| Gene Name | Oasl1 |
| HF Protein Name | 2'-5'-oligoadenylate synthase-like protein 1 |
| HF Function | Downregulates type I interferon production and increases viral infection |
| Uniprot ID | Q8VI94 |
| Protein Sequence | View Fasta Sequence |
| NCBI Gene ID | 231655 |
| Host Factor (HF) Name in Paper | OASL1 |
| Gene synonyms | oasl9 |
| Ensemble Gene ID | ENSMUSG00000041827 |
| Ensemble Transcript | ENSMUST00000031540;ENSMUST00000112143 |
| KEGG ID | Go to KEGG Database |
| Gene Ontology ID(s) | GO:0003677, GO:0003725, GO:0005524, GO:0005654, GO:0005730, GO:0005737, GO:0005829, GO:0009615, GO:0016740, GO:0045071, GO:0045087, GO:0051607, |
| MINT ID | N.A. |
| STRING | Click to see interaction map |
| GWAS Analysis | Click to see gwas analysis |
| OMIM ID | N.A. |
| PANTHER ID | PTHR11258 |
| PDB ID(s) | N.A., |
| pfam ID | PF10421, PF00240, |
| Drug Bank ID | N.A., |
| ChEMBL ID | N.A. |
| Organism | Mus musculus (Mouse) |
| Virus Name | Human herpesvirus 2 |
| Virus Short Name | HSV2 |
| Order | Herpesvirales |
| Virus Family | Herpesviridae |
| Virus Subfamily | Alphaherpesvirinae |
| Genus | Simplexvirus |
| Species | Herpes simplex virus 2 |
| 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 | OASL1 deficiency promotes antiviral protection against genital herpes simplex virus type 2 infection by enhancing type I interferon production |
| Author's Name | Ji EunOh, Myeong Sup Lee, Young-Joon Kim & Heung Kyu Lee |
| Journal Name | Scientific Reports |
| Pubmed ID | 26750802 |
| Abstract | Type I interferon (IFN) interferes with virus replication, promotes antiviral responses, and controls innate and adaptive immune responses to certain viruses. Recently, we reported that 2-5 oligoadenylate synthetase-like 1 (OASL1) negatively regulates type I IFN production by inhibiting the translation of the type I IFN-regulating master transcription factor, IRF7. Notably, while OASL1-deficient mice induce robust production of type I IFN and are resistant to systemic viral infection, the effects of OASL1 during localized viral infection has not been studied. To this end, we investigated the role of OASL1 during mucosal HSV-2 infection of the genital tract. Oasl1(-/-) mice exhibited better survival rates than wild type (WT) mice following intravaginal HSV-2 infection, and suppressed virus replication more efficiently despite comparable recruitment of effector immune cells. Moreover, Ly6C(high) monocytes, and not pDCs or other cell types, displayed enhanced production of type I IFNs in Oasl1(-/-) mice in response to HSV-2 infection. Furthermore, cytotoxic T cell responses including IFN-gamma production were accelerated in Oasl1(-/-) mice after mucosal HSV-2 infection. Collectively, these results demonstrate that OASL1 deficiency promotes antiviral immunity against local mucosal viral infection and suggest that OASL1 could be a therapeutic target for treatment of HSV-2 infection of the genital mucosa. |
| Used Model | Oasl1?/? mice and Oasl1?/? hematopoietic cells |
| DOI | 10.1038/srep19089 |
