Abstract
Influenza A viruses (IAVs) are known to impose a significant impact on both animal and human health due to its zoonotic potential. A growing body of evidence indicates that host long noncoding RNAs (lncRNAs) play crucial roles in regulating host-virus interactions during IAV infection. However, numerous lncRNAs associated with IAV infection have not been well-characterized. Here, we identified the LINC01197 as an antiviral host factor. LINC01197 was significantly upregulated after IAV infection which is controlled by NF-κB pathway. Functional analysis demonstrated that overexpression of LINC01197 inhibited IAV replication and virus production while knockdown of LINC01197 facilitated IAV replication. Mechanistically, LINC01197 directly interacted with poly(A) binding protein cytoplasmic 1 (PABPC1), which in turn sequesters and restricts its functions. This work demonstrates that LINC01197 functions as a protein decoy to suppress IAV replication, indicating a novel function of LINC01197 in controlling IAV replication.