Although influenza A virus (IAV) employs diverse strategies to evade IFN responses by inhibiting the synthesis of IFN, how IAV regulates signaling downstream of IFN is incompletely understood. In this study, we used Western blot-based protein analysis coupled with RT-qPCR, overexpression and RNA interference to investigate the regulation of JAK1 by IAV infection. The results indicated that JAK1 was ubiquitinated and degraded, resulting in inhibition of type I and type II IFN responses, demonstrating that IAV antagonizes the IFN-activated JAK/STAT signaling pathway by inducing the degradation of JAK1. Furthermore. IAV infection upregulated the suppressor of cytokine signaling (SOCS) protein SOCS1, and SOCS1 mediated the ubiquitination and degradation of JAK1. Collectively, our findings suggest that IAV infection induces SOCS1 expression to promote JAK1 degradation, which in turn inhibits host innate immune responses.

中文翻译：

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甲型流感病毒通过依赖SOCS1的泛素化和JAK1降解来拮抗I型和II型干扰素反应。

尽管甲型流感病毒（IAV）采用多种策略通过抑制IFN的合成来逃避IFN的应答，但IAV如何调节IFN下游信号的方式尚不完全清楚。在这项研究中，我们将基于蛋白质印迹的蛋白质分析与RT-qPCR，过表达和RNA干扰相结合，以研究IAV感染对JAK1的调控。结果表明，JAK1被泛素化和降解，导致抑制I型和II型IFN反应，表明IAV通过诱导JAK1降解来拮抗IFN激活的JAK / STAT信号通路。此外。IAV感染上调了细胞因子信号转导（SOCS）蛋白SOCS1的抑制因子，SOCS1介导JAK1的泛素化和降解。总的来说，