ArticleJournal of virology2003
Human parvovirus B19 nonstructural protein (NS1) induces cell cycle arrest at G(1) phase.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
50 citing papers in PubMed, 96 citations in OpenAlex.
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- Parvoviruses NS1 oncolytic attributes: mechanistic insights and synergistic anti-tumor therapeutic strategies.Frontiers in microbiology · 2025Review
- Analysis of the primary factors influencing donor derived cell-free DNA testing in kidney transplantation.Frontiers in immunology · 2024Review
- Nuclear entry and egress of parvoviruses.Molecular microbiology · 2022Review
- Parvovirus B19 induces cellular senescence in human dermal fibroblasts: putative role in systemic sclerosis-associated fibrosis.Rheumatology (Oxford, England) · 2022Article
- Duck hepatitis A virus type 1 mediates cell cycle arrest in the S phase.Virology journal · 2022Article
- G2/M checkpoint regulation and apoptosis facilitate the nuclear egress of parvoviral capsids.Frontiers in cell and developmental biology · 2022Article
- The Pathogenic Aspects of Human Parvovirus B19 NS1 Protein in Chronic and Inflammatory Diseases.Interdisciplinary perspectives on infectious diseases · 2022Article
- Canine Parvovirus and Its Non-Structural Gene 1 as Oncolytic Agents: Mechanism of Action and Induction of Anti-Tumor Immune Response.Frontiers in oncology · 2021Review
- Answered and Unanswered Questions in Early-Stage Viral Vector Transduction Biology and Innate Primary Cell Toxicity forFrontiers in immunology · 2021Review
- Therapeutic Plasma Exchange in Parvovirus B19-induced Acute Hepatic Failure.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2020Article
- Viral Nonstructural Protein 1 Induces Mitochondrion-Mediated Apoptosis in Mink Enteritis Virus Infection.Journal of virology · 2019Article
- Endonuclease Activity Inhibition of the NS1 Protein of Parvovirus B19 as a Novel Target for Antiviral Drug Development.Antimicrobial agents and chemotherapy · 2019Article
- Human Parvovirus B19 Utilizes Cellular DNA Replication Machinery for Viral DNA Replication.Journal of virology · 2018Article
- Recent Advances in Replication and Infection of Human Parvovirus B19.Frontiers in cellular and infection microbiology · 2018Review
- Protoparvovirus Knocking at the Nuclear Door.Viruses · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human parvovirus B19 infects predominantly erythroid precursor cells, leading to inhibition of erythropoiesis. This erythroid cell damage is mediated by the viral nonstructural protein 1 (NS1) through an apoptotic mechanism. We previously demonstrated that B19 virus infection induces G(2) arrest in erythroid UT7/Epo-S1 cells; however, the role of NS1 in regulating cell cycle arrest is unknown. In this report, by using paclitaxel, a mitotic inhibitor, we show that B19 virus infection induces not only G(2) arrest but also G(1) arrest. Interestingly, UV-irradiated B19 virus, which has inactivated the expression of NS1, still harbors the ability to induce G(2) arrest but not G(1) arrest. Furthermore, treatment with caffeine, a G(2) checkpoint inhibitor, abrogated the B19 virus-induced G(2) arrest despite expression of NS1. These results suggest that the B19 virus-induced G(2) arrest is not mediated by NS1 expression. We also found that NS1-transfected UT7/Epo-S1 and 293T cells induced cell cycle arrest at the G(1) phase. These results indicate that NS1 expression plays a critical role in G(1) arrest induced by B19 virus. Furthermore, NS1 expression significantly increased p21/WAF1 expression, a cyclin-dependent kinase inhibitor that induces G(1) arrest. Thus, G(1) arrest mediated by NS1 may be a prerequisite for the apoptotic damage of erythroid progenitor cells upon B19 virus infection.
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Registered trials
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.