{"doi":"10.1371/journal.ppat.1010301","title":"Host MOV10 is induced to restrict herpes simplex virus 1 lytic infection by promoting type I interferon response","abstract":"<jats:p>Moloney leukemia virus 10 protein (MOV10) is an interferon (IFN)-inducible RNA helicase implicated in antiviral activity against RNA viruses, yet its role in herpesvirus infection has not been investigated. After corneal inoculation of mice with herpes simplex virus 1 (HSV-1), we observed strong upregulation of both MOV10 mRNA and protein in acutely infected mouse trigeminal ganglia. MOV10 suppressed HSV-1 replication in both neuronal and non-neuronal cells, and this suppression required the N-terminus, but not C-terminal helicase domain of MOV10. MOV10 repressed expression of the viral gene ICP0 in transfected cells, but suppressed HSV-1 replication independently of ICP0. MOV10 increased expression of type I IFN in HSV-1 infected cells with little effect on IFN downstream signaling. Treating the cells with IFN-α or an inhibitor of the IFN receptor eliminated MOV10 suppression of HSV-1 replication. MOV10 enhanced IFN production stimulated by cytoplasmic RNA rather than DNA. IKKε co-immunoprecipitated with MOV10 and was required for MOV10 restriction of HSV-1 replication. Mass spectrometry identified ICP27 as a viral protein interacting with MOV10. Co-immunoprecipitation results suggested that this interaction depended on the RGG box of ICP27 and both termini of MOV10. Overexpressed ICP27, but not its RGG-Box deletion mutant, rendered MOV10 unable to regulate HSV-1 replication and type I IFN production. In summary, MOV10 is induced to restrict HSV-1 lytic infection by promoting the type I IFN response through an IKKε-mediated RNA sensing pathway, and its activity is potentially antagonized by ICP27 in an RGG box dependent manner.</jats:p>","journal":"PLOS Pathogens","year":2022,"id":614188,"datarank":0.41588830833596724,"base_score":2.772588722239781,"endowment":2.772588722239781,"self_citation_contribution":0.41588830833596724,"citation_network_contribution":0.0,"self_endowment_contribution":0.41588830833596724,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":15,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1024388,"name":"Ze Xiang","orcid":"0000-0002-0897-4550","position":1,"is_corresponding":false},{"id":453530,"name":"Zeyu Sun","orcid":"0000-0003-3465-4144","position":2,"is_corresponding":false},{"id":1582650,"name":"Feiyang Ji","orcid":null,"position":3,"is_corresponding":false},{"id":1582651,"name":"Keyi Ren","orcid":null,"position":4,"is_corresponding":false},{"id":118938,"name":"Dongli Pan","orcid":"0000-0002-0421-6242","position":5,"is_corresponding":false},{"id":1582649,"name":"Xiyuan Yang","orcid":"0000-0002-1662-266X","position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Host MOV10 is induced to restrict herpes simplex virus 1 lytic infection by promoting type I interferon response","abstract":"<jats:p>Moloney leukemia virus 10 protein (MOV10) is an interferon (IFN)-inducible RNA helicase implicated in antiviral activity against RNA viruses, yet its role in herpesvirus infection has not been investigated. After corneal inoculation of mice with herpes simplex virus 1 (HSV-1), we observed strong upregulation of both MOV10 mRNA and protein in acutely infected mouse trigeminal ganglia. MOV10 suppressed HSV-1 replication in both neuronal and non-neuronal cells, and this suppression required the N-terminus, but not C-terminal helicase domain of MOV10. MOV10 repressed expression of the viral gene ICP0 in transfected cells, but suppressed HSV-1 replication independently of ICP0. MOV10 increased expression of type I IFN in HSV-1 infected cells with little effect on IFN downstream signaling. Treating the cells with IFN-α or an inhibitor of the IFN receptor eliminated MOV10 suppression of HSV-1 replication. MOV10 enhanced IFN production stimulated by cytoplasmic RNA rather than DNA. IKKε co-immunoprecipitated with MOV10 and was required for MOV10 restriction of HSV-1 replication. Mass spectrometry identified ICP27 as a viral protein interacting with MOV10. Co-immunoprecipitation results suggested that this interaction depended on the RGG box of ICP27 and both termini of MOV10. Overexpressed ICP27, but not its RGG-Box deletion mutant, rendered MOV10 unable to regulate HSV-1 replication and type I IFN production. In summary, MOV10 is induced to restrict HSV-1 lytic infection by promoting the type I IFN response through an IKKε-mediated RNA sensing pathway, and its activity is potentially antagonized by ICP27 in an RGG box dependent manner.</jats:p>","is_dataset_classified":null,"base_score":2.772588722239781,"endowment":2.772588722239781,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"35157734","pmcid":"PMC8880913","openalex_id":"https://openalex.org/W4213112986","authors":[],"funders":[{"funder_name":"the National Key R & D Program of China","grant_id":"2017YFC1200204","title":null},{"funder_name":"Natural Science Foundation of Zhejiang Province","grant_id":"LR18H190001","title":null},{"funder_name":"State Key Laboratory for Diagnosis and Treatment of Infectious Diseases","grant_id":"SKLID2021KF03","title":null}],"total_grants":3,"fwci":1.0052,"citation_percentile":0.73293739,"influential_citations":0,"citation_trend":[{"year":2022,"count":2},{"year":2023,"count":4},{"year":2024,"count":3},{"year":2025,"count":3},{"year":2026,"count":3}],"oa_status":"gold","license":"cc-by","oa_locations":[{"url":"https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1010301&type=printable","host_type":"journal"},{"url":"https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1010301&type=printable","host_type":"publisher"},{"url":"https://dx.plos.org/10.1371/journal.ppat.1010301","host_type":"publisher"},{"url":"https://doi.org/10.1371/journal.ppat.1010301","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/35157734","host_type":"repository"},{"url":"https://doaj.org/article/f6b3b854c80c43b9b6a7f06aeb8824e9","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/8880913","host_type":"repository"},{"url":"https://europepmc.org/articles/PMC8880913","host_type":"Europe_PMC"},{"url":"https://europepmc.org/articles/PMC8880913?pdf=render","host_type":"Europe_PMC"}],"fields_of_study":["interferon and immune responses","Herpesvirus Infections and Treatments","Cytokine Signaling Pathways and Interactions","Animals","Herpes Simplex","Herpesvirus 1, Human","I-kappa B Kinase","Immediate-Early Proteins","Interferon Type I","Mice","RNA","Virus Replication"],"mesh_terms":["Animals","Herpes Simplex","Interferon Type I","RNA","Virus Replication","Immediate-Early Proteins","Herpesvirus 1, Human","Mice","I-kappa B Kinase"],"keywords":["Herpes simplex virus","Biology","Lytic cycle","Viral replication","Virology","Interferon","Molecular biology","Virus"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good health and well-being"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-02T11:23:01.417167Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}