| Virus Name | Japanese encephalitis virus |
| Virus Short Name | JEV |
| Order | Amarillovirales |
| Virus Family | Flaviviridae |
| Virus Subfamily | N.A. |
| Genus | Flavivirus |
| Species | Japanese encephalitis virus |
| Host | Vertebrates |
| Cell Tropism | Neurons |
| Associated Disease | Encephalitis |
| Mode of Transmission | Sexual contact, blood, breast feeding |
| VIPR DB link | https://www.viprbrc.org/brc/vipr_search.do?species=Japanese_encephalitis_virus |
| ICTV DB link | https://ictv.global/report/183/flaviviridae |
| Virus Host DB link |
| Paper Title | An RBM10 and NF-κB interacting host lncRNA promotes JEV replication and neuronal cell death |
| Author's Name | Shraddha Tripathi, Suryansh Sengar, Bakhya Shree, Stuti Mohapatra, Anirban Basu, Vivek Sharma, Mark T. Heise |
| Journal Name | Journal Of Virology |
| Pubmed ID | 37991381 |
| Abstract | Infection of the central nervous system by the Japanese encephalitis virus (JEV) is characterized by extensive neuronal cell death and neuroinflammation. 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 JINR1 (JEV-induced non-coding RNA 1), which is evolutionarily conserved in primates. JINR1 induction during JEV infection is regulated by nuclear factor-kappa B (NF-κB). Depletion of JINR1 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 JINR1 knockdown. JINR1 interacts with RBM10 and NF-κB to regulate the transcription of virus-induced genes. In addition, RBM10 and JINR1 form a feed-forward loop to reciprocally promote each other’s expression by regulating NF-κB activity. Our results suggest the role of JINR1 in promoting flavivirus replication and flavivirus-induced neuronal cell death. |
| Used Model | SH-SY5Y, Vero, PS, C6/36, HMC3, T98G |
| DOI | 10.1128/jvi.01183-24 |
