Infectious Bronchitis Virus Regulates Cellular Stress Granule Signaling

• Published in: Viruses 2020-05, Vol.12 (5), p.536
• Main Authors: Brownsword, Matthew J, Doyle, Nicole, Brocard, Michèle, Locker, Nicolas, Maier, Helena J
• Format: Article
• Language: English
• Subjects: Analysis; Animal diseases; Animals; Bronchitis; Cell regulation; Cellular stress response; Chlorocebus aethiops; Control; Coronavirus Infections - metabolism; Coronavirus Infections - physiopathology; Coronavirus Infections - veterinary; Coronavirus Infections - virology; Coronaviruses; Cytoplasmic Granules - metabolism; Cytoplasmic Granules - virology; Diagnosis; eIF2α; Eukaryotic Initiation Factor-2 - genetics; Eukaryotic Initiation Factor-2 - metabolism; host shut-off; Host-Pathogen Interactions; IBV; infectious bronchitis virus; Infectious bronchitis virus - genetics; Infectious bronchitis virus - physiology; Kinases; Middle East respiratory syndrome; Phosphorylation; Poultry Diseases - genetics; Poultry Diseases - metabolism; Poultry Diseases - physiopathology; Poultry Diseases - virology; Protein Biosynthesis; Ribonucleic acid; RNA; Stress (Physiology); stress granule; Translation; Vero Cells; Virus Replication; Viruses
• ISSN: 1999-4915; 1999-4915
• DOI: 10.3390/v12050536

Viruses must hijack cellular translation machinery to express viral genes. In many cases, this is impeded by cellular stress responses. These stress responses result in the global inhibition of translation and the storage of stalled mRNAs, into RNA-protein aggregates called stress granules. This results in the translational silencing of the majority of mRNAs excluding those beneficial for the cell to resolve the specific stress. For example, the expression of antiviral factors is maintained during viral infection. Here we investigated stress granule regulation by infectious bronchitis virus (IBV), which causes the economically important poultry disease, infectious bronchitis. Interestingly, we found that IBV is able to inhibit multiple cellular stress granule signaling pathways, whilst at the same time, IBV replication also results in the induction of seemingly canonical stress granules in a proportion of infected cells. Moreover, IBV infection uncouples translational repression and stress granule formation and both processes are independent of eIF2α phosphorylation. These results provide novel insights into how IBV modulates cellular translation and antiviral stress signaling.