We then dynamically examined the expression level of type I IFN and LINC02605after virus infection and found that the up-regulation of LINC02605 is behind the up-regulation of IFN-β, supporting the notion LINC02065 is an interferon stimulated lncRNA (Figure 1E).In order to further reveal the possible signaling pathways that induce the expression of LINC02605, we analyzed the transcription factors which have the potential to bind LINC02605 promoter region (Supplementary Information, Figure S1F), suggesting that NF-κB and STAT are potential binding transcription factors. This evidence concerns the gene NFKB1 and viral infectious disease.