ArticleJournal of virology2012
Human parvovirus B19 DNA replication induces a DNA damage response that is dispensable for cell cycle arrest at phase G2/M.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 49 citations in OpenAlex.
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- Parvovirus RNA Processing: Compact Genomic Organization and Unique Alternative mRNA Processing Mechanisms.Viruses · 2025Review
- 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
- Chaperonin TRiC/CCT subunit CCT7 is involved in the replication of canine parvovirus in F81 cells.Frontiers in microbiology · 2024Article
- For better or worse: crosstalk of parvovirus and host DNA damage response.Frontiers in immunology · 2024Review
- Article
- Duck hepatitis A virus type 1 mediates cell cycle arrest in the S phase.Virology journal · 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
- High-Throughput Screening Identifies Inhibitors for Parvovirus B19 Infection of Human Erythroid Progenitors.Journal of virology · 2022Article
- Structures and implications of the nuclease domain of human parvovirus B19 NS1 protein.Computational and structural biotechnology journal · 2022Article
- Chk1 and the Host Cell DNA Damage Response as a Potential Antiviral Target in BK Polyomavirus Infection.Viruses · 2021Article
- 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
- Recent Advances in Molecular Biology of Human Bocavirus 1 and Its Applications.Frontiers in microbiology · 2021Review
- Article
- Cellular Cleavage and Polyadenylation Specificity Factor 6 (CPSF6) Mediates Nuclear Import of Human Bocavirus 1 NP1 Protein and Modulates Viral Capsid Protein Expression.Journal of virology · 2020Article
- Establishment of a Parvovirus B19 NS1-Expressing Recombinant Adenoviral Vector for Killing Megakaryocytic Leukemia Cells.Viruses · 2019Article
- Endonuclease Activity Inhibition of the NS1 Protein of Parvovirus B19 as a Novel Target for Antiviral Drug Development.Antimicrobial agents and chemotherapy · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Human parvovirus B19 (B19V) infection is highly restricted to human erythroid progenitor cells, in which it induces a DNA damage response (DDR). The DDR signaling is mainly mediated by the ATR (ataxia telangiectasia-mutated and Rad3-related) pathway, which promotes replication of the viral genome; however, the exact mechanisms employed by B19V to take advantage of the DDR for virus replication remain unclear. In this study, we focused on the initiators of the DDR and the role of the DDR in cell cycle arrest during B19V infection. We examined the role of individual viral proteins, which were delivered by lentiviruses, in triggering a DDR in ex vivo-expanded primary human erythroid progenitor cells and the role of DNA replication of the B19V double-stranded DNA (dsDNA) genome in a human megakaryoblastoid cell line, UT7/Epo-S1 (S1). All the cells were cultured under hypoxic conditions. The results showed that none of the viral proteins induced phosphorylation of H2AX or replication protein A32 (RPA32), both hallmarks of a DDR. However, replication of the B19V dsDNA genome was capable of inducing the DDR. Moreover, the DDR per se did not arrest the cell cycle at the G(2)/M phase in cells with replicating B19V dsDNA genomes. Instead, the B19V nonstructural 1 (NS1) protein was the key factor in disrupting the cell cycle via a putative transactivation domain operating through a p53-independent pathway. Taken together, the results suggest that the replication of the B19V genome is largely responsible for triggering a DDR, which does not perturb cell cycle progression at G(2)/M significantly, during B19V 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.