Infectious bronchitis virus (IBV), a gammacoronavirus, causes the economically important poultry disease, infectious bronchitis, resulting in reduced weight gain and egg quality. As observed for many viruses, during replication, IBV shuts off translation of host proteins, preventing synthesis of important products of the innate immunity, which are pivotal in fighting viral infection. This work investigates the role of stress granules in IBV translational control. Stress granules are membranes-less aggregations of stalled translation initiation complexes comprising translation initiation factors, 40S ribosome and RNA binding proteins. These structures serve as sites of storage and sequestration of translational machinery and cellular mRNA while simultaneously enabling intracellular signalling and antiviral responses. It is shown here by immunofluorescence that IBV induces stress granules in only a proportion of infected cells. These stress granules occur late in the virus life cycle and appear canonical, containing multiple stress granule markers and showing mRNA exchange with ribosomes. In addition, stress granule markers are not diverted to sites of virus replication, as seen during replication of some other viruses. Interestingly, IBV infection results in resistance to chemicals that induce stress granules via eukaryotic initiation factor 2α (eIF2α). Consistent with this, eIF2α is not phosphorylated at any time during IBV infection. This also indicates a non-canonical signalling pathway for IBV-induced stress granules. Significantly, stress granule formation is uncoupled from translational arrest as visualised using ribopuromycylation. Therefore, IBV replication both induces and inhibits cellular stress granule signalling in a process that is uncoupled from shut off of host translation.

  • This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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