Influenza viruses represent a significant threat to global public health. MicroRNAs (miRNAs), a class of small non-coding RNA molecules, play pivotal roles in regulating gene expression and have emerged as critical modulators of host-virus interactions. To investigate the functions of miRNAs during influenza virus infection, a miRNA library was constructed and sequenced using DF1 cells infected with the H9N2 influenza virus. From the differentially expressed miRNAs, we identified miR-92 as a key antiviral host factor. Mechanistically, miR-92 inhibits viral replication by targeting TNFRSF1B, which, in turn, enhances type I interferon signaling responses. Promoter region analysis demonstrated that the transcription factor OCT1 binds to the miR-92 promoter and positively regulates its transcriptional activity. Additionally, our study revealed that TNFRSF1B interacts with TNF receptor-associated factor 3 (TRAF3) and mediates TRAF3 degradation via the autophagolysosomal pathway. Specifically, TNFRSF1B facilitates the removal of K63-linked polyubiquitin chains from TRAF3. Collectively, these findings indicate that TNFRSF1B negatively regulates IFN-I responses through autophagolysosomal-mediated TRAF3 degradation, while miR-92 counteracts this inhibitory effect to exert antiviral activity. In summary, our research delineates a novel regulatory axis that modulates the interferon pathway and H9N2 influenza virus replication, providing new insights into host antiviral defense mechanisms and potential therapeutic targets.