ArticlePloS one2014
Effects of human Parvovirus B19 and Bocavirus VP1 unique region on tight junction of human airway epithelial A549 cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Twenty years of human bocavirus research: from an unculturable virus of unclear pathogenicity to a culturable human pathogen and gene therapy vector candidate.Clinical microbiology reviews · 2025Review
- Effect of the Functional VP1 Unique Region of Human Parvovirus B19 in Causing Skin Fibrosis of Systemic Sclerosis.International journal of molecular sciences · 2023Article
- A cooperativity between virus and bacteria during respiratory infections.Frontiers in microbiology · 2023Review
- Airway Epithelial Cell Junctions as Targets for Pathogens and Antimicrobial Therapy.Pharmaceutics · 2022Review
- Respiratory syncytial virus disrupts the airway epithelial barrier by decreasing cortactin and destabilizing F-actin.Journal of cell science · 2022Article
- A Three-Dimensional Lung Cell Model to Leptospira Virulence Investigations.Current microbiology · 2022Article
- Biological Models of the Lower Human Airways-Challenges and Special Requirements of Human 3D Barrier Models for Biomedical Research.Pharmaceutics · 2021Review
- The Effect of a Unique Region of Parvovirus B19 Capsid Protein VP1 on Endothelial Cells.Biomolecules · 2021Article
- Airway tight junctions as targets of viral infections.Tissue barriers · 2021Article
- The effects of human parvovirus VP1 unique region in a mouse model of allergic asthma.PloS one · 2019Article
- The Antiviral Effects of Na,K-ATPase Inhibition: A Minireview.International journal of molecular sciences · 2018Review
- The Protective Effects of a Synthetic Geranyl Acetophenone in a Cellular Model of TNF-α-Induced Pulmonary Epithelial Barrier Dysfunction.Molecules (Basel, Switzerland) · 2018Article
- Escitalopram oxalate inhibits proliferation and migration and induces apoptosis in non-small cell lung cancer cells.Oncology letters · 2018Article
- Escitalopram oxalate induces apoptosis in U-87MG cells and autophagy in GBM8401 cells.Journal of cellular and molecular medicine · 2018Article
- The VP1 unique region of human parvovirus B19 and human bocavirus induce lung injury in naïve Balb/c mice.PloS one · 2018Article
- Structural Insights into Human Bocaparvoviruses.Journal of virology · 2017Article
- The effect of LDL particles on the behaviour of epithelial noncancer and cancer cell lines after in vitro induced injury.Protoplasma · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As is widely recognized, human parvovirus B19 (B19) and human bocavirus (HBoV) are important human pathogens. Obviously, both VP1 unique region (VP1u) of B19 and HBoV exhibit the secreted phospholipase A2 (sPLA2)-like enzymatic activity and are recognized to participate in the pathogenesis of lower respiratory tract illnesses. However, exactly how, both VP1u from B19 and HBoV affect tight junction has seldom been addressed. Therefore, this study investigates how B19-VP1u and HBoV-VP1u may affect the tight junction of the airway epithelial A549 cells by examining phospholipase A2 activity and transepithelial electrical resistance (TEER) as well as performing immunoblotting analyses. Experimental results indicate that TEER is more significantly decreased in A549 cells by treatment with TNF-α (10 ng), two dosages of B19-VP1u and BoV-VP1u (400 ng and 4000 ng) or bee venom PLA2 (10 ng) than that of the control. Accordingly, more significantly increased claudin-1 and decreased occludin are detected in A549 cells by treatment with TNF-α or both dosages of HBoV-VP1u than that of the control. Additionally, more significantly decreased Na+/K+ ATPase is observed in A549 cells by treatment with TNF-α, high dosage of B19-VP1u or both dosages of BoV-VP1u than that of the control. Above findings suggest that HBoV-VP1u rather than B19 VP1u likely plays more important roles in the disruption of tight junction in the airway tract. Meanwhile, this discrepancy appears not to be associated with the secreted phospholipase A2 (sPLA2)-like enzymatic activity.
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