The role of Lnc9101 and Lnc8475 in innate immunity against influenza virus

Recent studies have shown that host long-chain non-coding RNAs (LncRNAs) is a key regulator of host-virus interactions during viral infections, however, many LncRNAs have unknown functions in host-virus interactions, especially influenza A virus (IAV). Here, we demonstrate that expression of lncRNA 9101 and lncRNA8475 can be induced by IAV infection. Expression of lncRNA 9101 and lncRNA8475 was significantly stimulated by viral genomic RNA, poly (I:C), or LPS treatment. Furthermore, inhibition of lnc9101 expression in DF-1 cells enhanced IAV replication, whereas overexpression of lnc9101 suppressed virus production. Interestingly, the role lnc8475 in viral replication was the opposite of its role; inhibition of lnc8475 expression in DF-1 cells attenuated IAV replication, whereas overexpression of lnc8475 promoted viral replication. Further studies concluded that lnc9101 and lnc8475 affected the expression of type I and type III IFNs, multiple ISGs, and the activation of STAT1 triggered by IAV infection. In addition, lnc9101 deficiency impaired the expression of TLR7 and MDA5 and decreased the phosphorylation level of IRF7, whereas lnc8475 deficiency promoted the expression of TLR3 and TLR7. The outcomes suggest that lnc9101 inhibits IAV replication by positively regulating the innate immune response and lnc8475 subject promotes IAV replication by regulating the innate immune response. Overall design: To identify lncRNAs that play important roles in influenza virus infection, we infected 5-day-old chicks with or without H9N2 influenza virus for 48h, and performed RNA-seq to find differently expressed lncRNA .