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Updated: Nov 28, 2025
Generation, Amplification, and Titration of Recombinant Respiratory Syncytial Viruses
Published on: April 4, 2019
Luteolin inhibits respiratory syncytial virus replication by regulating the MiR-155/SOCS1/STAT1 signaling pathway
Saisai Wang1, Yiting Ling1, Yuanyuan Yao1
1Department of Colorectal Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou, 310003, Zhejiang, People's Republic of China.
Background:
Respiratory syncytial virus (RSV) is a major cause of acute lower respiratory tract infection in infants, children, immunocompromised adults, and elderly individuals. Currently, there are few therapeutic options available to prevent RSV infection. The present study aimed to investigate the effects of luteolin on RSV replication and the related mechanisms.
Material And Methods:
We pretreated cells and mice with luteolin before infection with RSV, the virus titer, expressions of RSV-F, interferon (IFN)-stimulated genes (ISGs), and production of IFN-α and IFN-β were determined by plaque assay, RT-qPCR, and ELISA, respectively. The activation of Janus kinase (JAK)-signal transducer and activator of transcription 1 (STAT1) signaling pathway was detected by Western blotting and luciferase assay. Proteins which negatively regulate STAT1 were determined by Western blotting. Then cells were transfected with suppressor of cytokine signaling 1 (SOCS1) plasmid and virus replication and ISGs expression were determined. Luciferase reporter assay and Western blotting were performed to detect the relationship between SOCS1 and miR-155.
Results:
Luteolin inhibited RSV replication, as shown by the decreased viral titer and RSV-F mRNA expression both in vitro and in vivo. The antiviral activity of luteolin was attributed to the enhanced phosphorylation of STAT1, resulting in the increased production of ISGs. Further study showed that SOCS1 was downregulated by luteolin and SOCS1 is a direct target of microRNA-155 (miR-155). Inhibition of miR-155 rescued luteolin-mediated SOCS1 downregulation, whereas upregulation of miR-155 enhanced the inhibitory effect of luteolin.
Conclusion:
Luteolin inhibits RSV replication by regulating the miR-155/SOCS1/STAT1 signaling pathway.
Insights
Luteolin effectively inhibits respiratory syncytial virus (RSV) replication by enhancing the STAT1 signaling pathway. This natural compound regulates the miR-155/SOCS1 axis, offering a potential therapeutic strategy against RSV infections.
Area of Science:
- Virology
- Immunology
- Pharmacology
Background:
- Respiratory syncytial virus (RSV) is a significant pathogen causing severe respiratory infections in vulnerable populations.
- Current therapeutic options for RSV prevention and treatment are limited.
- Luteolin, a natural flavonoid, was investigated for its potential antiviral properties against RSV.
Purpose of the Study:
- To evaluate the efficacy of luteolin in inhibiting RSV replication.
- To elucidate the underlying molecular mechanisms of luteolin's antiviral activity.
- To explore the role of the miR-155/SOCS1/STAT1 signaling pathway in luteolin's action against RSV.
Main Methods:
- Cells and mice were pretreated with luteolin before RSV infection.
- Viral titers, RSV-F mRNA expression, and interferon-stimulated genes (ISGs) were quantified.
- Western blotting and luciferase assays were used to analyze JAK-STAT1 pathway activation and miR-155/SOCS1 interactions.
Main Results:
- Luteolin significantly reduced RSV replication in vitro and in vivo, indicated by lower viral titers and RSV-F expression.
- Luteolin treatment enhanced STAT1 phosphorylation, leading to increased production of ISGs.
- Luteolin downregulated SOCS1, a direct target of miR-155, suggesting a regulatory role for miR-155 in luteolin's antiviral mechanism.
Conclusions:
- Luteolin demonstrates potent antiviral activity against RSV.
- The mechanism involves the regulation of the miR-155/SOCS1/STAT1 signaling pathway.
- Luteolin represents a promising therapeutic candidate for managing RSV infections.
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