Virus Details


VHFID10046

Host Factor Information

Gene Name MALAT1
HF Protein Name Metastasis-associated lung adenocarcinoma transcript 1
HF Function
Uniprot ID N.A.
Protein Sequence View Fasta Sequence
NCBI Gene ID N.A.
Host Factor (HF) Name in Paper MALAT1
Gene synonyms N.A.
Ensemble Gene ID N.A.
Ensemble Transcript N.A.
KEGG ID Go to KEGG Database
Gene Ontology ID(s) N.A.,
MINT ID N.A.
STRING Click to see interaction map
GWAS Analysis Click to see gwas analysis
OMIM ID N.A.
PANTHER ID N.A.
PDB ID(s) N.A.,
pfam ID N.A.,
Drug Bank ID N.A.,
ChEMBL ID N.A.
Organism N.A.

Pathogen Information

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

Publication Information

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.01183-35