The Effect of a Unique Region of Parvovirus B19 Capsid Protein VP1 on Endothelial Cells
Ieva Rinkūnaitė,
Egidijus Šimoliūnas,
Daiva Bironaitė,
Rasa Rutkienė,
Virginija Bukelskienė,
Rolandas Meškys,
Julius Bogomolovas
Affiliations
Ieva Rinkūnaitė
Department of Biological Models, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, Lithuania
Egidijus Šimoliūnas
Department of Biological Models, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, Lithuania
Daiva Bironaitė
Department of Regenerative Medicine, Center for Innovative Medicine, State Research Institute, LT-08406 Vilnius, Lithuania
Rasa Rutkienė
Department of Molecular Microbiology and Biotechnology, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, Lithuania
Virginija Bukelskienė
Department of Biological Models, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, Lithuania
Rolandas Meškys
Department of Molecular Microbiology and Biotechnology, Life Sciences Center, Institute of Biochemistry, Vilnius University, LT-10257 Vilnius, Lithuania
Julius Bogomolovas
Department of Medicine, School of Medicine, UCSD, La Jolla, CA 92093, USA
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.
