ArticleFuture virology2010
Parvovirus infection-induced cell death and cell cycle arrest.
Article in Future virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
54 citing papers in PubMed, 76 citations in OpenAlex.
- Article
- The SIRT1-Mediated p53 Deacetylation Pathway Modulates Apoptosis and Promotes Viral Replication in MVC-Infected Cells.Pathogens (Basel, Switzerland) · 2026Article
- Article
- 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
- Parvoviruses NS1 oncolytic attributes: mechanistic insights and synergistic anti-tumor therapeutic strategies.Frontiers in microbiology · 2025Review
- Temporal insights into molecular and cellular responses during rAAV production in HEK293T cells.Molecular therapy. Methods & clinical development · 2024Article
- Parvoviruses of Aquatic Animals.Pathogens (Basel, Switzerland) · 2024Review
- Transcriptional Differential Analysis of Nitazoxanide-Mediated Anticanine Parvovirus Effect in F81 Cells.Viruses · 2024Article
- 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
- TLR2-mediated NF-κB signaling pathway is involved in PPV1-induced apoptosis in PK-15 cells.Veterinary research communications · 2023Article
- Tracking of Human Parvovirus B19 Virus-Like Particles Using Short Peptide Tags Reveals a Membrane-Associated Extracellular Release of These Particles.Journal of virology · 2023Article
- Nuclear entry and egress of parvoviruses.Molecular microbiology · 2022Review
- A Functional Minigenome of Parvovirus B19.Viruses · 2022Article
- G2/M checkpoint regulation and apoptosis facilitate the nuclear egress of parvoviral capsids.Frontiers in cell and developmental biology · 2022Article
- Genome-wide activation screens to increase adeno-associated virus production.Molecular therapy. Nucleic acids · 2021Article
- Small but mighty: old and new parvoviruses of veterinary significance.Virology journal · 2021Review
- Review
- AMDV Vaccine: Challenges and Perspectives.Viruses · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The cytopathic effects induced during parvovirus infection have been widely documented. Parvovirus infection-induced cell death is often directly associated with disease outcomes (e.g., anemia resulting from loss of erythroid progenitors during parvovirus B19 infection). Apoptosis is the major form of cell death induced by parvovirus infection. However, nonapoptotic cell death, namely necrosis, has also been reported during infection of the minute virus of mice, parvovirus H-1 and bovine parvovirus. Recent studies have revealed multiple mechanisms underlying the cell death during parvovirus infection. These mechanisms vary in different parvoviruses, although the large nonstructural protein (NS)1 and the small NS proteins (e.g., the 11 kDa of parvovirus B19), as well as replication of the viral genome, are responsible for causing infection-induced cell death. Cell cycle arrest is also common, and contributes to the cytopathic effects induced during parvovirus infection. While viral NS proteins have been indicated to induce cell cycle arrest, increasing evidence suggests that a cellular DNA damage response triggered by an invading single-stranded parvoviral genome is the major inducer of cell cycle arrest in parvovirus-infected cells. Apparently, in response to infection, cell death and cell cycle arrest of parvovirus-infected cells are beneficial to the viral cell lifecycle (e.g., viral DNA replication and virus egress). In this article, we will discuss recent advances in the understanding of the mechanisms underlying parvovirus infection-induced cell death and cell cycle arrest.
Identifiers
What Socratic holds
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 Socratic graph.