JAK-STAT信号传导通路是一种在进化中保留的信号传导通路，能够调节各种生物过程。然而，JAK-STAT通路在昆虫媒介持续性病毒感染中的作用很少研究。在这里，我们利用两种不同植物病毒——稻瘟病毒（RSV）和稻黑条矮缩病毒（RBSDV），以及它们的昆虫媒介——小棕色稻飞虱构建了一个体系，阐明了JAK-STAT通路在持续性病毒感染中的调控机制。RSV和RBSDV感染均会激活JAK-STAT通路，并促进细胞因子抑制剂SOCS5的积累，该蛋白是由转录因子STAT5B调控的E3泛素连接酶。有趣的是，病毒诱导的SOCS5蛋白直接与抗凋亡的B细胞淋巴瘤-2（BCL2）相互作用，通过26S蛋白酶体途径促进BCL2的降解。因此，细胞凋亡的激活促进昆虫媒介的病毒持续感染。此外，STAT5B的激活促进病毒扩增，而STAT5B的抑制则抑制凋亡过程，减少病毒的积累。总之，我们的结果揭示了病毒诱导的JAK-STAT通路调控凋亡以促进病毒感染，并揭示了节肢动物媒介形式的植物病毒持续传播的JAK-STAT通路的新调控机制。版权所有：©2023 Zhang等，本文为开放获取文章，采用知识共享署名许可协议，允许任何人在任何媒介下自由使用、分发和再创作，只要原作者和出处被标明。

The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway is an evolutionarily conserved signaling pathway that can regulate various biological processes. However, the role of JAK-STAT pathway in the persistent viral infection in insect vectors has rarely been investigated. Here, using a system that comprised two different plant viruses, Rice stripe virus (RSV) and Rice black-streaked dwarf virus (RBSDV), as well as their insect vector small brown planthopper, we elucidated the regulatory mechanism of JAK-STAT pathway in persistent viral infection. Both RSV and RBSDV infection activated the JAK-STAT pathway and promoted the accumulation of suppressor of cytokine signaling 5 (SOCS5), an E3 ubiquitin ligase regulated by the transcription factor STAT5B. Interestingly, the virus-induced SOCS5 directly interacted with the anti-apoptotic B-cell lymphoma-2 (BCL2) to accelerate the BCL2 degradation through the 26S proteasome pathway. As a result, the activation of apoptosis facilitated persistent viral infection in their vector. Furthermore, STAT5B activation promoted virus amplification, whereas STAT5B suppression inhibited apoptosis and reduced virus accumulation. In summary, our results reveal that virus-induced JAK-STAT pathway regulates apoptosis to promote viral infection, and uncover a new regulatory mechanism of the JAK-STAT pathway in the persistent plant virus transmission by arthropod vectors.Copyright: © 2023 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.