The Pirbright Institute, Pirbright, Surrey GU24 0NF, UK.
Faculty of Health and Medical Sciences, School of Biosciences and Medicine, University of Surrey, Guildford, Surrey GU2 7XH, UK.
Viruses. 2020 May 14;12(5):536. 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.
病毒必须劫持细胞翻译机制来表达病毒基因。在许多情况下，这会受到细胞应激反应的阻碍。这些应激反应会导致翻译的全面抑制，并将停滞的 mRNA 储存为 RNA-蛋白质聚集体，称为应激颗粒。这导致大多数 mRNA 的翻译沉默，除了那些有利于细胞解决特定应激的 mRNA 除外。例如，抗病毒因子的表达在病毒感染期间得到维持。在这里，我们研究了传染性支气管炎病毒 (IBV) 对应激颗粒的调节作用，IBV 会导致具有重要经济意义的家禽疾病——传染性支气管炎。有趣的是，我们发现 IBV 能够抑制多种细胞应激颗粒信号通路，而与此同时，IBV 的复制也会导致一部分感染细胞中诱导出看似典型的应激颗粒。此外，IBV 感染会使翻译抑制和应激颗粒形成脱偶联，这两个过程都不依赖于 eIF2α 磷酸化。这些结果为 IBV 如何调节细胞翻译和抗病毒应激信号提供了新的见解。
