ArticleJournal of virology2010
Regulation of ICP0-null mutant herpes simplex virus type 1 infection by ND10 components ATRX and hDaxx.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 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
136 citing papers in PubMed, 172 citations in OpenAlex.
- Deciphering cassava brown streak virus infection in cassava through VPg mediated host protein interactions.Archives of virology · 2026Article
- Counteracting FOX proteins epigenetically control the herpesvirus lytic-latent balance.Nature communications · 2026Article
- Interferon dependent immune memory during HSV-1 neuronal latency via increased H3K9me3 and restriction by ATRX.Nature communications · 2025Article
- ATRX Promotes Transcription Initiation of HSV-1 Immediate Early Genes During Early Lytic Infection.Viruses · 2025Article
- Daxx mediated histone H3.3 deposition on HSV-1 DNA restricts genome decompaction and the progression of immediate-early transcription.PLoS pathogens · 2025Article
- Sp140L functions as a herpesvirus restriction factor suppressing viral transcription and activating interferon-stimulated genes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Daxx and HIRA go viral - How chromatin remodeling complexes affect DNA virus infection.Tumour virus research · 2025Review
- ATRX restricts Human Cytomegalovirus (HCMV) viral DNA replication through heterochromatinization and minimizes unpackaged viral genomes.PLoS pathogens · 2024Article
- Histone H2A variant H2A.B is enriched in transcriptionally active and replicating HSV-1 lytic chromatin.Journal of virology · 2024Article
- Article
- Single-genome analysis reveals heterogeneous association of the Herpes Simplex Virus genome with H3K27me2 and the reader PHF20L1 following infection of human fibroblasts.bioRxiv : the preprint server for biology · 2023Article
- The Intersection of Innate Immune Pathways with the Latent Herpes Simplex Virus Genome.Journal of virology · 2023Review
- Targeting telomeres: advances in telomere maintenance mechanism-specific cancer therapies.Nature reviews. Cancer · 2022Review
- The chromatin remodeling protein ATRX positively regulates IRF3-dependent type I interferon production and interferon-induced gene expression.PLoS pathogens · 2022Article
- PML Body Component Sp100A Restricts Wild-Type Herpes Simplex Virus 1 Infection.Journal of virology · 2022Article
- Functions and roles of IFIX, a member of the human HIN-200 family, in human diseases.Molecular and cellular biochemistry · 2022Review
- Schlafens Can Put Viruses to Sleep.Viruses · 2022Review
- Pathogenesis and virulence of herpes simplex virus.Virulence · 2021Review
- Advancing Our Understanding of Corneal Herpes Simplex Virus-1 Immune Evasion Mechanisms and Future Therapeutics.Viruses · 2021Review
- PML-NB-dependent type I interferon memory results in a restricted form of HSV latency.EMBO reports · 2021Article
76 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Herpes simplex virus type 1 (HSV-1) immediate-early gene product ICP0 activates lytic infection and relieves cell-mediated repression of viral gene expression. This repression is conferred by preexisting cellular proteins and is commonly referred to as intrinsic antiviral resistance or intrinsic defense. PML and Sp100, two core components of nuclear substructures known as ND10 or PML nuclear bodies, contribute to intrinsic resistance, but it is clear that other proteins must also be involved. We have tested the hypothesis that additional ND10 factors, particularly those that are involved in chromatin remodeling, may have roles in intrinsic resistance against HSV-1 infection. The two ND10 component proteins investigated in this report are ATRX and hDaxx, which are known to interact with each other and comprise components of a repressive chromatin-remodeling complex. We generated stable cell lines in which endogenous ATRX or hDaxx expression is severely suppressed by RNA interference. We found increases in both gene expression and plaque formation induced by ICP0-null mutant HSV-1 in both ATRX- and hDaxx-depleted cells. Reconstitution of wild-type hDaxx expression reversed the effects of hDaxx depletion, but reconstitution with a mutant form of hDaxx unable to interact with ATRX did not. Our results suggest that ATRX and hDaxx act as a complex that contributes to intrinsic antiviral resistance to HSV-1 infection, which is counteracted by ICP0.
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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.