Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

New Insights of Human Parvovirus B19 in Modulating Erythroid Progenitor Cells Differentiation

Version 1 : Received: 14 October 2019 / Approved: 16 October 2019 / Online: 16 October 2019 (05:37:39 CEST)

How to cite: Feng, S.; Zeng, D.; Zheng, J.; Zhao, D. New Insights of Human Parvovirus B19 in Modulating Erythroid Progenitor Cells Differentiation. Preprints 2019, 2019100179. https://doi.org/10.20944/preprints201910.0179.v1 Feng, S.; Zeng, D.; Zheng, J.; Zhao, D. New Insights of Human Parvovirus B19 in Modulating Erythroid Progenitor Cells Differentiation. Preprints 2019, 2019100179. https://doi.org/10.20944/preprints201910.0179.v1

Abstract

Background Human parvovirus B19, a human pathogen of the erythroparvovirus genus, is responsible for a variety of diseases. Despite less symptoms caused by B19 infection in healthy individuals, this pathogen can not be neglected in specific groups who exhibit severe anemia. Main body of abstract Transient aplastic crisis and pure red cell aplasia are two kinds of anemic hemogram respectively in acute phase and chronic B19 infection, especially occur in individuals with a shortened red cell survival or immunocompromised patients. In addition, B19 infected pregnant women may suffer risks of hydrops fetalis secondary to severe anemia and fetal loss. B19 possesses high affinity to bone marrow and fetal liver due to its extremely restricted cytotoxicity to erythroid progenitor cells mediated by viral proteins. The nonstructural protein NS1 is considered to be the major pathogenic factor, which takes parts in differentiational inhibition and apoptosis of erythroid progenitor cells 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. Conclusion In this review, we set up a hypothetic bridge between B19 NS1 and Notch signaling pathway or transcriptional factors GATA which are essential in hematopoiesis, to provide a new insight of the potential mechanism of B19-induced differentiational inhibition of erythroid progenitor cells.

Keywords

human parvovirus B19; nonstructural protein NS1; erythroid progenitor cells; differentiation; GATA; anemia

Subject

Medicine and Pharmacology, Pediatrics, Perinatology and Child Health

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