ArticleJournal of virology2011
Parvovirus B19 infection of human primary erythroid progenitor cells triggers ATR-Chk1 signaling, which promotes B19 virus replication.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 75 citations in OpenAlex.
- Screening out microRNAs and Their Molecular Pathways with a Potential Role in the Regulation of Parvovirus B19 Infection Through In Silico Analysis.International journal of molecular sciences · 2025Article
- Article
- For better or worse: crosstalk of parvovirus and host DNA damage response.Frontiers in immunology · 2024Review
- The Structures and Functions of Parvovirus Capsids and Missing Pieces: the Viral DNA and Its Packaging, Asymmetrical Features, Nonprotein Components, and Receptor or Antibody Binding and Interactions.Journal of virology · 2023Review
- Identification of AXL as a co-receptor for human parvovirus B19 infection of human erythroid progenitors.Science advances · 2023Article
- Parvovirus B19 induces cellular senescence in human dermal fibroblasts: putative role in systemic sclerosis-associated fibrosis.Rheumatology (Oxford, England) · 2022Article
- The small nonstructural protein NP1 of human bocavirus 1 directly interacts with Ku70 and RPA70 and facilitates viral DNA replication.PLoS pathogens · 2022Article
- Plasma-Enabled Smart Nanoexosome Platform as Emerging Immunopathogenesis for Clinical Viral Infection.Pharmaceutics · 2022Review
- The Large Nonstructural Protein (NS1) of Human Bocavirus 1 Directly Interacts with Ku70, Which Plays an Important Role in Virus Replication in Human Airway Epithelia.Journal of virology · 2022Article
- G2/M checkpoint regulation and apoptosis facilitate the nuclear egress of parvoviral capsids.Frontiers in cell and developmental biology · 2022Article
- Pregnancy and viral infections: Mechanisms of fetal damage, diagnosis and prevention of neonatal adverse outcomes from cytomegalovirus to SARS-CoV-2 and Zika virus.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- Concepts to Reveal Parvovirus-Nucleus Interactions.Viruses · 2021Review
- The N-terminal 5-68 amino acids domain of the minor capsid protein VP1 of human parvovirus B19 enters human erythroid progenitors and inhibits B19 infection.Journal of virology · 2021Article
- 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
- The Role of Ataxia Telangiectasia Mutant and Rad3-Related DNA Damage Response in Pathogenesis of Human Papillomavirus.Pathogens (Basel, Switzerland) · 2020Review
- Endonuclease Activity Inhibition of the NS1 Protein of Parvovirus B19 as a Novel Target for Antiviral Drug Development.Antimicrobial agents and chemotherapy · 2019Article
- Association between Parvovirus B19 and anemia in HIV-infected patients.Medical journal of the Islamic Republic of Iran · 2019Article
- The 11-Kilodalton Nonstructural Protein of Human Parvovirus B19 Facilitates Viral DNA Replication by Interacting with Grb2 through Its Proline-Rich Motifs.Journal of virology · 2019Article
- Virus DNA Replication and the Host DNA Damage Response.Annual review of virology · 2018Review
- RNA Binding Protein RBM38 Regulates Expression of the 11-Kilodalton Protein of Parvovirus B19, Which Facilitates Viral DNA Replication.Journal of virology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Human parvovirus B19 (B19V) infection is restricted to erythroid progenitor cells of the human bone marrow. Although the mechanism by which the B19V genome replicates in these cells has not been studied in great detail, accumulating evidence has implicated involvement of the cellular DNA damage machinery in this process. Here, we report that, in ex vivo-expanded human erythroid progenitor cells, B19V infection induces a broad range of DNA damage responses by triggering phosphorylation of all the upstream kinases of each of three repair pathways: ATM (ataxia-telangiectasi mutated), ATR (ATM and Rad3 related), and DNA-PKcs (DNA-dependent protein kinase catalytic subunit). We found that phosphorylated ATM, ATR, and DNA-PKcs, and also their downstream substrates and components (Chk2, Chk1, and Ku70/Ku80 complex, respectively), localized within the B19V replication center. Notably, inhibition of kinase phosphorylation (through treatment with either kinase-specific inhibitors or kinase-specific shRNAs) revealed requirements for signaling of ATR and DNA-PKcs, but not ATM, in virus replication. Inhibition of the ATR substrate Chk1 led to similar levels of decreased virus replication, indicating that signaling via the ATR-Chk1 pathway is critical to B19V replication. Notably, the cell cycle arrest characteristic of B19V infection was not rescued by interference with the activity of any of the three repair pathway kinases.
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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.