ArticleJournal of virology2008
Human parvovirus B19 NS1 protein modulates inflammatory signaling by activation of STAT3/PIAS3 in human endothelial cells.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 86 citations in OpenAlex.
- Intravenous immunoglobulin therapy in adult patients with idiopathic chronic cardiomyopathy and cardiac parvovirus B19 persistence: a prospective, double-blind, randomized, placebo-controlled clinical trial.European journal of heart failure · 2021Trial
- Article
- Parvoviruses at the Heart: Endothelial Injury and Myocyte Lysis in Human B19V and Canine CPV-2 Infections.Current issues in molecular biology · 2025Review
- Review
- Parvovirus B19 in Rheumatic Diseases.Microorganisms · 2024Review
- The inflammatory spectrum of cardiomyopathies.Frontiers in cardiovascular medicine · 2024Review
- Review
- Reproduction and pathogenesis of short beak and dwarfish syndrome in Cherry Valley Pekin ducks infected with the rescued novel goose parvovirus.Virulence · 2022Article
- High-Resolution Structure of the Nuclease Domain of the Human Parvovirus B19 Main Replication Protein NS1.Journal of virology · 2022Article
- COVID-lateral damage: cardiovascular manifestations of SARS-CoV-2 infection.Translational research : the journal of laboratory and clinical medicine · 2022Review
- The M2 Gene Is a Determinant of Reovirus-Induced Myocarditis.Journal of virology · 2022Article
- The Pathogenic Aspects of Human Parvovirus B19 NS1 Protein in Chronic and Inflammatory Diseases.Interdisciplinary perspectives on infectious diseases · 2022Article
- Persistent viral infections and their role in heart disease.Frontiers in microbiology · 2022Review
- Molecular Mechanisms behind Persistent Presence of Parvovirus B19 in Human Dilated Myocardium.Advances in experimental medicine and biology · 2022Article
- Cardiovascular consequences of viral infections: from COVID to other viral diseases.Cardiovascular research · 2021Review
- Effect of N‑terminal region of human parvovirus B19‑VP1 unique region on cardiac injury in naïve mice.Molecular medicine reports · 2021Article
- Review
- Viruses, SUMO, and immunity: the interplay between viruses and the host SUMOylation system.Journal of neurovirology · 2021Review
- Myocarditis and inflammatory cardiomyopathy: current evidence and future directions.Nature reviews. Cardiology · 2021Review
- Detection of parvovirus mRNAs as markers for viral activity in endomyocardial biopsy-based diagnosis of patients with unexplained heart failure.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenic mechanism by which parvovirus B19 may induce inflammatory cardiomyopathy (iCMP) is complex but is known to involve inflammatory processes, possibly including activation of JAK/STAT signaling. The nonstructural B19 protein NS1 acts as a transactivator triggering signaling cascades that eventually lead to activation of interleukin 6 (IL-6). We examined the impact of NS1 on modulation of STAT signaling in human endothelial cells (HMEC-1). The NS1 sequences were identified from B19 DNA isolated from the myocardia of patients with fatal iCMP. B19 infection as well as NS1 overexpression in HMEC-1 cells produced a significant upregulation in the phosphorylation of both tyrosine(705) and serine(727) STAT3 (P < 0.05). The increased STAT3 phosphorylation was accompanied by dimerization, nuclear translocation, and DNA binding of pSTAT3. In contrast, NS1 expression did not result in increased STAT1 activation. Notably, the expression levels of the negative regulators of STAT activation, SOCS1 and SOCS3, were not altered by NS1. However, the level of PIAS3 was upregulated in NS1-expressing HMEC-1 cells. Analysis of the transcriptional activation of target genes revealed that NS1-induced STAT3 signaling was associated with upregulation of genes involved in immune response (e.g., the IFNAR1 and IL-2 genes) and downregulation of genes associated with viral defense (e.g., the OAS1 and TYK2 genes). Our results demonstrate that B19 NS1 modulates the STAT/PIAS pathway. The NS1-induced upregulation of STAT3/PIAS3 in the absence of STAT1 phosphorylation and the lack of SOCS1/SOCS3 activation may contribute to the mechanisms by which B19 evades the immune response and establishes persistent infection in human endothelial cells. Thus, NS1 may play a critical role in the mechanism of viral pathogenesis in B19-associated iCMP.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.