ArticleThe Journal of experimental medicine2020
HSV1 VP1-2 deubiquitinates STING to block type I interferon expression and promote brain infection.
Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 90 citations in OpenAlex.
- Deletion of the N-terminal 400 amino acids of DPV pUL36 attenuated virulence and conferred effective protection against virulent challenge.Poultry science · 2026Article
- Lactylation: a novel post-translational modification for cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Herpes simplex virus type 1 R-loops are targets for APOBEC-mediated mutagenesis.Genome biology · 2026Article
- Unmasking the hidden catalyst: How infections trigger Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Review
- TRIM29 inhibits PRRSV replication by targeting nsp11 for degradation.Journal of virology · 2025Article
- Article
- Human herpesvirus 6B U65 binds to histone proteins and suppresses interferon production.Journal of virology · 2025Article
- Small intestinal γδ T17 cells promote SAE through STING/C1q-induced microglial synaptic pruning in male mice.Nature communications · 2025Article
- The STING Signaling: A Novel Target for Central Nervous System Diseases.Cellular and molecular neurobiology · 2025Review
- Herpes simplex virus assembly and spread in murine skin after infection from the outside.Journal of virology · 2025Article
- Rosmarinic Acid inhibits Pseudorabies Virus (PRV) infection by activating the cGAS-STING signaling pathway.BMC microbiology · 2025Article
- Grass carp reovirus VP4 manipulates TOLLIP to degrade STING for inhibition of IFN production.Journal of virology · 2025Article
- Co-option of mitochondrial nucleic acid-sensing pathways by HSV-1 UL12.5 for reactivation from latent infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Co-option of mitochondrial nucleic acid sensing pathways by HSV-1 UL12.5 for reactivation from latent Infection.bioRxiv : the preprint server for biology · 2024Article
- Multiple E3 ligases act as antiviral factors against SARS-CoV-2 via inducing the ubiquitination and degradation of ORF9b.Journal of virology · 2024Article
- Degradation of TRIM32 is induced by RTA for Kaposi's sarcoma-associated herpesvirus lytic replication.Journal of virology · 2024Article
- The HIF transcription network exerts innate antiviral activity in neurons and limits brain inflammation.Cell reports · 2024Article
- S-nitrosothiol homeostasis maintained by ADH5 facilitates STING-dependent host defense against pathogens.Nature communications · 2024Article
- Impaired STING Activation Due to a Variant in the E3 Ubiquitin Ligase AMFR in a Patient with Severe VZV Infection and Hemophagocytic Lymphohistiocytosis.Journal of clinical immunology · 2024Article
- Unraveling the cGAS/STING signaling mechanism: impact on glycerolipid metabolism and diseases.Frontiers in medicine · 2024Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 5 countries.
Funding
Abstract
Herpes simplex virus (HSV) is the main cause of viral encephalitis in the Western world, and the type I interferon (IFN) system is important for antiviral control in the brain. Here, we have compared Ifnb induction in mixed murine brain cell cultures by a panel of HSV1 mutants, each devoid of one mechanism to counteract the IFN-stimulating cGAS-STING pathway. We found that a mutant lacking the deubiquitinase (DUB) activity of the VP1-2 protein induced particularly strong expression of Ifnb and IFN-stimulated genes. HSV1 ΔDUB also induced elevated IFN expression in murine and human microglia and exhibited reduced viral replication in the brain. This was associated with increased ubiquitination of STING and elevated phosphorylation of STING, TBK1, and IRF3. VP1-2 associated directly with STING, leading to its deubiquitination. Recruitment of VP1-2 to STING was dependent on K150 of STING, which was ubiquitinated by TRIM32. Thus, the DUB activity of HSV1 VP1-2 is a major viral immune-evasion mechanism in the brain.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.