ArticleScientific reports2018
Epigenetic control of influenza virus: role of H3K79 methylation in interferon-induced antiviral response.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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.
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
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Pooled it
- Post-translational modification networks as master regulators of influenza virus replication, host adaptation, and immune evasion.Frontiers in immunology · 2026Review
- The long reach of influenza and other respiratory viruses: from acute epithelial injury to post-viral lung disease.Clinical microbiology reviews · 2025Review
- Harnessing Epigenetics: Innovative Approaches in Diagnosing and Combating Viral Acute Respiratory Infections.Pathogens (Basel, Switzerland) · 2025Review
- Epigenetic Control of Innate Immunity: Consequences of Acute Respiratory Virus Infection.Viruses · 2024Review
- The Mycobacterium tuberculosis methyltransferase Rv2067c manipulates host epigenetic programming to promote its own survival.Nature communications · 2023Article
- Host DNA Demethylation Induced by DNMT1 Inhibition Up-Regulates Antiviral OASL Protein during Influenza a Virus Infection.Viruses · 2023Article
- Pulmonary Pathogen-Induced Epigenetic Modifications.Epigenomes · 2023Review
- Neuronal Dot1l Activity Acts as a Mitochondrial Gene-Repressor Associated with Human Brain Aging via H3K79 Hypermethylation.International journal of molecular sciences · 2023Article
- DOT-1.1 (DOT1L) deficiency inBBA advances · 2023Article
- The battle for autophagy between host and influenza A virus.Virulence · 2022Review
- PRMT5 epigenetically regulates the E3 ubiquitin ligase ITCH to influence lipid accumulation during mycobacterial infection.PLoS pathogens · 2022Article
- Advances on Innate Immune Evasion by Avian Immunosuppressive Viruses.Frontiers in immunology · 2022Review
- An endogenously activated antiviral state restricts SARS-CoV-2 infection in differentiated primary airway epithelial cells.PloS one · 2022Article
- H3K23/H3K36 hypoacetylation and HDAC1 up-regulation are associated with adverse consequences in obstructive sleep apnea patients.Scientific reports · 2021Article
- Review
- Simeprevir Potently Suppresses SARS-CoV-2 Replication and Synergizes with Remdesivir.ACS central science · 2021Article
- Comparative transcriptome analysis reveals key epigenetic targets in SARS-CoV-2 infection.NPJ systems biology and applications · 2021Article
- An immune epigenetic insight to COVID-19 infection.Epigenomics · 2021Review
- Role of Host-Mediated Post-Translational Modifications (PTMs) in RNA Virus Pathogenesis.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza virus stablishes a network of virus-host functional interactions, which depends on chromatin dynamic and therefore on epigenetic modifications. Using an unbiased search, we analyzed the epigenetic changes at DNA methylation and post-translational histone modification levels induced by the infection. DNA methylation was unaltered, while we found a general decrease on histone acetylation, which correlates with transcriptional inactivation and may cooperate with the impairment of cellular transcription that causes influenza virus infection. A particular increase in H3K79 methylation was observed and the use of an inhibitor of the specific H3K79 methylase, Dot1L enzyme, or its silencing, increased influenza virus replication. The antiviral response was reduced in conditions of Dot1L downregulation, since decreased nuclear translocation of NF-kB complex, and IFN-β, Mx1 and ISG56 expression was detected. The data suggested a control of antiviral signaling by methylation of H3K79 and consequently, influenza virus replication was unaffected in IFN pathway-compromised, Dot1L-inhibited cells. H3K79 methylation also controlled replication of another potent interferon-inducing virus such as vesicular stomatitis virus, but did not modify amplification of respiratory syncytial virus that poorly induces interferon signaling. Epigenetic methylation of H3K79 might have an important role in controlling interferon-induced signaling against viral pathogens.
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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.