ArticlePloS one2011
Stepwise release of biologically active HMGB1 during HSV-2 infection.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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
30 citing papers in PubMed, 45 citations in OpenAlex.
- Proviral functions of HMGB1 in HAdV-C5 replication compartments.Microbiology spectrum · 2025Article
- Review
- Intracellular translocation of HMGB1 is important for Zika virus replication in Huh7 cells.Scientific reports · 2022Article
- Article
- Article
- Review
- Human Herpesvirus 6A Induces Dendritic Cell Death and HMGB1 Release without Virus Replication.Pathogens (Basel, Switzerland) · 2021Article
- Glycyrrhizin: An alternative drug for the treatment of COVID-19 infection and the associated respiratory syndrome?Pharmacology & therapeutics · 2020Review
- Decreased Expression of the High Mobility Group Box 1 (Microorganisms · 2020Article
- Released Tryptophanyl-tRNA Synthetase Stimulates Innate Immune Responses against Viral Infection.Journal of virology · 2019Article
- Inhibition of Homophilic Interactions and Ligand Binding of the Receptor for Advanced Glycation End Products by Heparin and Heparin-Related Carbohydrate Structures.Medicines (Basel, Switzerland) · 2018Article
- High Mobility Group Box 1 Influences HSV1716 Spread and Acts as an Adjuvant to Chemotherapy.Viruses · 2018Article
- Oncolytic Virotherapy and the Tumor Microenvironment.Advances in experimental medicine and biology · 2017Review
- Porcine epidemic diarrhea virus nucleoprotein contributes to HMGB1 transcription and release by interacting with C/EBP-β.Oncotarget · 2016Article
- Respiratory Syncytial Virus Infection Triggers Epithelial HMGB1 Release as a Damage-Associated Molecular Pattern Promoting a Monocytic Inflammatory Response.Journal of virology · 2016Article
- From Benchtop to Bedside: A Review of Oncolytic Virotherapy.Biomedicines · 2016Review
- HMGB1 Is a Potential Biomarker for Severe Viral Hemorrhagic Fevers.PLoS neglected tropical diseases · 2016Article
- Immunogenic cell death by oncolytic herpes simplex virus type 1 in squamous cell carcinoma cells.Cancer gene therapy · 2016Article
- Oncolytic viruses as immunotherapy: progress and remaining challenges.OncoTargets and therapy · 2016Review
- HMGB1 Promotes Hepatitis C Virus Replication by Interaction with Stem-Loop 4 in the Viral 5' Untranslated Region.Journal of virology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHigh mobility group box 1 protein (HMGB1) is a major endogenous danger signal that triggers inflammation and immunity during septic and aseptic stresses. HMGB1 recently emerged as a key soluble factor in the pathogenesis of various infectious diseases, but nothing is known of its behaviour during herpesvirus infection. We therefore investigated the dynamics and biological effects of HMGB1 during HSV-2 infection of epithelial HEC-1 cells. METHODOLOGY/PRINCIPAL
findingsDespite a transcriptional shutdown of HMGB1 gene expression during infection, the intracellular pool of HMGB1 protein remained unaffected, indicating its remarkable stability. However, the dynamics of HMGB1 was deeply modified in infected cells. Whereas viral multiplication was concomitant with apoptosis and HMGB1 retention on chromatin, a subsequent release of HMGB1 was observed in response to HSV-2 mediated necrosis. Importantly, extracellular HMGB1 was biologically active. Indeed, HMGB1-containing supernatants from HSV-2 infected cells induced the migration of fibroblasts from murine or human origin, and reactivated HIV-1 from latently infected T lymphocytes. These effects were specifically linked to HMGB1 since they were blocked by glycyrrhizin or by a neutralizing anti-HMGB1 antibody, and were mediated through TLR2 and the receptor for Advanced Glycation End-products (RAGE). Finally, we show that genital HSV-2 active infections also promote HMGB1 release in vivo, strengthening the clinical relevance of our experimental data.
conclusionsThese observations target HMGB1 as an important actor during HSV-2 genital infection, notably in the setting of HSV-HIV co-infection.
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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.