ArticlePLoS pathogens2016
An Epigenetic Compound Library Screen Identifies BET Inhibitors That Promote HSV-1 and -2 Replication by Bridging P-TEFb to Viral Gene Promoters through BRD4.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- BRD4: From molecular understanding to therapeutics development.Molecular cell · 2026Review
- A potent and selective PROTAC degrader of CDK9 as effective inhibitor of HIV-1 RNA synthesis.Molecular diversity · 2026Article
- Epigenetic drugs against human DNA viruses and retroviruses.Antiviral research · 2025Review
- A Review of the Bromodomain and Extraterminal Domain Epigenetic Reader Proteins: Function on Virus Infection and Cancer.Viruses · 2024Review
- An alpha-herpesvirus employs host HEXIM1 to promote viral transcription.Journal of virology · 2024Article
- Overcoming therapeutic resistance in oncolytic herpes virotherapy by targeting IGF2BP3-induced NETosis in malignant glioma.Nature communications · 2024Article
- Nucleotide metabolism-related host proteins RNA polymerase II subunit and uridine phosphorylase 1 interacting with porcine epidemic diarrhea virus N proteins affect viral replication.Frontiers in veterinary science · 2024Article
- Viral Hijacking of BET Proteins.Viruses · 2022Review
- Inhibition of BET Family Proteins Suppresses African Swine Fever Virus Infection.Microbiology spectrum · 2022Article
- Temporal dynamics of HCMV gene expression in lytic and latent infections.Cell reports · 2022Article
- Epigenetic reader BRD4 supports mycobacterial pathogenesis by co-modulating host lipophagy and angiogenesis.Autophagy · 2022Article
- Functional and tissue enrichment analyses suggest that SARS-CoV-2 infection affects host metabolism and catabolism mediated by interference on host proteins.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2021Article
- Chromatin-mediated epigenetic regulation of HSV-1 transcription as a potential target in antiviral therapy.Antiviral research · 2021Review
- Bromodomain proteins regulate human cytomegalovirus latency and reactivation allowing epigenetic therapeutic intervention.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Protocol Optimization for the Production of the Non-Cytotoxic JΔNI5 HSV Vector Deficient in Expression of Immediately Early Genes.Molecular therapy. Methods & clinical development · 2020Article
- Article
- BRD4 inhibition exerts anti-viral activity through DNA damage-dependent innate immune responses.PLoS pathogens · 2020Article
- Bromodomain Inhibitors as Therapeutics for Herpesvirus-Related Disease: All BETs Are Off?Frontiers in cellular and infection microbiology · 2020Review
- Degradation of Herpes Simplex Virus-1 Viral miRNA H11 by Vaccinia Virus Protein VP55 Attenuates Viral Replication.Frontiers in microbiology · 2020Article
- Enhancement of adenovirus infection and adenoviral vector-mediated gene delivery by bromodomain inhibitor JQ1.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human HSV-1 and -2 are common pathogens of human diseases. Both host and viral factors are involved in HSV lytic infection, although detailed mechanisms remain elusive. By screening a chemical library of epigenetic regulation, we identified bromodomain-containing protein 4 (BRD4) as a critical player in HSV infection. We show that treatment with pan BD domain inhibitor enhanced both HSV infection. Using JQ1 as a probe, we found that JQ1, a defined BD1 inhibitor, acts through BRD4 protein since knockdown of BRD4 expression ablated JQ1 effect on HSV infection. BRD4 regulates HSV replication through complex formation involving CDK9 and RNAP II; whereas, JQ1 promotes HSV-1 infection by allocating the complex to HSV gene promoters. Therefore, suppression of BRD4 expression or inhibition of CDK9 activity impeded HSV infection. Our data support a model that JQ1 enhances HSV infection by switching BRD4 to transcription regulation of viral gene expression from chromatin targeting since transient expression of BRD4 BD1 or BD1/2 domain had similar effect to that by JQ1 treatment. In addition to the identification that BRD4 is a modulator for JQ1 action on HSV infection, this study demonstrates BRD4 has an essential role in HSV 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.