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Several protein-coding genes and microRNAs are implicated in JEV-induced neuronal cell death. However, the global expression patterns and functional contributions of long non-coding RNAs (lncRNAs) during JEV-induced neuronal cell death have not been explored. Here, we profiled the transcriptome of the JEV-infected neuronal cell line and identified several lncRNAs whose expression is altered during JEV infection. We functionally characterized a lncRNA named\n            <jats:italic>JINR1<\/jats:italic>\n            (JEV-induced non-coding RNA 1), which is evolutionarily conserved in primates.\n            <jats:italic>JINR1<\/jats:italic>\n            induction during JEV infection is regulated by nuclear factor-kappa B (NF-\u03baB). Depletion of\n            <jats:italic>JINR1<\/jats:italic>\n            during infection reduces flavivirus replication, neuronal cell death, and the expression of genes involved in ER stress and neuroinflammation. Interestingly, GRP78 overexpression prevents the decrease in flavivirus replication due to\n            <jats:italic>JINR1<\/jats:italic>\n            knockdown.\n            <jats:italic>JINR1<\/jats:italic>\n            interacts with RBM10 and NF-\u03baB to regulate the transcription of virus\n            <jats:italic>-<\/jats:italic>\n            induced genes. In addition, RBM10 and\n            <jats:italic>JINR1<\/jats:italic>\n            form a feed-forward loop to reciprocally promote each other\u2019s expression by regulating NF-\u03baB activity. Our results suggest the role of\n            <jats:italic>JINR1<\/jats:italic>\n            in promoting flavivirus replication and flavivirus-induced neuronal cell death.\n          <\/jats:p>\n          <jats:sec>\n            <jats:title>IMPORTANCE<\/jats:title>\n            <jats:p>\n              Central nervous system infection by flaviviruses such as Japanese encephalitis virus, Dengue virus, and West Nile virus results in neuroinflammation and neuronal damage. However, little is known about the role of long non-coding RNAs (lncRNAs) in flavivirus-induced neuroinflammation and neuronal cell death. Here, we characterized the role of a flavivirus-induced lncRNA named\n              <jats:italic>JINR1<\/jats:italic>\n              during the infection of neuronal cells. Depletion of\n              <jats:italic>JINR1<\/jats:italic>\n              during virus infection reduces viral replication and cell death. An increase in GRP78 expression by\n              <jats:italic>JINR1<\/jats:italic>\n              is responsible for promoting virus replication. Flavivirus infection induces the expression of a cellular protein RBM10, which interacts with\n              <jats:italic>JINR1<\/jats:italic>\n              . RBM10 and JINR1 promote the proinflammatory transcription factor NF-\u03baB activity, which is detrimental to cell survival.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/jvi.01183-23","type":"journal-article","created":{"date-parts":[[2023,11,22]],"date-time":"2023-11-22T14:06:45Z","timestamp":1700662005000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":16,"title":["An RBM10 and NF-\u03baB interacting host lncRNA promotes JEV replication and neuronal cell death"],"prefix":"10.1128","volume":"97","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 Technology and Science, Pilani, Hyderabad Campus, Telangana, 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