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dc.contributor.authorIeva Rinkūnaitė
dc.contributor.authorEgidijus Šimoliūnas
dc.contributor.authorDaiva Bironaitė
dc.contributor.authorRasa Rutkienė
dc.contributor.authorVirginija Bukelskienė
dc.contributor.authorRolandas Meškys
dc.contributor.authorJulius Bogomolovas
dc.contributor.otherDepartment of Biological Models, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, Lithuania
dc.contributor.otherDepartment of Biological Models, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, Lithuania
dc.contributor.otherDepartment of Regenerative Medicine, Center for Innovative Medicine, State Research Institute, LT-08406 Vilnius, Lithuania
dc.contributor.otherDepartment of Molecular Microbiology and Biotechnology, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, Lithuania
dc.contributor.otherDepartment of Biological Models, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, Lithuania
dc.contributor.otherDepartment of Molecular Microbiology and Biotechnology, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, Lithuania
dc.contributor.otherDepartment of Medicine, School of Medicine, UCSD, La Jolla, CA 92093, USA
dc.date.accessioned2025-10-09T05:26:41Z
dc.date.available2025-10-09T05:26:41Z
dc.date.issued01-04-2021
dc.identifier.urihttps://www.mdpi.com/2218-273X/11/4/606
dc.identifier.urihttp://digilib.fisipol.ugm.ac.id/repo/handle/15717717/41021
dc.description.abstractParvovirus 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.
dc.language.isoEN
dc.publisherMDPI AG
dc.subject.lccMicrobiology
dc.titleThe Effect of a Unique Region of Parvovirus B19 Capsid Protein VP1 on Endothelial Cells
dc.typeArticle
dc.description.keywordsparvovirus B19
dc.description.keywordsendothelial cells
dc.description.keywordsVP1u
dc.description.keywordsendothelial stress
dc.description.doi10.3390/biom11040606
dc.title.journalBiomolecules
dc.identifier.e-issn2218-273X
dc.identifier.oaioai:doaj.org/journal:01d80b9165c045c8af4bbc9802c12a9b
dc.journal.infoVolume 11, Issue 4


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