Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2016, Article ID 1627184, 9 pages
Research Article

A Novel Murine Model of Parvovirus Associated Dilated Cardiomyopathy Induced by Immunization with VP1-Unique Region of Parvovirus B19

1Department of Integrative Pathophysiology, Medical Faculty Mannheim, Mannheim, Germany
2Department of Pathology, Forensic Medicine and Pharmacology, Faculty of Medicine, Vilnius University, Vilnius, Lithuania
3Department of Biological Models, Institute of Biochemistry, Vilnius University, Vilnius, Lithuania
4State Research Institute, Centre for Innovative Medicine, Department of Stem Cell Biology, Vilnius, Lithuania
5Medical Faculty Mannheim, Institute of Pathology, Mannheim, Germany
6Medical Faculty Mannheim, Medical Research Centre, Mannheim, Germany

Received 17 May 2016; Revised 9 August 2016; Accepted 14 September 2016

Academic Editor: Andrea Vecchione

Copyright © 2016 Julijus Bogomolovas et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Parvovirus B19 (B19V) is a common finding in endomyocardial biopsy specimens from myocarditis and dilated cardiomyopathy patients. However, current understanding of how B19V is contributing to cardiac damage is rather limited due to the lack of appropriate mice models. In this work we demonstrate that immunization of BALB/c mice with the major immunogenic determinant of B19V located in the unique sequence of capsid protein VP1 (VP1u) is an adequate model to study B19V associated heart damage. Methods and Results. We immunized mice in the experimental group with recombinant VP1u; immunization with cardiac myosin derived peptide served as a positive reference and phosphate buffered saline served as negative control. Cardiac function and dimensions were followed echocardiographically 69 days after immunization. Progressive dilatation of left ventricle and decline of ejection fraction were observed in VP1u- and myosin-immunized mice. Histologically, severe cardiac fibrosis and accumulation of heart failure cells in lungs were observed 69 days after immunization. Transcriptomic profiling revealed ongoing cardiac remodeling and immune process in VP1u- and myosin-immunized mice. Conclusions. Immunization of BALB/c mice with VP1u induces dilated cardiomyopathy in BALB/c mice and it could be used as a model to study clinically relevant B19V associated cardiac damage.