| Gene Name | EIF3M |
| HF Protein Name | Eukaryotic translation initiation factor 3 subunit M |
| HF Function | Essential for virus infection |
| Uniprot ID | Q7L2H7 |
| Protein Sequence | View Fasta Sequence |
| NCBI Gene ID | 10480 |
| Host Factor (HF) Name in Paper | eIF3m |
| Gene synonyms | HFLB5 PCID1 |
| Ensemble Gene ID | ENSG00000149100 |
| Ensemble Transcript | ENST00000524896 [Q7L2H7-2];ENST00000531120 [Q7L2H7-1] |
| KEGG ID | Go to KEGG Database |
| Gene Ontology ID(s) | GO:0002183, GO:0003743, GO:0005829, GO:0005852, GO:0006413, GO:0031369, GO:0071541, |
| MINT ID | Q7L2H7 |
| STRING | Click to see interaction map |
| GWAS Analysis | Click to see gwas analysis |
| OMIM ID | 609641 |
| PANTHER ID | N.A. |
| PDB ID(s) | 3J8B, 3J8C, 6FEC, |
| pfam ID | PF01399, |
| 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 | HSV usurps eukaryotic initiation factor 3 subunit M for viral protein translation: novel prevention target |
| Author's Name | Natalia Cheshenko, Janie B. Trepanier, Theodore J. Segarra, A. Oveta Fuller, Betsy C. Herold |
| Journal Name | PLOS One |
| Pubmed ID | 20676407 |
| Abstract | Prevention of genital herpes is a global health priority. B5, a recently identified ubiquitous human protein, was proposed as a candidate HSV entry receptor. The current studies explored its role in HSV infection. Viral plaque formation was reduced by approximately 90% in human cells transfected with small interfering RNA targeting B5 or nectin-1, an established entry receptor. However, the mechanisms were distinct. Silencing of nectin-1 prevented intracellular delivery of viral capsids, nuclear transport of a viral tegument protein, and release of calcium stores required for entry. In contrast, B5 silencing had no effect on these markers of entry, but inhibited viral protein translation. Specifically, viral immediate early genes, ICP0 and ICP4, were transcribed, polyadenylated and transported from the nucleus to the cytoplasm, but the viral transcripts did not associate with ribosomes or polysomes in B5-silenced cells. In contrast, immediate early gene viral transcripts were detected in polysome fractions isolated from control cells. These findings are consistent with sequencing studies demonstrating that B5 is eukaryotic initiation factor 3 subunit m (eIF3m). Although B5 silencing altered the polysome profile of cells, silencing had little effect on cellular RNA or protein expression and was not cytotoxic, suggesting that this subunit is not essential for host cellular protein synthesis. Together these results demonstrate that B5 plays a major role in the initiation of HSV protein translation and could provide a novel target for strategies to prevent primary and recurrent herpetic disease. |
| Used Model | CaSki cells |
| DOI | 10.1371/journal.pone.0011829 |
