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 in | Journal of medical virology Vol. 80; no. 7; pp. 1243 - 1251 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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Hoboken
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01.07.2008
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ISSN | 0146-6615 1096-9071 |
DOI | 10.1002/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. |
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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 |
Author_xml | – sequence: 1 fullname: Kühl, U – sequence: 2 fullname: Lassner, D – sequence: 3 fullname: Pauschinger, M – sequence: 4 fullname: Gross, U.M – sequence: 5 fullname: Seeberg, B – sequence: 6 fullname: Noutsias, M – sequence: 7 fullname: Poller, W – sequence: 8 fullname: Schultheiss, H.-P |
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Keywords | Human Heart failure Prevalence genotypes Cardiovascular disease Genotype Erythrovirus Myocardial disease Virus Dilated cardiomyopathy Parvoviridae Heart disease Molecular epidemiology Myocardium Parvovirinae |
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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 2002; 15 2003a; 108 2005; 111 2005a; 111 2002; 34 2002; 76 1986; 58 1995; 211 2005b; 112 2003; 34 2004; 31 1986; 60 2003; 107 2004; 73 1993; 39 1987; 61 1997; 53 1999; 37 1997; 78 2002; 66 2004; 193 2002; 302 2005; 75 1999; 99 2003; 48 2007; 81 2003; 28 2001; 1 2004; 318 2003; 102 2003; 42 2005; 79 2003b; 107 2006; 103 e_1_2_1_20_1 e_1_2_1_23_1 e_1_2_1_24_1 e_1_2_1_21_1 e_1_2_1_22_1 e_1_2_1_27_1 e_1_2_1_28_1 e_1_2_1_25_1 e_1_2_1_26_1 e_1_2_1_29_1 e_1_2_1_7_1 e_1_2_1_31_1 e_1_2_1_8_1 e_1_2_1_30_1 e_1_2_1_5_1 e_1_2_1_6_1 e_1_2_1_3_1 e_1_2_1_12_1 e_1_2_1_35_1 e_1_2_1_4_1 e_1_2_1_13_1 e_1_2_1_34_1 e_1_2_1_10_1 e_1_2_1_33_1 e_1_2_1_2_1 e_1_2_1_11_1 e_1_2_1_32_1 e_1_2_1_16_1 e_1_2_1_39_1 e_1_2_1_17_1 e_1_2_1_38_1 e_1_2_1_14_1 e_1_2_1_37_1 e_1_2_1_15_1 e_1_2_1_36_1 e_1_2_1_9_1 e_1_2_1_18_1 e_1_2_1_19_1 |
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. 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inflammatory cardiomyopathy publication-title: Med Microbiol Immunol (Berl) – volume: 48 start-page: 1939 year: 2003 end-page: 1947 article-title: Antiphospholipid antibodies in pediatric and adult patients with rheumatic disease are associated with parvovirus B19 infection publication-title: Arthritis Rheum – volume: 99 start-page: 1348 year: 1999 end-page: 1354 article-title: Detection of adenoviral genome in the myocardium of adult patients with idiopathic left ventricular dysfunction publication-title: Circulation – volume: 53 start-page: 229 year: 1997 end-page: 232 article-title: Evidence for persistence of human parvovirus B19 DNA in bone marrow publication-title: J Med Virol – volume: 31 start-page: 32 year: 2004 end-page: 39 article-title: Analysing myocardial tissue from explanted hearts of heart transplant recipients and multi‐organ donors for the presence of parvovirus B19 DNA publication-title: J Clin Virol – volume: 112 start-page: 1965 year: 2005b end-page: 1970 article-title: Viral persistence in the myocardium is associated with progressive cardiac dysfunction publication-title: Circulation – volume: 111 start-page: 887 year: 2005a end-page: 893 article-title: High prevalence of viral genomes and multiple viral infections in the myocardium of adults with “idiopathic” left ventricular dysfunction publication-title: Circulation – volume: 302 start-page: 224 year: 2002 end-page: 228 article-title: A new parvovirus genotype persistent in human skin publication-title: Virology – volume: 76 start-page: 2014 year: 2002 end-page: 2018 article-title: The VP1 unique region of parvovirus B19 and its constituent phospholipase A2‐like activity publication-title: J Virol – volume: 37 start-page: 2483 year: 1999 end-page: 2487 article-title: Novel human erythrovirus associated with transient aplastic anemia publication-title: J Clin Microbiol – volume: 42 start-page: 466 year: 2003 end-page: 472 article-title: Detection of viruses in myocardial tissues by polymerase chain reaction evidence of adenovirus as a common cause of myocarditis in children and adults publication-title: J Am Coll Cardiol – volume: 34 start-page: 92 year: 2002 end-page: 95 article-title: Fatal Parvovirus B19‐associated myocarditis clinically mimicking ischemic heart disease: An endothelial cell‐mediated disease publication-title: Hum Pathol – volume: 107 start-page: 857 year: 2003 end-page: 863 article-title: Immunosuppressive therapy for active lymphocytic myocarditis: Virological and immunologic profile of responders versus nonresponders publication-title: Circulation – volume: 28 start-page: 1 year: 2003 end-page: 13 article-title: B19 virus genome diversity: Epidemiological and clinical correlations publication-title: J Clin Virol – volume: 61 start-page: 2627 year: 1987 end-page: 2630 article-title: Characterization of capsid and noncapsid proteins of B19 parvovirus propagated in human erythroid bone marrow cell cultures publication-title: J Virol – volume: 75 start-page: 161 year: 2005 end-page: 169 article-title: 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 publication-title: J Med Virol – volume: 78 start-page: 539 year: 1997 end-page: 543 article-title: Meta‐analysis of the association of enteroviruses with human heart disease publication-title: Heart – volume: 81 start-page: 6927 year: 2007 end-page: 6935 article-title: Biological and immunological relations among human parvovirus B19 genotypes 1 to 3 publication-title: J Virol – volume: 76 start-page: 9124 year: 2002 end-page: 9134 article-title: Genetic diversity within human erythroviruses: Identification of three genotypes publication-title: J Virol – volume: 58 start-page: 921 year: 1986 end-page: 936 article-title: Nucleotide sequence and genome organization of human parvovirus B19 isolated from the serum of a child during aplastic crisis publication-title: J Virol 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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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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 |
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