelberg, Heidelberg, Germany.
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Belinda Hall
1Faculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford, United Kingdom.
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Glenys Lewis
1Faculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford, United Kingdom.
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Jia Lu
2Division of Virology, Department of Pathology, University of Cambridge, Addenbrooke’s Hospital, Hills Road, Cambridge CB2 2QQ, United Kingdom.
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James Burke
4Department of Biochemistry, University of Colorado, Boulder, CO
5Howard Hughes Medical Institute, University of Colorado, Boulder, CO.
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Roy Parker
4Department of Biochemistry, University of Colorado, Boulder, CO
5Howard Hughes Medical Institute, University of Colorado, Boulder, CO.
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Alessia Ruggieri
3Department of Infectious Diseases, Molecular Virology, Centre for Integrative Infectious Disease Research, University of Heidelberg, Heidelberg, Germany.
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Ian G. Goodfellow
2Division of Virology, Department of Pathology, University of Cambridge, Addenbrooke’s Hospital, Hills Road, Cambridge CB2 2QQ, United Kingdom.
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Nicolas Locker
1Faculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford, United Kingdom.
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  • ORCID record for Nicolas Locker
  • For correspondence: n.locker@surrey.ac.uk
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ABSTRACT

During viral infection, the accumulation of RNA replication intermediates or viral proteins imposes major stress on the host cell. In response, cellular stress pathways can rapidly impose defence mechanisms by shutting off the protein synthesis machinery, which viruses depend on, and triggering the accumulation of mRNAs into stress granules to limit the use of energy and nutrients. Because this threatens viral gene expression, viruses need to evade these pathways to propagate. Human norovirus is responsible for gastroenteritis outbreaks worldwide. Previously we showed that murine norovirus (MNV) regulates the activity of eukaryotic initiation factors (eIFs). Here we examined how MNV interacts with the eIF2α signaling axis controlling translation and stress granules accumulation. We show that while MNV infection represses host cell translation, it results in the assembly of virus-specific granules rather than stress granules. Further mechanistic analyses revealed that eIF2α signaling is uncoupled from translational stalling. Moreover the interaction of the RNA-binding protein G3BP1 with viral factors together with a redistribution of its cellular interacting partners could explain norovirus evasion of stress granules assembly. These results identify novel strategies by which norovirus ensure efficient replication propagation by manipulating the host stress response.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted December 09, 2018.
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Norovirus infection results in assembly of virus-specific G3BP1 granules and evasion of eIF2α signaling
Michèle Brocard, Valentina Iadevaia, Philipp Klein, Belinda Hall, Glenys Lewis, Jia Lu, James Burke, Roy Parker, Alessia Ruggieri, Ian G. Goodfellow, Nicolas Locker
bioRxiv 490318; doi: https://doi.org/10.1101/490318
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Norovirus infection results in assembly of virus-specific G3BP1 granules and evasion of eIF2α signaling
Michèle Brocard, Valentina Iadevaia, Philipp Klein, Belinda Hall, Glenys Lewis, Jia Lu, James Burke, Roy Parker, Alessia Ruggieri, Ian G. Goodfellow, Nicolas Locker
bioRxiv 490318; doi: https://doi.org/10.1101/490318

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