ArticleNature communications2018
KSHV episomes reveal dynamic chromatin loop formation with domain-specific gene regulation.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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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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
34 citing papers in PubMed, 52 citations in OpenAlex.
- Omics-Level Approaches to Studying Gammaherpesvirus Infection.Pathogens (Basel, Switzerland) · 2026Review
- Design, development, and evaluation of gene therapeutics specific to KSHV-associated diseases.Molecular therapy. Oncology · 2025Article
- Viral Enhancers Orchestrate Kaposi's Sarcoma-Associated Herpesvirus Transcription.Journal of medical virology · 2025Review
- Molecular Mechanisms of KSHV Latency Establishment and Maintenance.Current clinical microbiology reports · 2024Article
- Loopy virus or controlled contortionist? 3D regulation of HCMV gene expression by CTCF-driven chromatin interactions.Journal of virology · 2024Review
- The cellular Notch1 protein promotes KSHV reactivation in an Rta-dependent manner.Journal of virology · 2024Article
- From enhancers to genome conformation: complex transcriptional control underlies expression of a single herpesviral gene.bioRxiv : the preprint server for biology · 2024Article
- KSHV genome harbors both constitutive and lytically induced enhancers.Journal of virology · 2024Article
- Viral remodeling of the 4D nucleome.Experimental & molecular medicine · 2024Review
- Enhancer-promoter activation by the Kaposi sarcoma-associated herpesvirus episome maintenance protein LANA.Cell reports · 2024Article
- Kaposi's sarcoma-associated herpesvirus terminal repeat regulates inducible lytic gene promoters.Journal of virology · 2024Article
- Review
- Characterization of a new CCCTC-binding factor binding site as a dual regulator of Epstein-Barr virus latent infection.PLoS pathogens · 2023Article
- Dynamics of Viral and Host 3D Genome Structure upon Infection.Journal of microbiology and biotechnology · 2022Review
- The Contribution of Kaposi's Sarcoma-Associated Herpesvirus ORF7 and Its Zinc-Finger Motif to Viral Genome Cleavage and Capsid Formation.Journal of virology · 2022Article
- KSHV Topologically Associating Domains in Latent and Reactivated Viral Chromatin.Journal of virology · 2022Article
- KSHV episome tethering sites on host chromosomes and regulation of latency-lytic switch by CHD4.Cell reports · 2022Article
- A Panel of Kaposi's Sarcoma-Associated Herpesvirus Mutants in the Polycistronic Kaposin Locus for Precise Analysis of Individual Protein Products.Journal of virology · 2022Article
- Single-cell Hi-C data analysis: safety in numbers.Briefings in bioinformatics · 2021Article
- The Expression and Nuclear Retention Element of Polyadenylated Nuclear RNA Is Not Required for Productive Lytic Replication of Kaposi's Sarcoma-Associated Herpesvirus.Journal of virology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The three-dimensional structure of chromatin organized by genomic loops facilitates RNA polymerase II access to distal promoters. The Kaposi's sarcoma-associated herpesvirus (KSHV) lytic transcriptional program is initiated by a single viral transactivator, K-Rta. Here we report the KSHV genomic structure and its relationship with K-Rta recruitment sites using Capture Hi-C analyses. High-resolution 3D viral genomic maps identify a number of direct physical, long-range, and dynamic genomic interactions. Mutant KSHV chromosomes harboring point mutations in the K-Rta responsive elements (RE) significantly attenuate not only the directly proximate downstream gene, but also distal gene expression in a domain-specific manner. Genomic loops increase in the presence of K-Rta, while abrogation of K-Rta binding impairs the formation of inducible genomic loops, decreases the expression of genes networked through the looping, and diminishes KSHV replication. Our study demonstrates that genomic architectural dynamics plays an essential role in herpesvirus gene expression.
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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.