Long noncoding RNAs (lncRNAs) are important regulators of gene expression. Although evidence accumulated over the past decade shows that lncRNAs have key roles in the interaction between viruses and hosts, the functions of the majority of differentially expressed lncRNAs in response to viral infections remain uncharacterized so far. In this study, we have identified that USP30 antisense RNA 1 (USP30-AS1), a host antisense lncRNA, is hijacked by influenza A virus (IAV) to assist its replication. We show that USP30-AS1 is IAV-induced via the Janus protein tyrosine kinase-signal transducer and the activator of transcription (JAK-STAT) signaling pathway. Functionally, ectopic expression of USP30-AS1 significantly promotes IAV replication. Conversely, silencing USP30-AS1 suppresses IAV replication. Mechanistically, USP30-AS1 directly binds prohibitin 1 (PHB1) and modulates its protein stability and function. On the one hand, the binding of USP30-AS1 sequesters PHB1 away from the E3 ubiquitin ligase, tripartite motif containing 21 (TRIM21), thereby protecting the protein stability of PHB1. On the other hand, USP30-AS1 serves as a molecular scaffold for enhancing the interaction between PHB1 and interferon regulatory factor 3 (IRF3), which in turn impedes the nuclear import of IRF3. Therefore, our data unveil an important role of USP30-AS1 in promoting viral replication by modulating PHB1 stability and functions, providing a new insight into the role of lncRNAs in the interplay between IAV and host.