ArticleBlood2010
CpG-ODN 2006 and human parvovirus B19 genome consensus sequences selectively inhibit growth and development of erythroid progenitor cells.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 38 citations in OpenAlex.
- Rapid progression to end-stage renal disease in a child with IgA-dominant infection-related glomerulonephritis associated with parvovirus B19.CEN case reports · 2020Article
- Article
- RNA Binding Protein RBM38 Regulates Expression of the 11-Kilodalton Protein of Parvovirus B19, Which Facilitates Viral DNA Replication.Journal of virology · 2018Article
- Recent Advances in Replication and Infection of Human Parvovirus B19.Frontiers in cellular and infection microbiology · 2018Review
- Lentiviral vectors escape innate sensing but trigger p53 in human hematopoietic stem and progenitor cells.EMBO molecular medicine · 2017Article
- Parvovirus B19 NS1 protein induces cell cycle arrest at G2-phase by activating the ATR-CDC25C-CDK1 pathway.PLoS pathogens · 2017Article
- Human Parvoviruses.Clinical microbiology reviews · 2017Review
- Identification of a novel putative mitochondrial protein FAM210B associated with erythroid differentiation.International journal of hematology · 2016Article
- Parvovirus B19 Replication and Expression in Differentiating Erythroid Progenitor Cells.PloS one · 2016Article
- Human parvovirus B19 DNA replication induces a DNA damage response that is dispensable for cell cycle arrest at phase G2/M.Journal of virology · 2012Article
- Article
- Parvovirus b19 DNA CpG dinucleotide methylation and epigenetic regulation of viral expression.PloS one · 2012Article
- Guest editorial: the seven wonders of erythropoiesis.International journal of hematology · 2011Article
- Parvovirus infection-induced cell death and cell cycle arrest.Future virology · 2010Article
- Advances in human B19 erythrovirus biology.Journal of virology · 2010Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have shown that anemia is commonly observed after exposure to pathogens or pathogen-derived products, which are recognized via Toll-like receptor 9 (TLR9). In the current study, we demonstrate that CpG oligodeoxynucleotide-2006, a TLR9 ligand with phosphodiester (PO; 2006-PO) but not with the phosphorothioate backbone, selectively inhibits the erythroid growth derived from human CD34(+) cells. The 2006-PO was internalized by the erythroid progenitors within 30 minutes; however, expression of TLR9 mRNA was not detected in these cells. The 2006-PO directly inhibited burst-forming unit-erythroid growth, resulted in the accumulation of cells in S and G(2)/M phases, and increased cell size and frequency of apoptotic cells. These features were similar to those observed in erythroid progenitors infected with human parvovirus B19 that causes pure red cell aplasia. The consensus sequence of 2006-PO was defined as 5'-GTTTTGT-3', which was located in the P6-promoter region of B19 and inhibited erythroid growth in a sequence-specific manner and down-regulated expression of erythropoietin receptor (EPOR) mRNA and EPOR. B19 genome extracted from serum also inhibited erythroid growth and down-regulated expression of EPOR on glycophorin A(+) cells. These results provide a possible insight into our understanding of the mechanisms of human parvovirus B19-mediated inhibition of erythropoiesis.
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