PDF(Pubmed)
Abstract：
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: This study suggest that G3BP1 plays a crucial role in BPIV3 suppressing stress granule formation and viral replication.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: This study suggest that G3BP1 plays a crucial role in BPIV3 suppressing stress granule formation and viral replication.
摘要：
■尚不清楚BPIV3感染是否导致应激颗粒形成，以及G3BP1是否在此过程和病毒复制中起作用。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，并对BPIV3逃避宿主抗病毒免疫以支持其自身生存的机制提供了重要见解。
■这里，我们用免疫荧光染色观察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。检测细胞内G3BP1水平的过表达或siRNA沉默对BPIV3复制的调节控制。
■我们确定BPIV3感染引起eIF2α蛋白的磷酸化。然而,它没有诱导应力颗粒的组装；相反，它抑制了胁迫颗粒的形成并下调了G3BP1的表达。G3BP1过表达促进细胞内应激颗粒的形成并阻碍病毒复制，而G3BP1敲低增强了BPIV3的表达。
■这项研究表明，G3BP1在BPIV3抑制应激颗粒形成和病毒复制中起着至关重要的作用。
■这里，我们用免疫荧光染色观察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。检测细胞内G3BP1水平的过表达或siRNA沉默对BPIV3复制的调节控制。
■我们确定BPIV3感染引起eIF2α蛋白的磷酸化。然而,它没有诱导应力颗粒的组装；相反，它抑制了胁迫颗粒的形成并下调了G3BP1的表达。G3BP1过表达促进细胞内应激颗粒的形成并阻碍病毒复制，而G3BP1敲低增强了BPIV3的表达。
■这项研究表明，G3BP1在BPIV3抑制应激颗粒形成和病毒复制中起着至关重要的作用。
