Norovirus infection results in eIF2α independent host translation shut-off and remodels the G3BP1 interactome evading stress granule formation.

Michèle Brocard, Valentina Iadevaia, Philipp Klein, Belinda Hall, Glenys Lewis, Jia Lu, James Burke, Margaret M Willcocks, Roy Parker, Ian G Goodfellow, Alessia Ruggieri & Nicolas Locker
Viral infections impose major stress on the host cell. In response, stress pathways can rapidly deploy defence mechanisms by shutting off the protein synthesis machinery 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. Here we examined how norovirus interacts with the eIF2α signaling axis...
This data repository is not currently reporting usage information. For information on how your repository can submit usage information, please see our documentation.