ArticleMicroorganisms2021
The Epithelial-to-Mesenchymal Transition-Like Process Induced by TGF-β1 Enhances Rubella Virus Binding and Infection in A549 Cells via the Smad Pathway.
Article in Microorganisms, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Azelaic acid alleviates UVB-induced photoaging in keratinocytes by restoring Smad-dependent TGF-β signaling.Frontiers in medicine · 2026Article
- Multi-omics analysis reveals discordant proteome and transcriptome responses in larval guts of Frankliniella occidentalis infected with an orthotospovirus.Insect molecular biology · 2025Article
- Oxidative Stress Enhances Rubella Virus Infection in Immortalized Human First-Trimester Trophoblasts.International journal of molecular sciences · 2025Article
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Roles of TGF-β1 in Viral Infection during Pregnancy: Research Update and Perspectives.International journal of molecular sciences · 2023Review
- Article
- Single-cell transcriptome reveals cellular hierarchies and guides p-EMT-targeted trial in skull base chordoma.Cell discovery · 2022Article
- Article
- Enhancement of Rubella Virus Infection in Immortalized Human First-Trimester Trophoblasts Under Low-Glucose Stress Conditions.Frontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Virus-host cell interactions in rubella virus (RuV) are of great interest in current research in the field, as their mechanism is not yet well understood. By hypothesizing that the epithelial-to-mesenchymal transition (EMT) may play a role in RuV infection, this study aimed to investigate the influence of TGF-β1-induced EMT of human lung epithelial A549 cells on the infectivity of RuV. A549 cells were cultured and treated with TGF-β1 for 1 to 2 days prior to virus infection (with a clinical strain). Viral infectivity was determined by flow cytometry analysis of cells harvested at 24 and 48 h post-infection (hpi) and by titration of supernatants collected at 48 hpi. The results showed that the percentages of the TGF-β1-treated A549 cells that were positive for RuV were at least twofold higher than those of the control, and the viral progeny titers in the supernatants collected at 48 hpi were significantly higher in the treatment group than in the control group. In addition, the virus binding assay showed a strong increase (more than threefold) in the percentages of RuV-positive cells, as determined by flow cytometry analysis and further confirmed by real-time PCR. Such an enhancement effect on RuV infectivity was abolished using LY364947 or SB431542, inhibitors of the TGF-β/Smad signaling pathway. The findings suggest that the TGF-β1-induced EMT-like process enhances RuV binding and infection in A549 cells via the Smad pathway. Further studies are necessary to identify possible proteins that facilitate viral binding and entry into treated cells.
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