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

• DOI: 10.1371/journal.ppat.1008250
• Publication Date: 2020-01-06T18:31:03Z
• Authors: Michèle Brocard; Valentina Iadevaia; Philipp Klein; Belinda Hall; Glenys Lewis; Jia Lu; James Burke; Margaret M. Willc...; Roy Parker; Ian G. Goodfellow; Alessia Ruggieri; Nicolas Locker
• Keywords: Stress granule; Interactome; Integrated stress response

Viral infections impose major stress on the host cell. In response, pathways can rapidly deploy defence mechanisms by shutting off protein synthesis machinery and triggering accumulation of mRNAs into granules to limit use energy nutrients. Because this threatens viral gene expression, viruses need evade these propagate. Human norovirus is responsible for gastroenteritis outbreaks worldwide. Here we examined how interacts with eIF2α signaling axis controlling translation granules. While infection represses cell translation, our mechanistic analyses revealed that mediated kinase GCN2 uncoupled from translational stalling. Moreover, results in a redistribution RNA-binding G3BP1 replication complexes remodelling its interacting partners, allowing avoidance canonical These define novel strategies which undergo efficient whilst avoiding response manipulating interactome.