Critical role for G3BP1 in infectious bursal disease virus (IBDV)-induced stress granule formation and viral replication

• Published in: Veterinary microbiology Vol. 248; p. 108806
• Main Authors: Zhao, Dianzheng, Li, Jiaxin, Wang, Yongqiang, Li, Xiaoqi, Gao, Li, Cao, Hong, Zheng, Shijun J.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 01.09.2020; Elsevier BV
• Subjects: Ectopic expression; G3BP1; GTPase-activating protein; IBDV; Immune response; Innate immunity; mRNA; Replication; RNA-mediated interference; Stress granule; Stress granule; IBDV; Replication; G3BP1
• ISSN: 0378-1135; 1873-2542
• DOI: 10.1016/j.vetmic.2020.108806

•IBDV infection initiates stable typical stress granule formation and enhances G3BP1 expression in host cells.•Knockdown of G3BP1 inhibits IBDV-induced stress granule formation and decreases IBDV replication.•Overexpression of G3BP1 enhances IBDV-induced stress granule formation and promotes viral replication. 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.