New Insights of Human Parvovirus B19 in Modulating Erythroid Progenitor Cell Differentiation.

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
Read More Add to Saved list
  • Author(s): Feng S;Feng S; Zeng D; Zeng D; Zheng J; Zheng J; Zhao D; Zhao D
  • Source:
    Viral immunology [Viral Immunol] 2020 Oct; Vol. 33 (8), pp. 539-549. Date of Electronic Publication: 2020 May 15.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't; Review
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Mary Ann Liebert, Inc Country of Publication: United States NLM ID: 8801552 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1557-8976 (Electronic) Linking ISSN: 08828245 NLM ISO Abbreviation: Viral Immunol Subsets: MEDLINE
    • Publication Information:
      Original Publication: New York, NY : Mary Ann Liebert, Inc., c1987-
    • Subject Terms:
      Cell Differentiation*; Erythroid Precursor Cells/*physiology ; Erythroid Precursor Cells/*virology ; Parvovirus B19, Human/*pathogenicity ; Viral Nonstructural Proteins/*metabolism; Animals ; DNA Replication ; Female ; Humans ; Mice ; Parvoviridae Infections/virology ; Pregnancy ; Signal Transduction ; Viral Nonstructural Proteins/genetics ; Virus Replication
    • Abstract:
      Human parvovirus B19 (B19), a human pathogen of the erythroparvovirus genus, is responsible for a variety of diseases. B19 cause less symptoms in healthy individuals, also cause acute and chronic anemia in immunodeficiency patients. Transient aplastic crisis and pure red cell aplasia are two kinds of anemic hemogram, respectively, in acute and chronic B19 infection phase, especially occurring in patients with a shortened red cell survival or with immunodeficiency. In addition, B19-infected pregnant women may cause hydrops fetalis or fetal loss. B19 possesses high affinity to bone marrow and fetal liver due to its extremely restricted cytotoxicity to erythroid progenitor cells (EPCs) mediated by viral proteins. The nonstructural protein NS1 is considered to be the major pathogenic factor, which has been shown to inhibit the differentiation and maturation of EPCs through inducing viral DNA damage responses and cell cycle arrest. The time phase property of NS1 activity during DNA replication and conformity to transient change of hemogram are suggestive of its role in regulating differentiation of hematopoietic cells, which is not completely understood. In this review, we summarized the bridge between B19 NS1 and Notch signaling pathway or transcriptional factors GATA, which play an important role in erythroid cell proliferation and differentiation, to provide a new insight of the potential mechanism of B19-induced differential inhibition of EPCs.
    • Contributed Indexing:
      Keywords: GATA; anemia; differentiation; erythroid progenitor cells; human parvovirus B19; nonstructural protein NS1
    • Accession Number:
      0 (NS1 protein, parvovirus)
      0 (Viral Nonstructural Proteins)
    • Publication Date:
      Date Created: 20200516 Date Completed: 20210819 Latest Revision: 20210819
    • Publication Date:
      20240105
    • Accession Number:
      10.1089/vim.2020.0013
    • Accession Number:
      32412895