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Several long non-coding RNAs (lncRNAs) are differentially expressed during viral infection and regulate multiple aspects of viral pathogenesis. Previously, we have shown that JEV\/West Nile virus (WNV) infection promotes JEV-induced non-coding RNA 1 (\n              <jats:italic toggle=\"yes\">JINR1<\/jats:italic>\n              ) expression in SH-SY5Y cells, and it interacts with RNA-binding motif protein 10 (RBM10) to enhance cell death and viral replication. In this study, we show that JEV or WNV infection of the SH-SY5Y cells inhibits the expression of microRNAs (miRNAs)\n              <jats:italic toggle=\"yes\">miR-216b-5p<\/jats:italic>\n              and\n              <jats:italic toggle=\"yes\">miR-1-3p<\/jats:italic>\n              . These miRNAs bind to the JEV\/WNV genome, and their overexpression during JEV\/WNV infection reduces viral replication and cell death. Depleting\n              <jats:italic toggle=\"yes\">JINR1<\/jats:italic>\n              or RBM10 during viral infection prevents the downregulation of\n              <jats:italic toggle=\"yes\">miR-216b-5p<\/jats:italic>\n              and\n              <jats:italic toggle=\"yes\">miR-1-3p<\/jats:italic>\n              . In addition,\n              <jats:italic toggle=\"yes\">JINR1<\/jats:italic>\n              or RBM10 knockdown during JEV\/WNV infection enhances the binding of RNA Pol II and H3K4me3 at the promoters of\n              <jats:italic toggle=\"yes\">miR-216b-5p<\/jats:italic>\n              and\n              <jats:italic toggle=\"yes\">miR-1-3p. JINR1<\/jats:italic>\n              or RBM10 depletion also prevents the binding of H3K27me3 at the promoters of these miRNAs, suggesting that\n              <jats:italic toggle=\"yes\">JINR1<\/jats:italic>\n              and RBM10 are involved in their transcription repression. Interestingly\n              <jats:italic toggle=\"yes\">, JINR1<\/jats:italic>\n              also acts as a competing endogenous RNA (ceRNA) that directly binds to\n              <jats:italic toggle=\"yes\">miR-216b-5p<\/jats:italic>\n              and\n              <jats:italic toggle=\"yes\">miR-1-3p,<\/jats:italic>\n              resulting in the upregulation of their targets glucose-regulated protein 78 (GRP78) and DEAD-Box Helicase 5 (DDX5), respectively, which are involved in regulating viral replication. Our findings suggest that\n              <jats:italic toggle=\"yes\">JINR1<\/jats:italic>\n              uses multiple mechanisms to promote JEV and WNV infection in neuronal cells.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>IMPORTANCE<\/jats:title>\n            <jats:p>\n              Infection of the central nervous system (CNS) by Japanese encephalitis virus (JEV) or West Nile virus (WNV) leads to neuroinflammation and neuronal cell death. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) regulate viral infection by regulating the expression of host genes. However, knowledge about the interplay between lncRNAs and miRNAs during JEN\/WNV infection is limited. We show that JEV\/WNV infection inhibits the expression of anti-viral host miRNAs\n              <jats:italic toggle=\"yes\">miR-216b-5p<\/jats:italic>\n              and\n              <jats:italic toggle=\"yes\">miR-1-3p<\/jats:italic>\n              . These miRNAs inhibit the JEV and WNV replication by directly binding with their genome.\n              <jats:italic toggle=\"yes\">JINR1<\/jats:italic>\n              and its interacting protein, RBM10, inhibit the transcription of\n              <jats:italic toggle=\"yes\">miR-216b-5p<\/jats:italic>\n              and\n              <jats:italic toggle=\"yes\">miR-1-3p<\/jats:italic>\n              . Interestingly,\n              <jats:italic toggle=\"yes\">JINR1<\/jats:italic>\n              also binds and sequesters\n              <jats:italic toggle=\"yes\">miR-216b-5p<\/jats:italic>\n              and\n              <jats:italic toggle=\"yes\">miR-1-3p<\/jats:italic>\n              , resulting in upregulation of their targets GRP78 and DDX5, respectively, which promote viral infection. Our findings suggest that lncRNA\n              <jats:italic toggle=\"yes\">JINR1<\/jats:italic>\n              is a potential target for developing anti-virals against JEV\/WNV infection.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/jvi.00066-25","type":"journal-article","created":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T13:00:24Z","timestamp":1745499624000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":11,"title":["LncRNA\n            <i>JINR1<\/i>\n            regulates\n            <i>miR-216b-5p\/<\/i>\n            GRP78 and\n            <i>miR-1-3p\/<\/i>\n            DDX5 axis to promote JEV infection and cell death"],"prefix":"10.1128","volume":"99","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2840-4061","authenticated-orcid":false,"given":"Shraddha","family":"Tripathi","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, Birla Institute of 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