Japanese encephalitis virus-induced non-coding RNA 1 (JINR1)

Japanese encephalitis virus-induced non-coding RNA 1 (JINR1), also cataloged as LINC01518, is a primate-conserved long non-coding RNA that functions as a critical pro-viral host factor during the pathogenesis of neurotropic flaviviruses, including Japanese encephalitis virus (JEV) and West Nile virus (WNV). Primarily upregulated in neuronal cells via the NF-κB signaling pathway upon infection, JINR1 facilitates viral replication while concurrently promoting neuroinflammation and neuronal cell death [1, 4]. It exerts these effects by interacting with host proteins such as RBM10 to regulate pro-inflammatory gene transcription and by sequestering anti-viral microRNAs like miR-216b-5p and miR-1-3p, thereby upregulating pro-viral proteins such as GRP78 [2, 3]. Beyond its role in viral infection, JINR1 is increasingly recognized as an oncogene in various malignancies, including head and neck and esophageal squamous cell carcinomas, where it drives cell proliferation, migration, and resistance to chemotherapy [5]. Experimental studies have demonstrated that the knockdown of JINR1 significantly attenuates viral titers and reduces neuronal damage, suggesting it is a high-priority therapeutic target. Development of antisense oligonucleotides or RNA interference-based therapies targeting JINR1 represents a promising strategy for treating severe flaviviral encephalitis and certain chemoresistant cancers [1, 5].

Other names

JEV-induced non-coding RNA 1LINC01518JINR-1Long intergenic non-protein coding RNA 1518

JINR1 acts as a pro-viral host factor by facilitating viral replication and promoting neuronal apoptosis through a dual mechanism. It serves as a scaffold for the RNA-binding motif protein 10 (RBM10) and the p65 subunit of NF-κB, driving the transcription of genes associated with neuroinflammation and endoplasmic reticulum (ER) stress [1, 2]. Additionally, JINR1 functions as a competing endogenous RNA (ceRNA) or molecular sponge that sequesters anti-viral microRNAs, specifically miR-216b-5p and miR-1-3p. This sequestration leads to the upregulation of their respective targets, GRP78 and DDX5, which are essential for viral assembly and lifecycle [3, 4]. In oncological contexts, JINR1 promotes chemoresistance, and its depletion has been shown to sensitize tumor cells to cisplatin-induced apoptosis [5].