ArticleFrontiers in cellular and infection microbiology2021
Differential Expression of Human MicroRNAs During Dengue Virus Infection in THP-1 Monocytes.
Article in Frontiers in cellular and infection microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Identification of miRNA-mRNA Co-expression by network analysis in dengue virus infection.Virusdisease · 2025Article
- Regulation of Ferroptosis in Human Macrophage by Nitric Oxide Donors.Sovremennye tekhnologii v meditsine · 2025Article
- DENV-1 Infection of Macrophages Induces Pyroptosis and Causes Changes in MicroRNA Expression Profiles.Biomedicines · 2024Article
- Toward a Categorization of Virus-ncRNA Interactions in the World of RNA to Disentangle the Tiny Secrets of Dengue Virus.Viruses · 2024Review
- Micro-Players of Great Significance-Host microRNA Signature in Viral Infections in Humans and Animals.International journal of molecular sciences · 2022Review
- Suppression of TGF-β/Smad2 signaling by GW788388 enhances DENV-2 clearance in macrophages.Journal of medical virology · 2022Article
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Authors and funding
10 authors.
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Abstract
Dengue virus (DENV) is the most widespread arbovirus, responsible for a wide range of clinical manifestations, varying from self-limited illness to severe hemorrhagic fever. Dengue severity is associated with host intense proinflammatory response and monocytes have been considered one of the key cell types involved in the early steps of DENV infection and immunopathogenesis. To better understand cellular mechanisms involved in monocyte infection by DENV, we analyzed the expression levels of 754 human microRNAs in DENV-infected THP-1 cells, a human monocytic cell line. Eleven human microRNAs showed differential expression after DENV infection and gene ontology and enrichment analysis revealed biological processes potentially affected by these molecules. Five downregulated microRNAs were significantly linked to cellular response to stress, four to cell death/apoptosis, two to innate immune responses and one upregulated to vesicle mediated, TGF-β signaling, phosphatidylinositol mediated signaling, lipid metabolism process and blood coagulation.
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