ArticleScientific reports2016
Caveolae Restrict Tiger Frog Virus Release in HepG2 cells and Caveolae-Associated Proteins Incorporated into Virus Particles.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- RPSA enhances African swine fever virus entry via caveola-mediated endocytic pathway.Journal of virology · 2026Article
- Virus-Host Protein Interaction Network of the Hepatitis E Virus ORF2-4 by Mammalian Two-Hybrid Assays.Viruses · 2023Article
- Endothelial Transcytosis in Acute Lung Injury: Emerging Mechanisms and Therapeutic Approaches.Frontiers in physiology · 2022Review
- Evidence for a Novel Antiviral Mechanism of Teleost Fish: Serum-Derived Exosomes Inhibit Virus Replication through Incorporating Mx1 Protein.International journal of molecular sciences · 2021Article
- Review
- Lung Endothelial Transcytosis.Comprehensive Physiology · 2020Review
- Virion-Associated Cholesterol Regulates the Infection of Human Parainfluenza Virus Type 3.Viruses · 2019Article
- PTRF acts as an adipokine contributing to adipocyte dysfunctionality and ectopic lipid deposition.Journal of physiology and biochemistry · 2018Article
- MicroRNA and cellular targets profiling reveal miR-217 and miR-576-3p as proviral factors during Oropouche infection.PLoS neglected tropical diseases · 2018Article
- Caveolae provide a specialized membrane environment for respiratory syncytial virus assembly.Journal of cell science · 2017Article
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8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Caveolae are flask-shaped invaginations of the plasma membrane. Caveolae play important roles in the process of viruses entry into host cells, but the roles of caveolae at the late stage of virus infection were not completely understood. Tiger frog virus (TFV) has been isolated from the diseased tadpoles of the frog, Rana tigrina rugulosa, and causes high mortality of tiger frog tadpoles cultured in Southern China. In the present study, the roles of caveolae at the late stage of TFV infection were investigated. We showed that TFV virions were localized with the caveolae at the late stage of infection in HepG2 cells. Disruption of caveolae by methyl-β-cyclodextrin/nystatin or knockdown of caveolin-1 significantly increase the release of TFV. Moreover, the interaction between caveolin-1 and TFV major capsid protein was detected by co-immunoprecipitation. Those results suggested that caveolae restricted TFV release from the HepG2 cells. Caveolae-associated proteins (caveolin-1, caveolin-2, cavin-1, and cavin-2) were selectively incorporated into TFV virions. Different combinations of proteolytic and/or detergent treatments with virions showed that caveolae-associated proteins were located in viral capsid of TFV virons. Taken together, caveolae might be a restriction factor that affects virus release and caveolae-associated proteins were incorporated in TFV virions.
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