Stress granules (SGs), complexes for mRNA storage, are formed in host cellular response to stress stimuli and play an important role in innate immune response. GTPase-activating protein (SH3 domain)-binding protein 1 (G3BP1) is a key component of SGs. However, whether IBDV infection induces SG formation in host cells and what role of G3BP1 plays in this process are unclear. We report here that IBDV infection initiated typical stress granule formation and enhanced G3BP1 expression in DF-1 cells. Our data show that knockdown of G3BP1 by RNAi markedly inhibited IBDV-induced SG formation and viral replication in DF-1 cells. Conversely, ectopic expression of G3BP1 enhanced IBDV-induced SG formation and significantly promoted IBDV replication in host cells. Thus, G3BP1 plays a critical role in IBDV-induced SG formation and viral replication, providing an important clue to elucidating how IBDV employs cellular SGs for its own benefits.

应激颗粒（SGs​​）是用于mRNA存储的复合物，在宿主细胞对应激刺激的反应中形成，并在先天免疫反应中起重要作用。GTPase激活蛋白（SH3域）结合蛋白1（G3BP1）是SG的关键组成部分。但是，尚不清楚IBDV感染是否诱导宿主细胞中SG形成以及G3BP1在此过程中起什么作用。我们在这里报告IBDV感染开始典型的应激颗粒形成和DF-1细胞中增强的G3BP1表达。我们的数据表明，RNAi对G3BP1的抑制显着抑制了DF-1细胞中IBDV诱导的SG的形成和病毒复制。相反，G3BP1的异位表达增强了IBDV诱导的SG的形成，并显着促进了IBDV在宿主细胞中的复制。因此，G3BP1在IBDV诱导的SG形成和病毒复制中起关键作用，