ArticlemBio2017
Human Cytomegalovirus MicroRNAs miR-US5-1 and miR-UL112-3p Block Proinflammatory Cytokine Production in Response to NF-κB-Activating Factors through Direct Downregulation of IKKα and IKKβ.
Article in mBio, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 65 citations in OpenAlex.
- Human Cytomegalovirus UL4 is Required for Viral Reactivation via Cellular Reprogramming in Latently Infected CD34+ Progenitor Cells and Humanized Mice.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms of the Indirect Effects of CMV Infection in Solid Organ Transplant Recipients: A Narrative Review.Journal of clinical medicine · 2026Review
- Cytomegalovirus in HIV: A Modifiable Driver of Inflammation, Frailty, and Aging.Current HIV/AIDS reports · 2026Review
- Article
- Inhibition of type I interferon signaling is a conserved function of gamma-herpesvirus-encoded microRNAs.Journal of virology · 2026Article
- Review
- Third intracellular loop of HCMV US28 is necessary for signaling and viral reactivation.Journal of virology · 2025Article
- Human cytomegalovirus-IE2 suppresses antigen presentation of macrophage through the IL10/STAT3 signalling pathway in transgenic mouse.PloS one · 2025Article
- Viral microRNA regulation of Akt is necessary for reactivation of Human Cytomegalovirus from latency in CD34+ hematopoietic progenitor cells and humanized mice.PLoS pathogens · 2024Article
- Human cytomegalovirus: pathogenesis, prevention, and treatment.Molecular biomedicine · 2024Review
- Modulation of Monocyte Effector Functions and Gene Expression by Human Cytomegalovirus Infection.Viruses · 2024Review
- miRNA-Mediated Mechanisms in the Generation of Effective and Safe Oncolytic Viruses.Pharmaceutics · 2024Review
- MicroRNAs in infectious diseases: potential diagnostic biomarkers and therapeutic targets.Clinical microbiology reviews · 2023Review
- Current Knowledge on the Interaction of Human Cytomegalovirus Infection, Encoded miRNAs, and Acute Aortic Syndrome.Viruses · 2023Review
- Viral miRNA regulation of host gene expression.Seminars in cell & developmental biology · 2023Review
- Deletion of the non-adjacent genesFrontiers in immunology · 2023Article
- MicroRNA Regulation of Human Herpesvirus Latency.Viruses · 2022Review
- MicroRNAs: Harbingers and shapers of periodontal inflammation.Seminars in cell & developmental biology · 2022Review
- Human MicroRNAs Attenuate the Expression of Immediate Early Proteins and HCMV Replication during Lytic and Latent Infection in Connection with Enhancement of Phosphorylated RelA/p65 (Serine 536) That Binds to MIEP.International journal of molecular sciences · 2022Article
- Virus-host protein interactions as footprints of human cytomegalovirus replication.Current opinion in virology · 2022Review
Corrections and comments
- Commented on by
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Emerging evidence indicates that human cytomegalovirus (HCMV) manipulates host cell signaling pathways using both proteins and noncoding RNAs. Several studies have shown that HCMV induces NF-κB signaling early in infection, resulting in the induction of antiviral proinflammatory cytokines with a subsequent reduction of these cytokines late in infection. The mechanism for late cytokine reduction is unknown. In this study, we show that HCMV microRNAs (miRNAs) miR-US5-1 and miR-UL112-3p target the IκB kinase (IKK) complex components IKKα and IKKβ to limit production of proinflammatory cytokines in response to interleukin 1β (IL-1β) and tumor necrosis factor alpha (TNF-α). Transfection of miR-UL112-3p and miR-US5-1 mimics reduced endogenous IKKα and IKKβ protein levels, and site-directed mutagenesis of the 3' untranslated regions (UTRs) identified the binding sites for each miRNA. Infection with mutant viruses lacking these miRNAs resulted in increased levels of IKKα and IKKβ proteins, an impaired ability to control NF-κB signaling at late times of lytic infection, and increased production of proinflammatory cytokines compared to wild-type virus in cell types relevant to HCMV infection
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.