ArticleViruses2025
Parvovirus B19 and Cellular Transcriptome Dynamics in Differentiating Erythroid Progenitor Cells.
Article in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Article
- Article
- Viral receptors as host-pathogen control nodes linking entry, signalling, and system-level pathogenesis.FEMS microbiology reviews · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Parvovirus B19 (B19V) is a human ssDNA virus with ample pathogenic potential. It is characterized by a selective tropism for erythroid progenitor cells (EPC), exerting a cytotoxic effect with blockade of erythropoiesis. In our work, we investigated both viral and cellular expression profile in the course of infection of EPCs cultures via mRNA high throughput sequencing technology (HTS) and a dedicated bioinformatic pipeline, reconstructing both the viral and cellular transcriptome and their variations. A productive infection was confirmed as restricted to EPCs expressing mature differentiation markers and the specific receptor for virus VP1u region. mRNA HTS reconstructed the viral transcriptome in terms of localization and abundance of the different mRNA species, detailing the differential expression profile of B19V among early or late times in the course of infection. Analysis of cellular transcriptome indicated that variation was mainly driven by the cellular differentiation process, with the virus impacting to a lesser level, but still clearly separating infected vs. non-infected profiles. At early times post-infection, variations were typical of cellular sensing of viral infection and aimed at the induction of an antiviral state. At later times in the course of infection, the cellular population showed induction of an inflammatory response, related to TNF and IL-10, and a transition to adaptive immunity with evidence of upregulation of genes involved in MHC-II presentation. This dual-transcriptome analysis on infected EPCs population can lay the ground for future research aimed at a better definition of the pathogenetic mechanisms of B19V.
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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.