College of Veterinary Medicine, Northeast Agricultural University, Harbin, China.
Heilongjiang Key Laboratory for Animal Disease Control and Pharmaceutical Development, Harbin, China.
Front Immunol. 2024 Apr 16;15:1358036. doi: 10.3389/fimmu.2024.1358036. eCollection 2024.
It remains unclear whether BPIV3 infection leads to stress granules formation and whether G3BP1 plays a role in this process and in viral replication. This study aims to clarify the association between BPIV3 and stress granules, explore the effect of G3BP1 on BPIV3 replication, and provide significant insights into the mechanisms by which BPIV3 evades the host's antiviral immunity to support its own survival.
Here, we use Immunofluorescence staining to observe the effect of BPIV3 infection on the assembly of stress granules. Meanwhile, the expression changes of eIF2α and G3BP1 were determined. Overexpression or siRNA silencing of intracellular G3BP1 levels was examined for its regulatory control of BPIV3 replication.
We identify that the BPIV3 infection elicited phosphorylation of the eIF2α protein. However, it did not induce the assembly of stress granules; rather, it inhibited the formation of stress granules and downregulated the expression of G3BP1. G3BP1 overexpression facilitated the formation of stress granules within cells and hindered viral replication, while G3BP1 knockdown enhanced BPIV3 expression.
This study suggest that G3BP1 plays a crucial role in BPIV3 suppressing stress granule formation and viral replication.
BPIV3 感染是否会导致应激颗粒的形成，以及 G3BP1 是否在这一过程和病毒复制中发挥作用，目前仍不清楚。本研究旨在阐明 BPIV3 与应激颗粒之间的关联，探讨 G3BP1 对 BPIV3 复制的影响，为 BPIV3 逃避宿主抗病毒免疫以支持自身存活的机制提供重要见解。
在这里，我们使用免疫荧光染色来观察 BPIV3 感染对应激颗粒组装的影响。同时，测定 eIF2α 和 G3BP1 的表达变化。通过过表达或 siRNA 沉默细胞内 G3BP1 水平，研究其对 BPIV3 复制的调控作用。
我们发现 BPIV3 感染可诱导 eIF2α 蛋白磷酸化，但不会诱导应激颗粒的组装；相反，它抑制应激颗粒的形成并下调 G3BP1 的表达。G3BP1 的过表达促进了细胞内应激颗粒的形成并抑制了病毒复制，而 G3BP1 的敲低则增强了 BPIV3 的表达。
本研究表明，G3BP1 在 BPIV3 抑制应激颗粒形成和病毒复制中发挥关键作用。
