ArticleJournal of virology2012
Inhibition of TANK binding kinase 1 by herpes simplex virus 1 facilitates productive infection.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 79 citations in OpenAlex.
- Oncolytic viruses: advanced strategies in cancer therapy.Signal transduction and targeted therapy · 2026Review
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- Regulation of the innate immune response in human neurons by ICP34.5 maintains herpes simplex virus 1 latency.bioRxiv : the preprint server for biology · 2025Article
- Current status and research progress of oncolytic virus.Pharmaceutical science advances · 2024Review
- Interplay between Autophagy and Herpes Simplex Virus Type 1: ICP34.5, One of the Main Actors.International journal of molecular sciences · 2022Review
- Review
- The Molecular Mechanism of Herpes Simplex Virus 1 UL31 in Antagonizing the Activity of IFN-β.Microbiology spectrum · 2022Article
- Herpesvirus-mediated stabilization of ICP0 expression neutralizes restriction by TRIM23.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Oncolytic HSV: Underpinnings of Tumor Susceptibility.Viruses · 2021Review
- The herpesvirus accessory protein γ134.5 facilitates viral replication by disabling mitochondrial translocation of RIG-I.PLoS pathogens · 2021Article
- Defects inScience immunology · 2020Article
- Lentiviral delivery of combinatorial CAR/CRISPRi circuit into human primary T cells is enhanced by TBK1/IKKɛ complex inhibitor BX795.Journal of translational medicine · 2020Article
- HSV1 VP1-2 deubiquitinates STING to block type I interferon expression and promote brain infection.The Journal of experimental medicine · 2020Article
- Herpes Simplex Virus 1 ICP34.5 Alters Mitochondrial Dynamics in Neurons.Journal of virology · 2020Article
- Preclinical Toxicology of rQNestin34.5v.2: An Oncolytic Herpes Virus with Transcriptional Regulation of the ICP34.5 Neurovirulence Gene.Molecular therapy. Methods & clinical development · 2020Article
- Regulation of cGAS-Mediated Immune Responses and Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Review
- The E3 Ubiquitin Ligase TBK1 Mediates the Degradation of Multiple Picornavirus VP3 Proteins by Phosphorylation and Ubiquitination.Journal of virology · 2019Article
- Disassembly of the TRIM23-TBK1 Complex by the Us11 Protein of Herpes Simplex Virus 1 Impairs Autophagy.Journal of virology · 2019Article
- Article
- Coevolution pays off: Herpesviruses have the license to escape the DNA sensing pathway.Medical microbiology and immunology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The γ(1)34.5 protein of herpes simplex viruses (HSV) is essential for viral pathogenesis, where it precludes translational arrest mediated by double-stranded-RNA-dependent protein kinase (PKR). Paradoxically, inhibition of PKR alone is not sufficient for HSV to exhibit viral virulence. Here we report that γ(1)34.5 inhibits TANK binding kinase 1 (TBK1) through its amino-terminal sequences, which facilitates viral replication and neuroinvasion. Compared to wild-type virus, the γ(1)34.5 mutant lacking the amino terminus induces stronger antiviral immunity. This parallels a defect of γ(1)34.5 for interacting with TBK1 and reducing phosphorylation of interferon (IFN) regulatory factor 3. This activity is independent of PKR. Although resistant to IFN treatment, the γ(1)34.5 amino-terminal deletion mutant replicates at an intermediate level between replication of wild-type virus and that of the γ(1)34.5 null mutant in TBK1(+/+) cells. However, such impaired viral growth is not observed in TBK1(-/-) cells, indicating that the interaction of γ(1)34.5 with TBK1 dictates HSV infection. Upon corneal infection, this mutant replicates transiently but barely invades the trigeminal ganglia or brain, which is a difference from wild-type virus and the γ(1)34.5 null mutant. Therefore, in addition to PKR, γ(1)34.5 negatively regulates TBK1, which contributes viral replication and spread in vivo.
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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.