ArticleJournal of virology2013
The open chromatin landscape of Kaposi's sarcoma-associated herpesvirus.
Article in Journal of virology, 2013. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 40 citations in OpenAlex.
- Omics-Level Approaches to Studying Gammaherpesvirus Infection.Pathogens (Basel, Switzerland) · 2026Review
- Viral Enhancers Orchestrate Kaposi's Sarcoma-Associated Herpesvirus Transcription.Journal of medical virology · 2025Review
- KSHV genome harbors both constitutive and lytically induced enhancers.Journal of virology · 2024Article
- Today's Kaposi sarcoma is not the same as it was 40 years ago, or is it?Journal of medical virology · 2023Review
- Article
- NDRG1 facilitates lytic replication of Kaposi's sarcoma-associated herpesvirus by maintaining the stability of the KSHV helicase.PLoS pathogens · 2021Article
- Regulation of KSHV Latency and Lytic Reactivation.Viruses · 2020Review
- Global epigenomic analysis of KSHV-infected primary effusion lymphoma identifies functionalProceedings of the National Academy of Sciences of the United States of America · 2020Article
- RNA decay during gammaherpesvirus infection reduces RNA polymerase II occupancy of host promoters but spares viral promoters.PLoS pathogens · 2020Article
- Epigenetic Regulation of Kaposi's Sarcoma-Associated Herpesvirus Latency.Frontiers in microbiology · 2020Review
- A comparative epigenome analysis of gammaherpesviruses suggests cis-acting sequence features as critical mediators of rapid polycomb recruitment.PLoS pathogens · 2019Article
- Viperin catalyzes methionine oxidation to promote protein expression and function of helicases.Science advances · 2019Article
- The landscape of transcription initiation across latent and lytic KSHV genomes.PLoS pathogens · 2019Article
- Extracellular vesicles from Kaposi Sarcoma-associated herpesvirus lymphoma induce long-term endothelial cell reprogramming.PLoS pathogens · 2019Article
- Epstein-Barr virus enhances genome maintenance of Kaposi sarcoma-associated herpesvirus.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Chromatin remodeling controls Kaposi's sarcoma-associated herpesvirus reactivation from latency.PLoS pathogens · 2018Article
- ZIC2 Is Essential for Maintenance of Latency and Is a Target of an Immediate Early Protein during Kaposi's Sarcoma-Associated Herpesvirus Lytic Reactivation.Journal of virology · 2017Article
- KSHV encoded ORF59 modulates histone arginine methylation of the viral genome to promote viral reactivation.PLoS pathogens · 2017Article
- Epigenetic Landscape during Coronavirus Infection.Pathogens (Basel, Switzerland) · 2017Article
- Expression of the Antisense-to-Latency Transcript Long Noncoding RNA in Kaposi's Sarcoma-Associated Herpesvirus.Journal of virology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic gammaherpesvirus which establishes latent infection in endothelial and B cells, as well as in primary effusion lymphoma (PEL). During latency, the viral genome exists as a circular DNA minichromosome (episome) and is packaged into chromatin analogous to human chromosomes. Only a small subset of promoters, those which drive latent RNAs, are active in latent episomes. In general, nucleosome depletion ("open chromatin") is a hallmark of eukaryotic regulatory elements such as promoters and transcriptional enhancers or insulators. We applied formaldehyde-assisted isolation of regulatory elements (FAIRE) followed by next-generation sequencing to identify regulatory elements in the KSHV genome and integrated these data with previously identified locations of histone modifications, RNA polymerase II occupancy, and CTCF binding sites. We found that (i) regions of open chromatin were not restricted to the transcriptionally defined latent loci; (ii) open chromatin was adjacent to regions harboring activating histone modifications, even at transcriptionally inactive loci; and (iii) CTCF binding sites fell within regions of open chromatin with few exceptions, including the constitutive LANA promoter and the vIL6 promoter. FAIRE-identified nucleosome depletion was similar among B and endothelial cell lineages, suggesting a common viral genome architecture in all forms of latency.
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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 Socratic graph.