ArticleJournal of virology2010
Role of erythropoietin receptor signaling in parvovirus B19 replication in human erythroid progenitor cells.
Article in Journal of virology, 2010. 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, 72 citations in OpenAlex.
- Article
- Cellular determinants of parvovirus B19 susceptibility in the human placenta.PLoS pathogens · 2026Article
- Article
- Identification of SLC35A1 as an essential host factor for the transduction of multi-serotype recombinant adeno-associated virus (AAV) vectors.bioRxiv : the preprint server for biology · 2024Article
- Parvovirus B19 in Rheumatic Diseases.Microorganisms · 2024Review
- Inhibition of DNA-dependent protein kinase catalytic subunit boosts rAAV transduction of polarized human airway epithelium.Molecular therapy. Methods & clinical development · 2023Article
- Globoside and the mucosal pH mediate parvovirus B19 entry through the epithelial barrier.PLoS pathogens · 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
- Article
- Identification of AXL as a co-receptor for human parvovirus B19 infection of human erythroid progenitors.Science advances · 2023Article
- The cytokine receptor CRLF3 is a human neuroprotective EV-3 (Epo) receptor.Frontiers in molecular neuroscience · 2023Article
- Small but mighty: old and new parvoviruses of veterinary significance.Virology journal · 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
- Human parvovirus B19 interacts with globoside under acidic conditions as an essential step in endocytic trafficking.PLoS pathogens · 2021Article
- The VP1u of Human Parvovirus B19: A Multifunctional Capsid Protein with Biotechnological Applications.Viruses · 2020Review
- Oxygen: viral friend or foe?Virology journal · 2020Review
- Article
- Globoside Is Dispensable for Parvovirus B19 Entry but Essential at a Postentry Step for Productive Infection.Journal of virology · 2019Article
- Review
- Pure Red Cell Aplasia After Kidney Transplantation: Parvovirus B19 Culprit or Coincidence?Annals of transplantation · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Parvovirus B19 (B19V) infection is highly restricted to human erythroid progenitor cells. Although previous studies have led to the theory that the basis of this tropism is receptor expression, this has been questioned by more recent observation. In the study reported here, we have investigated the basis of this tropism, and a potential role of erythropoietin (Epo) signaling, in erythroid progenitor cells (EPCs) expanded ex vivo from CD34(+) hematopoietic cells in the absence of Epo (CD36(+)/Epo(-) EPCs). We show, first, that CD36(+)/Epo(-) EPCs do not support B19V replication, in spite of B19V entry, but Epo exposure either prior to infection or after virus entry enabled active B19V replication. Second, when Janus kinase 2 (Jak2) phosphorylation was inhibited using the inhibitor AG490, phosphorylation of the Epo receptor (EpoR) was also inhibited, and B19V replication in ex vivo-expanded erythroid progenitor cells exposed to Epo (CD36(+)/Epo(+) EPCs) was abolished. Third, expression of constitutively active EpoR in CD36(+)/Epo(-) EPCs led to efficient B19V replication. Finally, B19V replication in CD36(+)/Epo(+) EPCs required Epo, and the replication response was dose dependent. Our findings demonstrate that EpoR signaling is absolutely required for B19V replication in ex vivo-expanded erythroid progenitor cells after initial virus entry and at least partly accounts for the remarkable tropism of B19V infection for human erythroid progenitors.
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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.