ArticleScientific reports2018
Up-regulation of microRNA-203 in influenza A virus infection inhibits viral replication by targeting DR1.
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 28 papers.
What it found
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
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- Glucosidase alpha neutral C promotes influenza virus replication by inhibiting proteosome-dependent degradation of hemagglutinin.Signal transduction and targeted therapy · 2025Article
- A comprehensive overview on the crosstalk between microRNAs and viral pathogenesis and infection.Medicinal research reviews · 2025Review
- Role of miRNA in Highly Pathogenic H5 Avian Influenza Virus Infection: An Emphasis on Cellular and Chicken Models.Viruses · 2024Review
- microRNA-guided immunity against respiratory virus infection in human and mouse lung cells.Biology open · 2024Article
- ZNF219, a novel transcriptional repressor, inhibits transcription of the prototype foamy virus by interacting with the viral LTR promoter.Virus research · 2023Article
- Host DNA Demethylation Induced by DNMT1 Inhibition Up-Regulates Antiviral OASL Protein during Influenza a Virus Infection.Viruses · 2023Article
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- MicroRNAs based regulation of cytokine regulating immune expressed genes and their transcription factors in COVID-19.Meta gene · 2022Article
- Involvement of host microRNAs in flavivirus-induced neuropathology: An update.Journal of biosciences · 2022Review
- Review
- Identifying Putative Causal Links between MicroRNAs and Severe COVID-19 Using Mendelian Randomization.Cells · 2021Article
- The potential use of microRNAs as a therapeutic strategy for SARS-CoV-2 infection.Archives of virology · 2021Review
- Perspective: Milk microRNAs as Important Players in Infant Physiology and Development.Advances in nutrition (Bethesda, Md.) · 2021Article
- Polyphenols Could Prevent SARS-CoV-2 Infection by Modulating the Expression of miRNAs in the Host Cells.Aging and disease · 2021Article
- Article
- Review
- Zika Virus Pathogenesis: A Battle for Immune Evasion.Vaccines · 2021Review
- COVID-19: fighting the invisible enemy with microRNAs.Expert review of anti-infective therapy · 2021Review
- The Relationship of the Mechanisms of the Pathogenesis of Multiple Sclerosis and the Expression of Endogenous Retroviruses.Biology · 2020Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) are small noncoding RNA molecules that play important roles in various biological processes. Much evidence shows that miRNAs are closely associated with numerous virus infections; however, involvement of cellular miRNAs in influenza A virus (IAV) infection is unclear. Here, we found that expression of miR-203 was up-regulated markedly via two different mechanisms during IAV infection. First, we examined the effects of type I interferon induced by IAV on direct activation of miR-203 expression. Next, we showed that DNA demethylation within the miR-203 promoter region in A549 cells induced its up-regulation, and that expression of DNA methyltransferase 1 was down-regulated following H5N1 virus infection. Ectopic expression of miR-203 in turn inhibited H5N1 virus replication by targeting down-regulator of transcription 1 (DR1), which was identified as a novel target of miR-203. Silencing DR1 in miR-203 knockout cells using a specific siRNA inhibited replication of the H5N1 virus, an effect similar to that of miR-203. In summary, the data show that host cell expression of miR-203 is up-regulated upon IAV infection, which increases antiviral responses by suppressing a novel target gene, DR1. Thus, we have identified a novel mechanism underlying the relationship between miR-203 and IAV infection.
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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.