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Impaired Endothelial Regeneration Through Human Parvovirus B19-Infected Circulating Angiogenic Cells in Patients With Cardiomyopathy

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Impaired Endothelial Regeneration Through Human Parvovirus B19-Infected Circulating Angiogenic Cells in Patients With Cardiomyopathy. / Schmidt-Lucke, Caroline; Zobel, Thomas; Schrepfer, Sonja; Kuhl, Uwe; Wang, Dong; Klingel, Karin; Becher, Peter Moritz; Fechner, Henry; Pozzuto, Tanja; Van Linthout, Sophie; Lassner, Dirk; Spillmann, Frank; Escher, Felicitas; Holinski, Sebastian; Volk, Hans-Dieter; Schultheiss, Heinz-Peter; Tschope, Carsten.

In: J INFECT DIS, Vol. 212, No. 7, 01.10.2015, p. 1070-1081.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Schmidt-Lucke, C, Zobel, T, Schrepfer, S, Kuhl, U, Wang, D, Klingel, K, Becher, PM, Fechner, H, Pozzuto, T, Van Linthout, S, Lassner, D, Spillmann, F, Escher, F, Holinski, S, Volk, H-D, Schultheiss, H-P & Tschope, C 2015, 'Impaired Endothelial Regeneration Through Human Parvovirus B19-Infected Circulating Angiogenic Cells in Patients With Cardiomyopathy', J INFECT DIS, vol. 212, no. 7, pp. 1070-1081. https://doi.org/10.1093/infdis/jiv178

APA

Schmidt-Lucke, C., Zobel, T., Schrepfer, S., Kuhl, U., Wang, D., Klingel, K., Becher, P. M., Fechner, H., Pozzuto, T., Van Linthout, S., Lassner, D., Spillmann, F., Escher, F., Holinski, S., Volk, H-D., Schultheiss, H-P., & Tschope, C. (2015). Impaired Endothelial Regeneration Through Human Parvovirus B19-Infected Circulating Angiogenic Cells in Patients With Cardiomyopathy. J INFECT DIS, 212(7), 1070-1081. https://doi.org/10.1093/infdis/jiv178

Vancouver

Schmidt-Lucke C, Zobel T, Schrepfer S, Kuhl U, Wang D, Klingel K et al. Impaired Endothelial Regeneration Through Human Parvovirus B19-Infected Circulating Angiogenic Cells in Patients With Cardiomyopathy. J INFECT DIS. 2015 Oct 1;212(7):1070-1081. https://doi.org/10.1093/infdis/jiv178

Bibtex

@article{37e53050ea664cecbf7a109a49212d81,
title = "Impaired Endothelial Regeneration Through Human Parvovirus B19-Infected Circulating Angiogenic Cells in Patients With Cardiomyopathy",
abstract = "Human parvovirus B19 (B19V) is a common pathogen in microvascular disease and cardiomyopathy, owing to infection of endothelial cells. B19V replication, however, is almost restricted to erythroid progenitor cells (ErPCs). Endothelial regeneration attributable to bone marrow-derived circulating angiogenic cells (CACs) is a prerequisite for organ function. Because of many similarities of ErPCs and CACs, we hypothesized that B19V is a perpetrator of impaired endogenous endothelial regeneration. B19V DNA and messenger RNA from endomyocardial biopsy specimens, bone marrow specimens, and circulating progenitor cells were quantified by polymerase chain reaction analysis. The highest B19V DNA concentrations were found in CD34(+)KDR(+) cells from 17 patients with chronic B19V-associated cardiomyopathy. B19V replication intermediates could be detected in nearly half of the patients. Furthermore, chronic B19V infection was associated with impaired endothelial regenerative capacity. B19V infection of CACs in vitro resulted in expression of transcripts encoding B19V proteins. The capsid protein VP1 was identified as a novel inducer of apoptosis, as were nonstructural proteins. Inhibition studies identified so-called death receptor signaling with activation of caspase-8 and caspase-10 to be responsible for apoptosis induction. B19V causally impaired endothelial regeneration with spreading of B19V in CACs in an animal model in vivo. We thus conclude that B19V infection and damage to CACs result in dysfunctional endogenous vascular repair, supporting the emergence of primary bone marrow disease with secondary end-organ damage. ",
keywords = "Adult, Aged, Animals, Apoptosis, Capsid Proteins/genetics, Cardiomyopathies/complications, Case-Control Studies, Caspase 10/genetics, Cell Line, Endothelial Cells/physiology, Erythema Infectiosum/virology, Erythroid Precursor Cells/physiology, Female, Humans, Male, Mice, Middle Aged, Parvovirus B19, Human/genetics, Regeneration, Signal Transduction, Virus Replication",
author = "Caroline Schmidt-Lucke and Thomas Zobel and Sonja Schrepfer and Uwe Kuhl and Dong Wang and Karin Klingel and Becher, {Peter Moritz} and Henry Fechner and Tanja Pozzuto and {Van Linthout}, Sophie and Dirk Lassner and Frank Spillmann and Felicitas Escher and Sebastian Holinski and Hans-Dieter Volk and Heinz-Peter Schultheiss and Carsten Tschope",
note = "{\textcopyright} The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.",
year = "2015",
month = oct,
day = "1",
doi = "10.1093/infdis/jiv178",
language = "English",
volume = "212",
pages = "1070--1081",
journal = "J INFECT DIS",
issn = "0022-1899",
publisher = "Oxford University Press",
number = "7",

}

RIS

TY - JOUR

T1 - Impaired Endothelial Regeneration Through Human Parvovirus B19-Infected Circulating Angiogenic Cells in Patients With Cardiomyopathy

AU - Schmidt-Lucke, Caroline

AU - Zobel, Thomas

AU - Schrepfer, Sonja

AU - Kuhl, Uwe

AU - Wang, Dong

AU - Klingel, Karin

AU - Becher, Peter Moritz

AU - Fechner, Henry

AU - Pozzuto, Tanja

AU - Van Linthout, Sophie

AU - Lassner, Dirk

AU - Spillmann, Frank

AU - Escher, Felicitas

AU - Holinski, Sebastian

AU - Volk, Hans-Dieter

AU - Schultheiss, Heinz-Peter

AU - Tschope, Carsten

N1 - © The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

PY - 2015/10/1

Y1 - 2015/10/1

N2 - Human parvovirus B19 (B19V) is a common pathogen in microvascular disease and cardiomyopathy, owing to infection of endothelial cells. B19V replication, however, is almost restricted to erythroid progenitor cells (ErPCs). Endothelial regeneration attributable to bone marrow-derived circulating angiogenic cells (CACs) is a prerequisite for organ function. Because of many similarities of ErPCs and CACs, we hypothesized that B19V is a perpetrator of impaired endogenous endothelial regeneration. B19V DNA and messenger RNA from endomyocardial biopsy specimens, bone marrow specimens, and circulating progenitor cells were quantified by polymerase chain reaction analysis. The highest B19V DNA concentrations were found in CD34(+)KDR(+) cells from 17 patients with chronic B19V-associated cardiomyopathy. B19V replication intermediates could be detected in nearly half of the patients. Furthermore, chronic B19V infection was associated with impaired endothelial regenerative capacity. B19V infection of CACs in vitro resulted in expression of transcripts encoding B19V proteins. The capsid protein VP1 was identified as a novel inducer of apoptosis, as were nonstructural proteins. Inhibition studies identified so-called death receptor signaling with activation of caspase-8 and caspase-10 to be responsible for apoptosis induction. B19V causally impaired endothelial regeneration with spreading of B19V in CACs in an animal model in vivo. We thus conclude that B19V infection and damage to CACs result in dysfunctional endogenous vascular repair, supporting the emergence of primary bone marrow disease with secondary end-organ damage.

AB - Human parvovirus B19 (B19V) is a common pathogen in microvascular disease and cardiomyopathy, owing to infection of endothelial cells. B19V replication, however, is almost restricted to erythroid progenitor cells (ErPCs). Endothelial regeneration attributable to bone marrow-derived circulating angiogenic cells (CACs) is a prerequisite for organ function. Because of many similarities of ErPCs and CACs, we hypothesized that B19V is a perpetrator of impaired endogenous endothelial regeneration. B19V DNA and messenger RNA from endomyocardial biopsy specimens, bone marrow specimens, and circulating progenitor cells were quantified by polymerase chain reaction analysis. The highest B19V DNA concentrations were found in CD34(+)KDR(+) cells from 17 patients with chronic B19V-associated cardiomyopathy. B19V replication intermediates could be detected in nearly half of the patients. Furthermore, chronic B19V infection was associated with impaired endothelial regenerative capacity. B19V infection of CACs in vitro resulted in expression of transcripts encoding B19V proteins. The capsid protein VP1 was identified as a novel inducer of apoptosis, as were nonstructural proteins. Inhibition studies identified so-called death receptor signaling with activation of caspase-8 and caspase-10 to be responsible for apoptosis induction. B19V causally impaired endothelial regeneration with spreading of B19V in CACs in an animal model in vivo. We thus conclude that B19V infection and damage to CACs result in dysfunctional endogenous vascular repair, supporting the emergence of primary bone marrow disease with secondary end-organ damage.

KW - Adult

KW - Aged

KW - Animals

KW - Apoptosis

KW - Capsid Proteins/genetics

KW - Cardiomyopathies/complications

KW - Case-Control Studies

KW - Caspase 10/genetics

KW - Cell Line

KW - Endothelial Cells/physiology

KW - Erythema Infectiosum/virology

KW - Erythroid Precursor Cells/physiology

KW - Female

KW - Humans

KW - Male

KW - Mice

KW - Middle Aged

KW - Parvovirus B19, Human/genetics

KW - Regeneration

KW - Signal Transduction

KW - Virus Replication

U2 - 10.1093/infdis/jiv178

DO - 10.1093/infdis/jiv178

M3 - SCORING: Journal article

C2 - 25805750

VL - 212

SP - 1070

EP - 1081

JO - J INFECT DIS

JF - J INFECT DIS

SN - 0022-1899

IS - 7

ER -