Nicolas LOCKER

Professor, Virology, School of Biosciences and Medicine, Faculty of Health and Medical Sciences, University of Surrey, Guildford,UK

Thursday 24 October 2019 | 12:00 noon – ICGEB Trieste, ITALY

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

Host: A. Marcello

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. We have examined how norovirus interacts with the eIF2 α signaling axis controlling translation and stress granules. While norovirus infection represses host cell translation, our mechanistic analyses revealed that eIF2 α signaling is uncoupled from translational stalling. Moreover, infection results in the assembly of virus-specific granules, evidenced by a redistribution of the RNA-binding protein G3BP1 interacting partners, rather than canonical stress granules. These results define novel strategies by which norovirus undergo efficient replication whilst avoiding and manipulating the host stress response.