Prevalence of erythrovirus genotypes in the myocardium of patients with dilated cardiomyopathy

Parvovirus B19 (PVB19) is a member of the human erythrovirus family detected frequently in endomyocardial biopsies from patients with dilated cardiomyopathy. Human erythroviruses cluster into three genotypes 1-3 which share a high degree of homology between major structural proteins and may cause in...

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Published inJournal of medical virology Vol. 80; no. 7; pp. 1243 - 1251
Main Authors Kühl, U, Lassner, D, Pauschinger, M, Gross, U.M, Seeberg, B, Noutsias, M, Poller, W, Schultheiss, H.-P
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.07.2008
Wiley-Liss
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ISSN0146-6615
1096-9071
DOI10.1002/jmv.21187

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Abstract Parvovirus B19 (PVB19) is a member of the human erythrovirus family detected frequently in endomyocardial biopsies from patients with dilated cardiomyopathy. Human erythroviruses cluster into three genotypes 1-3 which share a high degree of homology between major structural proteins and may cause indistinguishable infections clinically and serologically. In human cardiac tissue erythrovirus genotypes other than PVB19 have not yet been reported. Three hundred seventeen consecutive patients with symptomatic dilated cardiomyopathy (median left ventricular ejection fraction: 28.6%, range 5-45%) who underwent endomyocardial biopsy for the elucidation of the etiology, were analyzed using a new consensus PCR assay designed for the detection of the three erythrovirus genotype sequences. Endomyocardial biopsies of 151 (47.6%) patients were erythrovirus-positive. Genotype 1 specific sequences were detected in 43/151 (28.5%) of positive biopsy samples, whereas genotype 2-specific sequences so far considered rare in human disease and not yet been described in human heart tissue was identified in 108/151 (71.5%) of virus-positive endomyocardial biopsies with a preference in patients above 50 years of age. In spite of younger age, systolic left ventricular dysfunction of genotype 1-positive patients was significantly reduced as compared to genotype 2-positive patients (24.4 ± 10.4% vs. 31.0 ± 9.5%, P = 0.0001) at the initial presentation. The data show that two genetically distinct erythrovirus variants with a different age distribution are detectable in endomyocardial biopsies of patients with dilated cardiomyopathy. The erythrovirus genotype 2, not described previously in human heart tissue, is highly prevalent in the heart but the less prevalent genotype 1 is associated with more severe disturbed cardiac function. J. Med. Virol. 80: 1243-1251, 2008.
AbstractList Parvovirus B19 (PVB19) is a member of the human erythrovirus family detected frequently in endomyocardial biopsies from patients with dilated cardiomyopathy. Human erythroviruses cluster into three genotypes 1-3 which share a high degree of homology between major structural proteins and may cause indistinguishable infections clinically and serologically. In human cardiac tissue erythrovirus genotypes other than PVB19 have not yet been reported. Three hundred seventeen consecutive patients with symptomatic dilated cardiomyopathy (median left ventricular ejection fraction: 28.6%, range 5-45%) who underwent endomyocardial biopsy for the elucidation of the etiology, were analyzed using a new consensus PCR assay designed for the detection of the three erythrovirus genotype sequences. Endomyocardial biopsies of 151 (47.6%) patients were erythrovirus-positive. Genotype 1 specific sequences were detected in 43/151 (28.5%) of positive biopsy samples, whereas genotype 2-specific sequences so far considered rare in human disease and not yet been described in human heart tissue was identified in 108/151 (71.5%) of virus-positive endomyocardial biopsies with a preference in patients above 50 years of age. In spite of younger age, systolic left ventricular dysfunction of genotype 1-positive patients was significantly reduced as compared to genotype 2-positive patients (24.4 ± 10.4% vs. 31.0 ± 9.5%, P = 0.0001) at the initial presentation. The data show that two genetically distinct erythrovirus variants with a different age distribution are detectable in endomyocardial biopsies of patients with dilated cardiomyopathy. The erythrovirus genotype 2, not described previously in human heart tissue, is highly prevalent in the heart but the less prevalent genotype 1 is associated with more severe disturbed cardiac function. J. Med. Virol. 80: 1243-1251, 2008.
Parvovirus B19 (PVB19) is a member of the human erythrovirus family detected frequently in endomyocardial biopsies from patients with dilated cardiomyopathy. Human erythroviruses cluster into three genotypes 1-3 which share a high degree of homology between major structural proteins and may cause indistinguishable infections clinically and serologically. In human cardiac tissue erythrovirus genotypes other than PVB19 have not yet been reported. Three hundred seventeen consecutive patients with symptomatic dilated cardiomyopathy (median left ventricular ejection fraction: 28.6%, range 5-45%) who underwent endomyocardial biopsy for the elucidation of the etiology, were analyzed using a new consensus PCR assay designed for the detection of the three erythrovirus genotype sequences. Endomyocardial biopsies of 151 (47.6%) patients were erythrovirus-positive. Genotype 1 specific sequences were detected in 43/151 (28.5%) of positive biopsy samples, whereas genotype 2-specific sequences so far considered rare in human disease and not yet been described in human heart tissue was identified in 108/151 (71.5%) of virus-positive endomyocardial biopsies with a preference in patients above 50 years of age. In spite of younger age, systolic left ventricular dysfunction of genotype 1-positive patients was significantly reduced as compared to genotype 2-positive patients (24.4±10.4% vs. 31.0±9.5%, P=0.0001) at the initial presentation. The data show that two genetically distinct erythrovirus variants with a different age distribution are detectable in endomyocardial biopsies of patients with dilated cardiomyopathy. The erythrovirus genotype 2, not described previously in human heart tissue, is highly prevalent in the heart but the less prevalent genotype 1 is associated with more severe disturbed cardiac function. J. Med. Virol. 80: 1243-1251, 2008.
Parvovirus B19 (PVB19) is a member of the human erythrovirus family detected frequently in endomyocardial biopsies from patients with dilated cardiomyopathy. Human erythroviruses cluster into three genotypes 1–3 which share a high degree of homology between major structural proteins and may cause indistinguishable infections clinically and serologically. In human cardiac tissue erythrovirus genotypes other than PVB19 have not yet been reported. Three hundred seventeen consecutive patients with symptomatic dilated cardiomyopathy (median left ventricular ejection fraction: 28.6%, range 5–45%) who underwent endomyocardial biopsy for the elucidation of the etiology, were analyzed using a new consensus PCR assay designed for the detection of the three erythrovirus genotype sequences. Endomyocardial biopsies of 151 (47.6%) patients were erythrovirus‐positive. Genotype 1 specific sequences were detected in 43/151 (28.5%) of positive biopsy samples, whereas genotype 2‐specific sequences so far considered rare in human disease and not yet been described in human heart tissue was identified in 108/151 (71.5%) of virus‐positive endomyocardial biopsies with a preference in patients above 50 years of age. In spite of younger age, systolic left ventricular dysfunction of genotype 1‐positive patients was significantly reduced as compared to genotype 2‐positive patients (24.4 ± 10.4% vs. 31.0 ± 9.5%, P  = 0.0001) at the initial presentation. The data show that two genetically distinct erythrovirus variants with a different age distribution are detectable in endomyocardial biopsies of patients with dilated cardiomyopathy. The erythrovirus genotype 2, not described previously in human heart tissue, is highly prevalent in the heart but the less prevalent genotype 1 is associated with more severe disturbed cardiac function. J. Med. Virol. 80: 1243–1251, 2008. © 2008 Wiley‐Liss, Inc.
Parvovirus B19 (PVB19) is a member of the human erythrovirus family detected frequently in endomyocardial biopsies from patients with dilated cardiomyopathy. Human erythroviruses cluster into three genotypes 1-3 which share a high degree of homology between major structural proteins and may cause indistinguishable infections clinically and serologically. In human cardiac tissue erythrovirus genotypes other than PVB19 have not yet been reported. Three hundred seventeen consecutive patients with symptomatic dilated cardiomyopathy (median left ventricular ejection fraction: 28.6%, range 5-45%) who underwent endomyocardial biopsy for the elucidation of the etiology, were analyzed using a new consensus PCR assay designed for the detection of the three erythrovirus genotype sequences. Endomyocardial biopsies of 151 (47.6%) patients were erythrovirus-positive. Genotype 1 specific sequences were detected in 43/151 (28.5%) of positive biopsy samples, whereas genotype 2-specific sequences so far considered rare in human disease and not yet been described in human heart tissue was identified in 108/151 (71.5%) of virus-positive endomyocardial biopsies with a preference in patients above 50 years of age. In spite of younger age, systolic left ventricular dysfunction of genotype 1-positive patients was significantly reduced as compared to genotype 2-positive patients (24.4+/-10.4% vs. 31.0+/-9.5%, P=0.0001) at the initial presentation. The data show that two genetically distinct erythrovirus variants with a different age distribution are detectable in endomyocardial biopsies of patients with dilated cardiomyopathy. The erythrovirus genotype 2, not described previously in human heart tissue, is highly prevalent in the heart but the less prevalent genotype 1 is associated with more severe disturbed cardiac function.Parvovirus B19 (PVB19) is a member of the human erythrovirus family detected frequently in endomyocardial biopsies from patients with dilated cardiomyopathy. Human erythroviruses cluster into three genotypes 1-3 which share a high degree of homology between major structural proteins and may cause indistinguishable infections clinically and serologically. In human cardiac tissue erythrovirus genotypes other than PVB19 have not yet been reported. Three hundred seventeen consecutive patients with symptomatic dilated cardiomyopathy (median left ventricular ejection fraction: 28.6%, range 5-45%) who underwent endomyocardial biopsy for the elucidation of the etiology, were analyzed using a new consensus PCR assay designed for the detection of the three erythrovirus genotype sequences. Endomyocardial biopsies of 151 (47.6%) patients were erythrovirus-positive. Genotype 1 specific sequences were detected in 43/151 (28.5%) of positive biopsy samples, whereas genotype 2-specific sequences so far considered rare in human disease and not yet been described in human heart tissue was identified in 108/151 (71.5%) of virus-positive endomyocardial biopsies with a preference in patients above 50 years of age. In spite of younger age, systolic left ventricular dysfunction of genotype 1-positive patients was significantly reduced as compared to genotype 2-positive patients (24.4+/-10.4% vs. 31.0+/-9.5%, P=0.0001) at the initial presentation. The data show that two genetically distinct erythrovirus variants with a different age distribution are detectable in endomyocardial biopsies of patients with dilated cardiomyopathy. The erythrovirus genotype 2, not described previously in human heart tissue, is highly prevalent in the heart but the less prevalent genotype 1 is associated with more severe disturbed cardiac function.
Parvovirus B19 (PVB19) is a member of the human erythrovirus family detected frequently in endomyocardial biopsies from patients with dilated cardiomyopathy. Human erythroviruses cluster into three genotypes 1–3 which share a high degree of homology between major structural proteins and may cause indistinguishable infections clinically and serologically. In human cardiac tissue erythrovirus genotypes other than PVB19 have not yet been reported. Three hundred seventeen consecutive patients with symptomatic dilated cardiomyopathy (median left ventricular ejection fraction: 28.6%, range 5–45%) who underwent endomyocardial biopsy for the elucidation of the etiology, were analyzed using a new consensus PCR assay designed for the detection of the three erythrovirus genotype sequences. Endomyocardial biopsies of 151 (47.6%) patients were erythrovirus‐positive. Genotype 1 specific sequences were detected in 43/151 (28.5%) of positive biopsy samples, whereas genotype 2‐specific sequences so far considered rare in human disease and not yet been described in human heart tissue was identified in 108/151 (71.5%) of virus‐positive endomyocardial biopsies with a preference in patients above 50 years of age. In spite of younger age, systolic left ventricular dysfunction of genotype 1‐positive patients was significantly reduced as compared to genotype 2‐positive patients (24.4 ± 10.4% vs. 31.0 ± 9.5%, P = 0.0001) at the initial presentation. The data show that two genetically distinct erythrovirus variants with a different age distribution are detectable in endomyocardial biopsies of patients with dilated cardiomyopathy. The erythrovirus genotype 2, not described previously in human heart tissue, is highly prevalent in the heart but the less prevalent genotype 1 is associated with more severe disturbed cardiac function. J. Med. Virol. 80: 1243–1251, 2008. © 2008 Wiley‐Liss, Inc.
Parvovirus B19 (PVB19) is a member of the human erythrovirus family detected frequently in endomyocardial biopsies from patients with dilated cardiomyopathy. Human erythroviruses cluster into three genotypes 1-3 which share a high degree of homology between major structural proteins and may cause indistinguishable infections clinically and serologically. In human cardiac tissue erythrovirus genotypes other than PVB19 have not yet been reported. Three hundred seventeen consecutive patients with symptomatic dilated cardiomyopathy (median left ventricular ejection fraction: 28.6%, range 5-45%) who underwent endomyocardial biopsy for the elucidation of the etiology, were analyzed using a new consensus PCR assay designed for the detection of the three erythrovirus genotype sequences. Endomyocardial biopsies of 151 (47.6%) patients were erythrovirus-positive. Genotype 1 specific sequences were detected in 43/151 (28.5%) of positive biopsy samples, whereas genotype 2-specific sequences so far considered rare in human disease and not yet been described in human heart tissue was identified in 108/151 (71.5%) of virus-positive endomyocardial biopsies with a preference in patients above 50 years of age. In spite of younger age, systolic left ventricular dysfunction of genotype 1-positive patients was significantly reduced as compared to genotype 2-positive patients (24.4+/-10.4% vs. 31.0+/-9.5%, P=0.0001) at the initial presentation. The data show that two genetically distinct erythrovirus variants with a different age distribution are detectable in endomyocardial biopsies of patients with dilated cardiomyopathy. The erythrovirus genotype 2, not described previously in human heart tissue, is highly prevalent in the heart but the less prevalent genotype 1 is associated with more severe disturbed cardiac function.
Author Lassner, D
Poller, W
Schultheiss, H.-P
Pauschinger, M
Seeberg, B
Noutsias, M
Gross, U.M
Kühl, U
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IsScholarly true
Issue 7
Keywords Human
Heart failure
Prevalence
genotypes
Cardiovascular disease
Genotype
Erythrovirus
Myocardial disease
Virus
Dilated cardiomyopathy
Parvoviridae
Heart disease
Molecular epidemiology
Myocardium
Parvovirinae
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
CC BY 4.0
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Notes http://dx.doi.org/10.1002/jmv.21187
German Research Foundation (DFG)
Transregional Collaborative Research Centre "Inflammatory Cardiomyopathy-Molecular Pathogenesis and Therapy" - No. SFB TR 19
ark:/67375/WNG-79NVRKT5-F
U. Kühl and D. Lassner contributed equally to this study.
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PublicationDate July 2008
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PublicationTitle Journal of medical virology
PublicationTitleAlternate J. Med. Virol
PublicationYear 2008
Publisher Wiley Subscription Services, Inc., A Wiley Company
Wiley-Liss
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References Blumel J, Eis-Hubinger AM, Stuhler A, Bonsch C, Gessner M, Lower J. 2005. Characterization of parvovirus B19 genotype 2 in KU812Ep6 cells. J Virol 79: 14197-14206.
Zhi N, Zadori Z, Brown KE, Tijssen P. 2004. Construction and sequencing of an infectious clone of the human parvovirus B19. Virology 318: 142-152.
Bowles NE, Ni J, Kearney DL, Pauschinger M, Schultheiss HP, McCarthy R, Hare J, Bricker JT, Bowles KR, Towbin JA. 2003. Detection of viruses in myocardial tissues by polymerase chain reaction evidence of adenovirus as a common cause of myocarditis in children and adults. J Am Coll Cardiol 42: 466-472.
Ozawa K, Young NS. 1987. Characterization of capsid and noncapsid proteins of B19 parvovirus propagated in human erythroid bone marrow cell cultures. J Virol 61: 2627-2630.
Frustaci A, Chimenti C, Calabrese F, Pieroni M, Thiene G, Maseri A. 2003. Immunosuppressive therapy for active lymphocytic myocarditis: Virological and immunologic profile of responders versus nonresponders. Circulation 107: 857-863.
Liefeldt L, Plentz A, Klempa B, Kershaw O, Endres AS, Raab U, Neumayer HH, Meisel H, Modrow S. 2005. Recurrent high level parvovirus B19/genotype 2 viremia in a renal transplant recipient analyzed by real-time PCR for simultaneous detection of genotypes 1 to 3. J Med Virol 75: 161-169.
von Landenberg P, Lehmann HW, Knoll A, Dorsch S, Modrow S. 2003. Antiphospholipid antibodies in pediatric and adult patients with rheumatic disease are associated with parvovirus B19 infection. Arthritis Rheum 48: 1939-1947.
Gallinella G, Venturoli S, Manaresi E, Musiani M, Zerbini M. 2003. B19 virus genome diversity: Epidemiological and clinical correlations. J Clin Virol 28: 1-13.
Kawase M, Momoeda M, Young NS, Kajigaya S. 1995. Most of the VP1 unique region of B19 parvovirus is on the capsid surface. Virology 211: 359-366.
Hokynar K, Soderlund-Venermo M, Pesonen M, Ranki A, Kiviluoto O, Partio EK, Hedman K. 2002. A new parvovirus genotype persistent in human skin. Virology 302: 224-228.
Servant A, Laperche S, Lallemand F, Marinho V, De Saint Maur G, Meritet JF, Garbarg-Chenon A. 2002. Genetic diversity within human erythroviruses: Identification of three genotypes. J Virol 76: 9124-9134.
Tschope C, Bock CT, Kasner M, Noutsias M, Westermann D, Schwimmbeck PL, Pauschinger M, Poller WC, Kuhl U, Kandolf R, Schultheiss HP. 2005. High prevalence of cardiac parvovirus B19 infection in patients with isolated left ventricular diastolic dysfunction. Circulation 111: 879-886.
Cotmore SF, McKie VC, Anderson LJ, Astell CR, Tattersall P. 1986. Identification of the major structural and nonstructural proteins encoded by human parvovirus B19 and mapping of their genes by procaryotic expression of isolated genomic fragments. J Virol 60: 548-557.
Heegaard ED, Brown KE. 2002. Human parvovirus B19. Clin Microbiol Rev 15: 485-505.
Schalasta G, Schmid M, Lachmund T, Enders G. 2004. LightCycler consensus PCR for rapid and differential detection of human erythrovirus B19 and V9 isolates. J Med Virol 73: 54-59.
Kühl U, Pauschinger M, Noutsias M, Seeberg B, Bock T, Lassner D, Poller W, Kandolf R, Schultheiss HP. 2005a. High prevalence of viral genomes and multiple viral infections in the myocardium of adults with "idiopathic" left ventricular dysfunction. Circulation 111: 887-893.
Umene K, Nunoue T. 1993. Partial nucleotide sequencing and characterization of human parvovirus B19 genome DNAs from damaged human fetuses and from patients with leukemia. J Med Virol 39: 333-339.
Heegaard ED, Qvortrup K, Christensen J. 2002. Baculovirus expression of erythrovirus V9 capsids and screening by ELISA: Serologic cross-reactivity with erythrovirus B19. J Med Virol 66: 246-252.
Vallbracht KB, Schwimmbeck PL, Kuhl U, Rauch U, Seeberg B, Schultheiss HP. 2005. Differential aspects of endothelial function of the coronary microcirculation considering myocardial virus persistence, endothelial activation, and myocardial leukocyte infiltrates. Circulation 111: 1784-1791.
Zadori Z, Szelei J, Lacoste MC. 2001. A viral phospholipase A2 is required for parvovirus infectivity. Dev Cell 1: 291-302.
Ekman A, Hokynar K, Kakkola L, Kantola K, Hedman L, Bondén H, Gessner M, Aberham C, Norja P, Miettinen S, Hedman K, Söderlund-Venermo M. 2007. Biological and immunological relations among human parvovirus B19 genotypes 1 to 3. J Virol 81: 6927-6935.
Baboonian C, Treasure T. 1997. Meta-analysis of the association of enteroviruses with human heart disease. Heart 78: 539-543.
Dorsch S, Liebsch G, Kaufmann B, von Landenberg P, Hoffmann JH, Drobnik W, Modrow S. 2002. The VP1 unique region of parvovirus B19 and its constituent phospholipase A2-like activity. J Virol 76: 2014-2018.
Lamparter S, Schoppet M, Pankuweit S, Maisch B. 2003. Acute parvovirus B19 infection associated with myocarditis in an immunocompetent adult. Hum Pathol 34: 725-728.
Kühl U, Pauschinger M, Schwimmbeck PL, Seeberg B, Lober C, Noutsias M, Poller W, Schultheiss HP. 2003b. Interferon-beta treatment eliminates cardiotropic viruses and improves left ventricular function in patients with myocardial persistence of viral genomes and left ventricular dysfunction. Circulation 107: 2793-2798.
Bueltmann BD, Klingel K, Soltar K, Bock CT, Baba HA, Sauter M, Kandolf R. 2002. Fatal Parvovirus B19-associated myocarditis clinically mimicking ischemic heart disease: An endothelial cell-mediated disease. Hum Pathol 34: 92-95.
Kühl U, Pauschinger M, Bock T, Klingel K, Schwimmbeck CP, Seeberg B, Krautwurm L, Poller W, Schultheiss HP, Kandolf R. 2003a. Parvovirus B19 infection mimicking acute myocardial infarction. Circulation 108: 945-950.
Noutsias M, Seeberg B, Schultheiss HP, Kuhl U. 1999. Expression of cell adhesion molecules in dilated cardiomyopathy: Evidence for endothelial activation in inflammatory cardiomyopathy. Circulation 99: 2124-2131.
Weigel-Kelley KA, Yoder MC, Srivastava A. 2003. Alpha5beta1 integrin as a cellular coreceptor for human parvovirus B19: Requirement of functional activation of beta1 integrin for viral entry. Blood 102: 3927-3933.
Nguyen QT, Sifer C, Schneider V, Allaume X, Servant A, Bernaudin F, Auguste V, Garbarg-Chenon A. 1999. Novel human erythrovirus associated with transient aplastic anemia. J Clin Microbiol 37: 2483-2487.
Norja P, Hokynar K, Aaltonen LM, Chen R, Ranki A, Partio EK, Kiviluoto O, Davidkin I, Leivo T, Eis-Hubinger AM, Schneider B, Fischer HP, Tolba R, Vapalahti O, Vaheri A, Soderlund-Venermo M, Hedman K. 2006. Bioportfolio: Lifelong persistence of variant and prototypic erythrovirus DNA genomes in human tissue. Proc Natl Acad Sci USA 103: 7450-7453.
Donoso Mantke O, Nitsche A, Meyer R, Klingel K, Niedrig M, 2004. Analysing myocardial tissue from explanted hearts of heart transplant recipients and multi-organ donors for the presence of parvovirus B19 DNA. J Clin Virol 31: 32-39.
Kaufmann B, Simpson AA, Rossmann MG. 2004. The structure of human parvovirus B19. Proc Natl Acad Sci 101: 11628-11633.
Pauschinger M, Bowles NE, Fuentes-Garcia FJ, Pham V, Kuhl U, Schwimmbeck PL, Schultheiss HP, Towbin JA. 1999. Detection of adenoviral genome in the myocardium of adult patients with idiopathic left ventricular dysfunction. Circulation 99: 1348-1354.
Klingel K, Sauter M, Bock CT, Szalay G, Schnorr JJ, Kandolf R. 2004. Molecular pathology of inflammatory cardiomyopathy. Med Microbiol Immunol (Berl) 193: 101-107.
Kühl U, Pauschinger M, Seeberg B, Lassner D, Noutsias M, Poller W, Schultheiss HP. 2005b. Viral persistence in the myocardium is associated with progressive cardiac dysfunction. Circulation 112: 1965-1970.
Shade RO, Blundell MC, Cotmore SF, Tattersall PC, Astell CR. 1986. Nucleotide sequence and genome organization of human parvovirus B19 isolated from the serum of a child during aplastic crisis. J Virol 58: 921-936.
Cassinotti P, Burtonboy G, Fopp M, Siegl G. 1997. Evidence for persistence of human parvovirus B19 DNA in bone marrow. J Med Virol 53: 229-232.
2004; 101
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1986; 60
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2004; 73
1993; 39
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1997; 78
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2004; 193
2002; 302
2005; 75
1999; 99
2003; 48
2007; 81
2003; 28
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2003; 102
2003; 42
2005; 79
2003b; 107
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References_xml – reference: Bowles NE, Ni J, Kearney DL, Pauschinger M, Schultheiss HP, McCarthy R, Hare J, Bricker JT, Bowles KR, Towbin JA. 2003. Detection of viruses in myocardial tissues by polymerase chain reaction evidence of adenovirus as a common cause of myocarditis in children and adults. J Am Coll Cardiol 42: 466-472.
– reference: Blumel J, Eis-Hubinger AM, Stuhler A, Bonsch C, Gessner M, Lower J. 2005. Characterization of parvovirus B19 genotype 2 in KU812Ep6 cells. J Virol 79: 14197-14206.
– reference: Kawase M, Momoeda M, Young NS, Kajigaya S. 1995. Most of the VP1 unique region of B19 parvovirus is on the capsid surface. Virology 211: 359-366.
– reference: Weigel-Kelley KA, Yoder MC, Srivastava A. 2003. Alpha5beta1 integrin as a cellular coreceptor for human parvovirus B19: Requirement of functional activation of beta1 integrin for viral entry. Blood 102: 3927-3933.
– reference: Cassinotti P, Burtonboy G, Fopp M, Siegl G. 1997. Evidence for persistence of human parvovirus B19 DNA in bone marrow. J Med Virol 53: 229-232.
– reference: Lamparter S, Schoppet M, Pankuweit S, Maisch B. 2003. Acute parvovirus B19 infection associated with myocarditis in an immunocompetent adult. Hum Pathol 34: 725-728.
– reference: Zhi N, Zadori Z, Brown KE, Tijssen P. 2004. Construction and sequencing of an infectious clone of the human parvovirus B19. Virology 318: 142-152.
– reference: Noutsias M, Seeberg B, Schultheiss HP, Kuhl U. 1999. Expression of cell adhesion molecules in dilated cardiomyopathy: Evidence for endothelial activation in inflammatory cardiomyopathy. Circulation 99: 2124-2131.
– reference: Tschope C, Bock CT, Kasner M, Noutsias M, Westermann D, Schwimmbeck PL, Pauschinger M, Poller WC, Kuhl U, Kandolf R, Schultheiss HP. 2005. High prevalence of cardiac parvovirus B19 infection in patients with isolated left ventricular diastolic dysfunction. Circulation 111: 879-886.
– reference: Klingel K, Sauter M, Bock CT, Szalay G, Schnorr JJ, Kandolf R. 2004. Molecular pathology of inflammatory cardiomyopathy. Med Microbiol Immunol (Berl) 193: 101-107.
– reference: Hokynar K, Soderlund-Venermo M, Pesonen M, Ranki A, Kiviluoto O, Partio EK, Hedman K. 2002. A new parvovirus genotype persistent in human skin. Virology 302: 224-228.
– reference: Kaufmann B, Simpson AA, Rossmann MG. 2004. The structure of human parvovirus B19. Proc Natl Acad Sci 101: 11628-11633.
– reference: Dorsch S, Liebsch G, Kaufmann B, von Landenberg P, Hoffmann JH, Drobnik W, Modrow S. 2002. The VP1 unique region of parvovirus B19 and its constituent phospholipase A2-like activity. J Virol 76: 2014-2018.
– reference: Donoso Mantke O, Nitsche A, Meyer R, Klingel K, Niedrig M, 2004. Analysing myocardial tissue from explanted hearts of heart transplant recipients and multi-organ donors for the presence of parvovirus B19 DNA. J Clin Virol 31: 32-39.
– reference: Bueltmann BD, Klingel K, Soltar K, Bock CT, Baba HA, Sauter M, Kandolf R. 2002. Fatal Parvovirus B19-associated myocarditis clinically mimicking ischemic heart disease: An endothelial cell-mediated disease. Hum Pathol 34: 92-95.
– reference: Ozawa K, Young NS. 1987. Characterization of capsid and noncapsid proteins of B19 parvovirus propagated in human erythroid bone marrow cell cultures. J Virol 61: 2627-2630.
– reference: Baboonian C, Treasure T. 1997. Meta-analysis of the association of enteroviruses with human heart disease. Heart 78: 539-543.
– reference: Kühl U, Pauschinger M, Schwimmbeck PL, Seeberg B, Lober C, Noutsias M, Poller W, Schultheiss HP. 2003b. Interferon-beta treatment eliminates cardiotropic viruses and improves left ventricular function in patients with myocardial persistence of viral genomes and left ventricular dysfunction. Circulation 107: 2793-2798.
– reference: Kühl U, Pauschinger M, Seeberg B, Lassner D, Noutsias M, Poller W, Schultheiss HP. 2005b. Viral persistence in the myocardium is associated with progressive cardiac dysfunction. Circulation 112: 1965-1970.
– reference: Heegaard ED, Brown KE. 2002. Human parvovirus B19. Clin Microbiol Rev 15: 485-505.
– reference: Schalasta G, Schmid M, Lachmund T, Enders G. 2004. LightCycler consensus PCR for rapid and differential detection of human erythrovirus B19 and V9 isolates. J Med Virol 73: 54-59.
– reference: Shade RO, Blundell MC, Cotmore SF, Tattersall PC, Astell CR. 1986. Nucleotide sequence and genome organization of human parvovirus B19 isolated from the serum of a child during aplastic crisis. J Virol 58: 921-936.
– reference: von Landenberg P, Lehmann HW, Knoll A, Dorsch S, Modrow S. 2003. Antiphospholipid antibodies in pediatric and adult patients with rheumatic disease are associated with parvovirus B19 infection. Arthritis Rheum 48: 1939-1947.
– reference: Gallinella G, Venturoli S, Manaresi E, Musiani M, Zerbini M. 2003. B19 virus genome diversity: Epidemiological and clinical correlations. J Clin Virol 28: 1-13.
– reference: Pauschinger M, Bowles NE, Fuentes-Garcia FJ, Pham V, Kuhl U, Schwimmbeck PL, Schultheiss HP, Towbin JA. 1999. Detection of adenoviral genome in the myocardium of adult patients with idiopathic left ventricular dysfunction. Circulation 99: 1348-1354.
– reference: Kühl U, Pauschinger M, Noutsias M, Seeberg B, Bock T, Lassner D, Poller W, Kandolf R, Schultheiss HP. 2005a. High prevalence of viral genomes and multiple viral infections in the myocardium of adults with "idiopathic" left ventricular dysfunction. Circulation 111: 887-893.
– reference: Kühl U, Pauschinger M, Bock T, Klingel K, Schwimmbeck CP, Seeberg B, Krautwurm L, Poller W, Schultheiss HP, Kandolf R. 2003a. Parvovirus B19 infection mimicking acute myocardial infarction. Circulation 108: 945-950.
– reference: Zadori Z, Szelei J, Lacoste MC. 2001. A viral phospholipase A2 is required for parvovirus infectivity. Dev Cell 1: 291-302.
– reference: Servant A, Laperche S, Lallemand F, Marinho V, De Saint Maur G, Meritet JF, Garbarg-Chenon A. 2002. Genetic diversity within human erythroviruses: Identification of three genotypes. J Virol 76: 9124-9134.
– reference: Ekman A, Hokynar K, Kakkola L, Kantola K, Hedman L, Bondén H, Gessner M, Aberham C, Norja P, Miettinen S, Hedman K, Söderlund-Venermo M. 2007. Biological and immunological relations among human parvovirus B19 genotypes 1 to 3. J Virol 81: 6927-6935.
– reference: Heegaard ED, Qvortrup K, Christensen J. 2002. Baculovirus expression of erythrovirus V9 capsids and screening by ELISA: Serologic cross-reactivity with erythrovirus B19. J Med Virol 66: 246-252.
– reference: Umene K, Nunoue T. 1993. Partial nucleotide sequencing and characterization of human parvovirus B19 genome DNAs from damaged human fetuses and from patients with leukemia. J Med Virol 39: 333-339.
– reference: Norja P, Hokynar K, Aaltonen LM, Chen R, Ranki A, Partio EK, Kiviluoto O, Davidkin I, Leivo T, Eis-Hubinger AM, Schneider B, Fischer HP, Tolba R, Vapalahti O, Vaheri A, Soderlund-Venermo M, Hedman K. 2006. Bioportfolio: Lifelong persistence of variant and prototypic erythrovirus DNA genomes in human tissue. Proc Natl Acad Sci USA 103: 7450-7453.
– reference: Liefeldt L, Plentz A, Klempa B, Kershaw O, Endres AS, Raab U, Neumayer HH, Meisel H, Modrow S. 2005. Recurrent high level parvovirus B19/genotype 2 viremia in a renal transplant recipient analyzed by real-time PCR for simultaneous detection of genotypes 1 to 3. J Med Virol 75: 161-169.
– reference: Nguyen QT, Sifer C, Schneider V, Allaume X, Servant A, Bernaudin F, Auguste V, Garbarg-Chenon A. 1999. Novel human erythrovirus associated with transient aplastic anemia. J Clin Microbiol 37: 2483-2487.
– reference: Cotmore SF, McKie VC, Anderson LJ, Astell CR, Tattersall P. 1986. Identification of the major structural and nonstructural proteins encoded by human parvovirus B19 and mapping of their genes by procaryotic expression of isolated genomic fragments. J Virol 60: 548-557.
– reference: Vallbracht KB, Schwimmbeck PL, Kuhl U, Rauch U, Seeberg B, Schultheiss HP. 2005. Differential aspects of endothelial function of the coronary microcirculation considering myocardial virus persistence, endothelial activation, and myocardial leukocyte infiltrates. Circulation 111: 1784-1791.
– reference: Frustaci A, Chimenti C, Calabrese F, Pieroni M, Thiene G, Maseri A. 2003. Immunosuppressive therapy for active lymphocytic myocarditis: Virological and immunologic profile of responders versus nonresponders. Circulation 107: 857-863.
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– volume: 31
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  article-title: Analysing myocardial tissue from explanted hearts of heart transplant recipients and multi‐organ donors for the presence of parvovirus B19 DNA
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  article-title: High prevalence of viral genomes and multiple viral infections in the myocardium of adults with “idiopathic” left ventricular dysfunction
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  article-title: A new parvovirus genotype persistent in human skin
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Snippet Parvovirus B19 (PVB19) is a member of the human erythrovirus family detected frequently in endomyocardial biopsies from patients with dilated cardiomyopathy....
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StartPage 1243
SubjectTerms Adult
Aged
Amino Acid Sequence
Base Sequence
Biological and medical sciences
Capsid Proteins - chemistry
Cardiomyopathy, Dilated - virology
dilated cardiomyopathy
Epidemiology
Erythrovirus
Erythrovirus - genetics
Erythrovirus - isolation & purification
Female
Fundamental and applied biological sciences. Psychology
Genotype
genotypes
Heart - virology
heart failure
Human viral diseases
Humans
Infectious diseases
Male
Medical sciences
Microbiology
Middle Aged
Miscellaneous
Molecular Sequence Data
Parvoviridae Infections - virology
Parvovirus B19
Prevalence
Sequence Alignment
Viral diseases
Viral Load
Virology
Title Prevalence of erythrovirus genotypes in the myocardium of patients with dilated cardiomyopathy
URI https://api.istex.fr/ark:/67375/WNG-79NVRKT5-F/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjmv.21187
https://www.ncbi.nlm.nih.gov/pubmed/18461615
https://www.proquest.com/docview/20301415
https://www.proquest.com/docview/47655463
https://www.proquest.com/docview/69202995
Volume 80
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