ArticleJournal of virology2010
Herpes simplex virus type 1 (HSV-1)-induced apoptosis in human dendritic cells as a result of downregulation of cellular FLICE-inhibitory protein and reduced expression of HSV-1 antiapoptotic latency-associated transcript sequences.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
- 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
- Review
- Life-death trade-offs: HSV-1 ICP27 differentially modulates intrinsic apoptotic signaling in epithelial and neuron-like cells.Frontiers in microbiology · 2026Article
- Hexokinase-2 as a Therapeutic Target: Alleviating Herpes Simplex Keratitis Through Metabolic Reprogramming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- An updated review of HSV-1 infection-associated diseases and treatment, vaccine development, and vector therapy application.Virulence · 2024Review
- Article
- Low Prevalence of HSV-1 andDiagnostics (Basel, Switzerland) · 2023Article
- Caspase-8 is required for HSV-1-induced apoptosis and promotes effective viral particle release via autophagy inhibition.Cell death and differentiation · 2023Article
- Apoptosis and Phagocytosis as Antiviral Mechanisms.Sub-cellular biochemistry · 2023Article
- Direct cleavage of caspase-8 by herpes simplex virus 1 tegument protein US11.Scientific reports · 2022Article
- Interaction between the Hepatitis B Virus and Cellular FLIP Variants in Viral Replication and the Innate Immune System.Viruses · 2022Review
- Review
- Pathobiology and treatment of viral keratitis.Experimental eye research · 2021Review
- Herpes Simplex Virus type 1 infects Langerhans cells and the novel epidermal dendritic cell, Epi-cDC2s, via different entry pathways.PLoS pathogens · 2021Article
- The latency-associated transcript locus of herpes simplex virus 1 is a virulence determinant in human skin.PLoS pathogens · 2020Article
- Article
- The PD-1/PD-L1 Axis and Virus Infections: A Delicate Balance.Frontiers in cellular and infection microbiology · 2019Review
- Herpes Simplex Virus Evasion of Early Host Antiviral Responses.Frontiers in cellular and infection microbiology · 2019Review
- The suppression of apoptosis by α-herpesvirus.Cell death & disease · 2017Review
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Herpes simplex virus type 1 (HSV-1) is one of the most frequent and successful human pathogens. It targets immature dendritic cells (iDCs) to interfere with the antiviral immune response. The mechanisms underlying apoptosis of HSV-1-infected iDCs are not fully understood. Previously, we have shown that HSV-1-induced apoptosis of iDCs is associated with downregulation of the cellular FLICE-inhibitory protein (c-FLIP), a potent inhibitor of caspase-8-mediated apoptosis. In this study, we prove that HSV-1 induces degradation of c-FLIP in a proteasome-independent manner. In addition, by using c-FLIP-specific small interfering RNA (siRNA) we show for the first time that downregulation of c-FLIP expression is sufficient to drive uninfected iDCs into apoptosis, underlining the importance of this molecule for iDC survival. Surprisingly, we also observed virus-induced c-FLIP downregulation in epithelial cells and many other cell types that do not undergo apoptosis after HSV-1 infection. Microarray analyses revealed that HSV-1-encoded latency-associated transcript (LAT) sequences, which can substitute for c-FLIP as an inhibitor of caspase-8-mediated apoptosis, are much less abundant in iDCs as compared to epithelial cells. Finally, iDCs infected with an HSV-1 LAT knockout mutant showed increased apoptosis when compared to iDCs infected with the corresponding wild-type HSV-1. Taken together, our results demonstrate that apoptosis of HSV-1-infected iDCs requires both c-FLIP downregulation and diminished expression of viral LAT.
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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.