The Effect of a Unique Region of Parvovirus B19 Capsid Protein VP1 on Endothelial Cells

Parvovirus B19 (B19V) is a widespread human pathogen possessing a high tropism for erythroid precursor cells. However, the persistence or active replication of B19V in endothelial cells (EC) has been detected in diverse human pathologies. The VP1 unique region (VP1u) of the viral capsid has been rep...

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Main Authors: Ieva Rinkūnaitė, Egidijus Šimoliūnas, Daiva Bironaitė, Rasa Rutkienė, Virginija Bukelskienė, Rolandas Meškys, Julius Bogomolovas
Format: Article
Language:English
Published: MDPI AG 2021-04-01
Series:Biomolecules
Subjects:
Online Access:https://www.mdpi.com/2218-273X/11/4/606
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author Ieva Rinkūnaitė
Egidijus Šimoliūnas
Daiva Bironaitė
Rasa Rutkienė
Virginija Bukelskienė
Rolandas Meškys
Julius Bogomolovas
author_facet Ieva Rinkūnaitė
Egidijus Šimoliūnas
Daiva Bironaitė
Rasa Rutkienė
Virginija Bukelskienė
Rolandas Meškys
Julius Bogomolovas
author_sort Ieva Rinkūnaitė
collection DOAJ
description Parvovirus B19 (B19V) is a widespread human pathogen possessing a high tropism for erythroid precursor cells. However, the persistence or active replication of B19V in endothelial cells (EC) has been detected in diverse human pathologies. The VP1 unique region (VP1u) of the viral capsid has been reported to act as a major determinant of viral tropism for erythroid precursor cells. Nevertheless, the interaction of VP1u with EC has not been studied. We demonstrate that recombinant VP1u is efficiently internalized by rats’ pulmonary trunk blood vessel-derived EC in vitro compared to the human umbilical vein EC line. The exposure to VP1u was not acutely cytotoxic to either human- or rat-derived ECs, but led to the upregulation of cellular stress signaling-related pathways. Our data suggest that high levels of circulating B19V during acute infection can cause endothelial damage, even without active replication or direct internalization into the cells.
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spelling doaj.art-01d80b9165c045c8af4bbc9802c12a9b2023-11-21T16:14:28ZengMDPI AGBiomolecules2218-273X2021-04-0111460610.3390/biom11040606The Effect of a Unique Region of Parvovirus B19 Capsid Protein VP1 on Endothelial CellsIeva Rinkūnaitė0Egidijus Šimoliūnas1Daiva Bironaitė2Rasa Rutkienė3Virginija Bukelskienė4Rolandas Meškys5Julius Bogomolovas6Department of Biological Models, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, LithuaniaDepartment of Biological Models, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, LithuaniaDepartment of Regenerative Medicine, Center for Innovative Medicine, State Research Institute, LT-08406 Vilnius, LithuaniaDepartment of Molecular Microbiology and Biotechnology, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, LithuaniaDepartment of Biological Models, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, LithuaniaDepartment of Molecular Microbiology and Biotechnology, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, LithuaniaDepartment of Medicine, School of Medicine, UCSD, La Jolla, CA 92093, USAParvovirus B19 (B19V) is a widespread human pathogen possessing a high tropism for erythroid precursor cells. However, the persistence or active replication of B19V in endothelial cells (EC) has been detected in diverse human pathologies. The VP1 unique region (VP1u) of the viral capsid has been reported to act as a major determinant of viral tropism for erythroid precursor cells. Nevertheless, the interaction of VP1u with EC has not been studied. We demonstrate that recombinant VP1u is efficiently internalized by rats’ pulmonary trunk blood vessel-derived EC in vitro compared to the human umbilical vein EC line. The exposure to VP1u was not acutely cytotoxic to either human- or rat-derived ECs, but led to the upregulation of cellular stress signaling-related pathways. Our data suggest that high levels of circulating B19V during acute infection can cause endothelial damage, even without active replication or direct internalization into the cells.https://www.mdpi.com/2218-273X/11/4/606parvovirus B19endothelial cellsVP1uendothelial stress
spellingShingle Ieva Rinkūnaitė
Egidijus Šimoliūnas
Daiva Bironaitė
Rasa Rutkienė
Virginija Bukelskienė
Rolandas Meškys
Julius Bogomolovas
The Effect of a Unique Region of Parvovirus B19 Capsid Protein VP1 on Endothelial Cells
Biomolecules
parvovirus B19
endothelial cells
VP1u
endothelial stress
title The Effect of a Unique Region of Parvovirus B19 Capsid Protein VP1 on Endothelial Cells
title_full The Effect of a Unique Region of Parvovirus B19 Capsid Protein VP1 on Endothelial Cells
title_fullStr The Effect of a Unique Region of Parvovirus B19 Capsid Protein VP1 on Endothelial Cells
title_full_unstemmed The Effect of a Unique Region of Parvovirus B19 Capsid Protein VP1 on Endothelial Cells
title_short The Effect of a Unique Region of Parvovirus B19 Capsid Protein VP1 on Endothelial Cells
title_sort effect of a unique region of parvovirus b19 capsid protein vp1 on endothelial cells
topic parvovirus B19
endothelial cells
VP1u
endothelial stress
url https://www.mdpi.com/2218-273X/11/4/606
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