| Gene Name | N.A. |
| HF Protein Name | HSV-1 infection response repressive protein |
| HF Function | Antiviral protein, induces feedback repression of virus transcription by interacting with ATF5 |
| Uniprot ID | N.A. |
| Protein Sequence | View Fasta Sequence |
| NCBI Gene ID | N.A. |
| Host Factor (HF) Name in Paper | HIRPP |
| 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. |
| 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 | A cellular response protein induced during HSV-1 infection inhibits viral replication by interactingwith ATF5 |
| Author's Name | WU LianQiu, ZHANG XueMei, CHE YanChun, ZHANG Ying, TANG SongQing, LIAO Yun, NA RuiXiong, XIONG XiangLin, LIU LongDing & LI QiHan |
| Journal Name | SCIENCE CHINA-lifesciences (Springer) |
| Pubmed ID | 24302293 |
| Abstract | Studies of herpes simplex virus type 1 (HSV-1) infection have shown that many known and unknown cellular molecules involved in viral proliferation are up-regulated following HSV-1 infection. In this study, using two-dimensional polyacrylamide gel electrophoresis, we found that the expression of the HSV-1 infection response repressive protein (HIRRP, GI 16552881) was up-regulated in human L02 cells infected with HSV-1. HIRRP, an unknown protein, was initially localized in the cytoplasm and then translocated into the nucleus of HSV-1-infected cells. Further analysis showed that HIRRP represses HSV-1 proliferation by inhibiting transcription of the viral genome by interacting with the cellular transcription factor, ATF5, via its N-terminal domain. ATF5 represses the transcription of many host genes but can also act as an activator of genes containing a specific motif. We found that ATF5 promotes the proliferation of HSV-1 via a potential mechanism by which ATF5 enhances the transcription of viral genes during the course of an HSV-1 infection HIRRP then induces feedback repression of this transcription by interacting with ATF5. |
| Used Model | L02, vero, hela and 293 T |
| DOI | 10.1007/s11427-013-4569-y |
