ArticleJournal of virology2007
Herpes simplex virus type 1 induces CD83 degradation in mature dendritic cells with immediate-early kinetics via the cellular proteasome.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
44 citing papers in PubMed, 78 citations in OpenAlex.
- Host factor SAMHD1 restricts DNA viruses in non-dividing myeloid cells.PLoS pathogens · 2013Trial
- Herpes simplex virus type 1 interferes with signal transducer and activator of transcription 3 expression in infected mature dendritic cells.The Journal of general virology · 2026Article
- Alzheimer's disease-associated CD83(+) microglia are linked with increased immunoglobulin G4 and human cytomegalovirus in the gut, vagal nerve, and brain.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Single cell transcriptomes and multiscale networks from persons with and without Alzheimer's disease.Nature communications · 2024Article
- CD83 Regulates the Immune Responses in Inflammatory Disorders.International journal of molecular sciences · 2023Review
- HSV-1 Infection of Epithelial Dendritic Cells Is a Critical Strategy for Interfering with Antiviral Immunity.Viruses · 2022Article
- PKHB1 peptide induces antiviral effects through induction of immunogenic cell death in herpes simplex keratitis.Frontiers in pharmacology · 2022Article
- Review
- Review
- CD83 expression regulates antibody production in response to influenza A virus infection.Virology journal · 2020Article
- Herpes Simplex Virus Type-2 Paralyzes the Function of Monocyte-Derived Dendritic Cells.Viruses · 2020Article
- HSV-1 Modulates IL-6 Receptor Expression on Human Dendritic Cells.Frontiers in immunology · 2020Article
- Replication in the Mononuclear Phagocyte System (MPS) as a Determinant of Hantavirus Pathogenicity.Frontiers in cellular and infection microbiology · 2020Article
- The CD83 Molecule - An Important Immune Checkpoint.Frontiers in immunology · 2020Review
- Characteristics of herpes simplex virus infection and pathogenesis suggest a strategy for vaccine development.Reviews in medical virology · 2019Review
- Inhibition of CD83 Alleviates Systemic Inflammation in Herpes Simplex Virus Type 1-Induced Behçet's Disease Model Mouse.Mediators of inflammation · 2019Article
- Invasive Salmonella exploits divergent immune evasion strategies in infected and bystander dendritic cell subsets.Nature communications · 2018Article
- RING-Domain E3 Ligase-Mediated Host-Virus Interactions: Orchestrating Immune Responses by the Host and Antagonizing Immune Defense by Viruses.Frontiers in immunology · 2018Review
- Viral Ubiquitin Ligase Stimulates Selective Host MicroRNA Expression by Targeting ZEB Transcriptional Repressors.Viruses · 2017Article
- An Engineered Herpesvirus Activates Dendritic Cells and Induces Protective Immunity.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Mature dendritic cells (DCs) are the most potent antigen-presenting cells within the human immune system. However, Herpes simplex virus type 1 (HSV-1) is able to interfere with DC biology and to establish latency in infected individuals. In this study, we provide new insights into the mechanism by which HSV-1 disarms DCs by the manipulation of CD83, a functionally important molecule for DC activation. Fluorescence-activated cell sorter (FACS) analyses revealed a rapid downmodulation of CD83 surface expression within 6 to 8 h after HSV-1 infection, in a manner strictly dependent on viral gene expression. Soluble CD83 enzyme-linked immunosorbent assays, together with Western blot analysis, demonstrated that CD83 rapidly disappears from the cell surface after contact with HSV-1 by a mechanism that involves protein degradation rather than shedding of CD83 from the cell surface into the medium. Infection experiments with an ICP0 deletion mutant demonstrated an important role for this viral immediate-early protein during CD83 degradation, since this particular mutant strain leads to strongly reduced CD83 degradation. This hypothesis was further strengthened by cotransfection of plasmids expressing CD83 and ICP0 into 293T cells, which led to significantly reduced accumulation of CD83. In strong contrast, transfection of plasmids expressing CD83 and a mutant ICP0 defective in its RING finger-mediated E3 ubiquitin ligase function did not reduce CD83 expression. Inhibition of the proteasome, the cellular protein degradation machinery, almost completely restored CD83 surface expression during HSV-1 infection, indicating that proteasome-mediated degradation and HSV-1 ICP0 play crucial roles in this novel viral immune escape mechanism.
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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.