| Gene Name | TNFRSF14 |
| HF Protein Name | Tumor necrosis factor receptor superfamily member 14 |
| HF Function | Essential for virus entry |
| Uniprot ID | Q92956 |
| Protein Sequence | View Fasta Sequence |
| NCBI Gene ID | 8764 |
| Host Factor (HF) Name in Paper | TNFRSF14 |
| Gene synonyms | HVEA HVEM |
| Ensemble Gene ID | ENSG00000157873 |
| Ensemble Transcript | ENST00000355716 [Q92956-1];ENST00000621877 [Q92956-1] |
| KEGG ID | Go to KEGG Database |
| Gene Ontology ID(s) | GO:0001618, GO:0005031, GO:0005886, GO:0005887, GO:0006954, GO:0006955, GO:0007166, GO:0007275, GO:0031295, GO:0031625, GO:0032496, GO:0033209, GO:0042127, GO:0042981, GO:0097190, |
| MINT ID | Q92956 |
| STRING | Click to see interaction map |
| GWAS Analysis | Click to see gwas analysis |
| OMIM ID | 602746 |
| PANTHER ID | N.A. |
| PDB ID(s) | 1JMA, 2AW2, 4FHQ, 4RSU, |
| pfam ID | PF00020, |
| Drug Bank ID | N.A., |
| ChEMBL ID | N.A. |
| Organism | Homo sapiens (Human) |
| Virus Name | Human herpesvirus 1 |
| Virus Short Name | HSV1 |
| Order | Herpesvirales |
| Virus Family | Herpesviridae |
| Virus Subfamily | Alphaherpesvirinae |
| Genus | Simplexvirus |
| Species | Herpes simplex virus 1 |
| Host | Human, mammals |
| Cell Tropism | Primary site of infection: epithelial mucosal cells , latency: remains latent in sensory neurons (ganglions) |
| Associated Disease | Skin vesicles or mucosal ulcers, rarely encephalitis and meningitis |
| Mode of Transmission | Contact, saliva |
| VIPR DB link | http://www.viprbrc.org/brc/vipr_allSpecies_search.do?method=SubmitForm&decorator=herpes |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/91/herpesviridae |
| Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Herpesviridae |
| Paper Title | Interactions between herpesvirus entry mediator (TNFRSF14) and latency-associated transcript during herpes simplex virus 1 latency |
| Author's Name | Sariah J. Allen, Antje Rhode-Kurnow, Kevin R. Mott, Xianzhi Jiang, Dale Carpenter, J. Ignacio Rodriguez-Barbosa, Clinton Jones, Steven L. Wechsler, Carl F. Ware, Homayon Ghiasi |
| Journal Name | Journal Of Virology |
| Pubmed ID | 24307582 |
| Abstract | Herpesvirus entry mediator (HVEM) is one of several cell surface proteins herpes simplex virus (HSV) uses for attachment/entry. HVEM regulates cellular immune responses and can also increase cell survival. Interestingly, latency-associated transcript (LAT), the only viral gene consistently expressed during neuronal latency, enhances latency and reactivation by promoting cell survival and by helping the virus evade the host immune response. However, the mechanisms of these LAT activities are not well understood. We show here for the first time that one mechanism by which LAT enhances latency and reactivation appears to be by upregulating HVEM expression. HSV-1 latency/reactivation was significantly reduced in Hvem(-/-) mice, indicating that HVEM plays a significant role in HSV-1 latency/reactivation. Furthermore, LAT upregulated HVEM expression during latency in vivo and also when expressed in vitro in the absence of other viral factors. This study suggests a mechanism whereby LAT upregulates HVEM expression potentially through binding of two LAT small noncoding RNAs to the HVEM promoter and that the increased HVEM then leads to downregulation of immune responses in the latent microenvironment and increased survival of latently infected cells. Thus, one of the mechanisms by which LAT enhances latency/reactivation appears to be through increasing expression of HVEM. |
| Used Model | C57BL/6 and C57BL/6-Hvem / mice |
| DOI | 10.1128/JVI.02467-13 |
