盖塔病毒感染诱导类似于应激颗粒的G3BP聚集体的产生OA

Stress granules(SGs)are a crucial host antiviral defense mechanism.This study investigated the role and mechanisms of SG formation during Getah virus(GETV)infection.To enable specific detection,we generated a polyclonal antibody to the GETV nonstructural protein NSP3 by immunizing BALB/c mice with bacterially expressed and purified recombinant NSP3 protein.By using this antibody alongside immunofluorescence and confocal microscopy,we analyzed SG dynamics in GETV-infected PK-15 cells.GETV infection induced the formation of cytoplasmic aggregates containing the core SG marker G3BP1.However,these G3BP aggre-gates persisted after cycloheximide(CHX)treatment,which typically disperses canonical SGs,and they crucially lacked the essential SG component TIA1.Western blot analysis revealed that GETV significantly enhanced the phosphorylation of eIF2α and its upstream kinase PKR but not PERK.Furthermore,global protein synthesis was suppressed over the infection course.Additionally,G3BP1/2 knockout in NCI-H1299 cells did not impair GETV replication.In conclusion,GETV infection subverts the host antiviral SG re-sponse.Instead of triggering canonical SG assembly,it induces the accumulation of persistent G3BP-positive aggregates that lack key SG components such as TIA1.This process is mechanistically dependent on the PKR/eIF2α signaling pathway and represents a viral strategy to evade the suppressive effects of functional SGs on viral replication.