Abstract
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 Gammacoronavirus 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.
Highlights
During replication within a host cell, all viruses must regulate a variety of cellular processes to generate an environment that allows progeny virus to be produced to continue the infection cycle.This includes promoting pathways that are favorable to replication and overcoming intrinsic immune pathways
Vero cells were infected with infectious bronchitis virus (IBV) and at the indicated time points, cells were fixed and labelled with anti-dsRNA to detect virus infection and with anti-GAP SH3-domain binding protein 1 (G3BP1) to detect stress granules (SG)
At each of the time points tested, G3BP1 puncta were detected in a proportion of, but not all, infected cells, with diffuse G3BP1 found in the remaining infected and uninfected cells
Summary
During replication within a host cell, all viruses must regulate a variety of cellular processes to generate an environment that allows progeny virus to be produced to continue the infection cycle. This includes promoting pathways that are favorable to replication and overcoming intrinsic immune pathways. SG are cytoplasmic, non-membrane bound aggregations of mRNA associated with translation initiation factors, the 40S ribosome and RNA binding proteins. They primarily form under stress conditions that trigger the phosphorylation of translation initiation factor eIF2α [3]. SG can be Viruses 2020, 12, 536; doi:10.3390/v12050536 www.mdpi.com/journal/viruses
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