Pseudorabies virus (PRV) is one of the most notorious pathogens in the global pig industry. During infection, viruses may evolve various strategies, such as modulating stress granules (SGs) formation, to create an optimal surroundings for viral replication. However, the interplay between PRV infection and SGs formation remains largely unknown. Here we showed that PRV infection markedly blocked SGs formation induced by sodium arsenate (AS) and DL-Dithiothreitol (DTT). Accordantly, the phosphorylation of eIF2α was markedly inhibited in PRV-infected cells, although two eIF2α kinases double-stranded RNA-activated protein kinase (PKR) and PKR-like ER kinase (PERK) were activated during PRV infection. Furthermore, we also found that the dephosphorylation of eIF2α occurred at the early stage of virus infection but without the elevated production of GADD34 and PP1. Moreover, inhibition of PP1 activity by salubrinal could counteract PRV-mediated eIF2α dephosphorylation partially and inhibit virus replication. Our results revealed that, on the one hand, PRV infection activated eIF2α kinases PKR (latter inhibited) and PERK, and on the other hand, PRV encoded-functions dephosphorylated eIF2α and inhibited SGs formation to facilitate virus replication.

伪狂犬病病毒（PRV）是全球养猪业中最臭名昭著的病原体之一。在感染过程中，病毒可能会进化各种策略，例如调节应激颗粒（SGs​​）的形成，从而为病毒复制创造最佳环境。然而，PRV感染和SGs形成之间的相互作用仍然未知。在这里，我们显示PRV感染显着阻断了由砷酸钠（AS）和DL-二硫苏糖醇（DTT）诱导的SGs的形成。因此，尽管在PRV感染过程中激活了两个eIF2α激酶双链RNA激活蛋白激酶（PKR）和PKR样ER激酶（PERK），但ePR2α的磷酸化在PRV感染的细胞中被显着抑制。此外，我们还发现eIF2α的去磷酸化发生在病毒感染的早期，但GADD34和PP1的产生却没有升高。此外，金枪鱼对PP1活性的抑制作用可以部分抵消PRV介导的eIF2α去磷酸化并抑制病毒复制。我们的研究结果表明，一方面，PRV感染激活了eIF2α激酶PKR（被抑制）和PERK，另一方面，PRV编码的功能使eIF2α磷酸化并抑制了SGs的形成，从而促进了病毒的复制。