RIG-I dependent antiviral response regulator RNA (RDUR)

RIG-I dependent antiviral response regulator RNA (RDUR) is a long non-coding RNA (lncRNA) that is robustly upregulated upon infection with influenza A virus (IAV) and other viruses in a manner dependent on the RIG-I/NF-κB signaling pathway. RDUR promotes the host antiviral response by upregulating the expression of critical interferons (such as IFN-β) and interferon-stimulated genes (such as IFITM3, MX1, and ISG15), which suppress viral replication both in vitro and in vivo. RDUR achieves part of this activity by interacting with ILF2 and ILF3, proteins necessary for efficient ISG expression. Furthermore, RDUR provides feedback inhibition of NF-κB activation, thus restraining excessive inflammation during infection. Loss of RDUR expression leads to increased viral replication, heightened inflammation, tissue damage, and lower survival rates in animal models of IAV infection. RDUR maps to the human gene locus LINC02085 (previously LOC152225). RDUR is not a classic drug target (such as a receptor or enzyme) but is a regulatory RNA involved in innate immune regulation. There are no known drugs or established biomarkers or specific safety concerns directly related to manipulating RDUR as of current knowledge.

Other names

RIG-I-dependent IAV-upregulated noncoding RNALINC02085long intergenic non-protein coding RNA 2085LOC152225