ArticlePloS one2017
The Smc5/6 Complex Restricts HBV when Localized to ND10 without Inducing an Innate Immune Response and Is Counteracted by the HBV X Protein Shortly after Infection.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 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
105 citing papers in PubMed, 150 citations in OpenAlex.
- Human cytomegalovirus antagonizes SMC5/6 driven genome silencing via UL35 instituted proteasomal degradation of SLF2.PLoS pathogens · 2026Article
- The PTM switches of HBx: Master regulators of HBV infection and liver oncogenesis.Virus research · 2026Review
- The Multifunctional SMC5/6 Complex in Genome Stability, Antiviral Restriction, and Human Disease.Current issues in molecular biology · 2026Review
- ddOTs: A multiplexed quantitative ddPCR approach for resolving overlapping hepatitis B virus transcripts to decipher cccDNA-driven transcription.PLoS pathogens · 2026Article
- Secretion of the HBV small surface antigen is driven by an ER autophagic pathway.Hepatology communications · 2026Article
- Role of cccDNA in the Quest for HBV Cure- Implications for HIV-HBV Coinfection.Current HIV/AIDS reports · 2025Review
- The Intrinsic Innate Immunity of Hepatocytes Suppresses HBV Replication and Is Antagonized by HBx.Viruses · 2025Article
- SMC5/6-mediated plasmid silencing is directed by SIMC1-SLF2 and antagonized by the SV40 large T antigen.eLife · 2025Article
- Emerging Serum Biomarkers for Chronic Hepatitis B: Focus on Serum HBV RNA and HBcrAg.Journal of clinical and translational hepatology · 2025Review
- Conserved Yet Divergent Smc5/6 Complex Degradation by Mammalian Hepatitis B Virus X Proteins.International journal of molecular sciences · 2025Article
- Lamin A/C promotes HBV transcription by modulating histone modification associated with cccDNA minichromosome in an HBx-dependent manner.Virology journal · 2025Article
- HBV-driven host chromatin accessibility changes affect liver metabolic pathways, iron homeostasis and promote a preneoplastic phenotype.Journal of experimental & clinical cancer research : CR · 2025Article
- Article
- RAB3GAP2 dysregulation in adult T-cell leukemia/lymphoma (ATLL) compared to acute lymphoblastic leukemia (ALL): a molecular perspective.BMC research notes · 2025Article
- Review
- SARS-CoV-2 nsp13 suppresses hepatitis B virus replication by targeting cccDNA transcription.Journal of virology · 2024Article
- Article
- SMC5/6-Mediated Transcriptional Regulation of Hepatitis B Virus and Its Therapeutic Potential.Viruses · 2024Review
- Regulation of R-Loops in DNA Tumor Viruses.Pathogens (Basel, Switzerland) · 2024Review
- Human Smc5/6 recognises transcription-generated positive DNA supercoils.Nature communications · 2024Article
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The structural maintenance of chromosome 5/6 complex (Smc5/6) is a restriction factor that represses hepatitis B virus (HBV) transcription. HBV counters this restriction by expressing HBV X protein (HBx), which targets Smc5/6 for degradation. However, the mechanism by which Smc5/6 suppresses HBV transcription and how HBx is initially expressed is not known. In this study we characterized viral kinetics and the host response during HBV infection of primary human hepatocytes (PHH) to address these unresolved questions. We determined that Smc5/6 localizes with Nuclear Domain 10 (ND10) in PHH. Co-localization has functional implications since depletion of ND10 structural components alters the nuclear distribution of Smc6 and induces HBV gene expression in the absence of HBx. We also found that HBV infection and replication does not induce a prominent global host transcriptional response in PHH, either shortly after infection when Smc5/6 is present, or at later times post-infection when Smc5/6 has been degraded. Notably, HBV and an HBx-negative virus establish high level infection in PHH without inducing expression of interferon-stimulated genes or production of interferons or other cytokines. Our study also revealed that Smc5/6 is degraded in the majority of infected PHH by the time cccDNA transcription could be detected and that HBx RNA is present in cell culture-derived virus preparations as well as HBV patient plasma. Collectively, these data indicate that Smc5/6 is an intrinsic antiviral restriction factor that suppresses HBV transcription when localized to ND10 without inducing a detectable innate immune response. Our data also suggest that HBx protein may be initially expressed by delivery of extracellular HBx RNA into HBV-infected cells.
Indexed as
Identifiers
What OpenQuestion holds
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.