ArticleJournal of medical virology2022
Suppression of TGF-β/Smad2 signaling by GW788388 enhances DENV-2 clearance in macrophages.
Article in Journal of medical virology, 2022. 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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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
6 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- Article
- Review
- Pilot proteomic analysis of immune dysregulation in dengue with prior SARS-CoV-2 infection.Frontiers in immunology · 2025Observational
- The Role of Growth Factors in the Pathogenesis of Dengue: A Scoping Review.Pathogens (Basel, Switzerland) · 2022Article
- 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
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dengue fever, caused by the dengue virus (DENV-1, -2, -3, and -4), affects millions of people in the tropical and subtropical regions worldwide. Severe dengue is correlated with high viraemia and cytokine storm, such as high levels of transforming growth factor-β1 (TGF-β1) in the patient's serum. Here, the TGF-β1 signaling was investigated in the context of in vitro viral clearance. Macrophages were infected with DENV-2 at MOI 5 and treated with the TGF-β receptor 1 and 2 inhibitor, GW788388. TGF-β1 expression, signal transduction and viral load were evaluated 48 h after DENV-2 infection by enzyme-linked immunoassay, immunofluorescence, and RT-qPCR assays. Total TGF-β1 level was reduced in 15% after DENV-2 infection, but the secretion of its biologically active form increased threefold during infection, which was followed by the phosphorylation of Smad2 protein. Phosphorylation of Smad2 was reduced by treatment with GW788388 and it was correlated with reduced cytokine production. Importantly, treatment led to a dose-dependent reduction in viral load, ranging from 6.6 × 10
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