CORRESPONDENCE: LETTER TO THE EDITOR
A Geographical Mystery: Do Cardiotropic Viruses Respect National Borders?
Ali Yilmaz, MD,
Karin Klingel, MD,
Reinhard Kandolf, MD and
Udo Sechtem, MD*
* Robert-Bosch-Krankenhaus, Auerbachstrasse 110, 70376 Stuttgart, Germany (Email: udo.sechtem{at}rbk.de).
We read the interesting article of Andréoletti et al. (1) showing active coxsackieviral B (CV-B) infection in post-mortem endomyocardial tissue of patients who died suddenly due to acute myocardial infarction. The demonstration of sarcolemmal dystrophin disruption in the same tissue areas that were infected by CV-B is of potential groundbreaking value for the understanding of viral pathogen-induced myocardial damage in humans. Both CV-B genomes and CV-B capsid proteins were detected in the heart tissues of patients with myocardial infarction by reverse transcriptase-polymerase chain reaction and immunohistochemistry, thereby suggesting active virus replication.
However, it is interesting to find that about one-half of the myocytes (exemplary pictured in Fig. 1 of this article [1]) reveal virus replication in patients with coronary artery disease as demonstrated by the presence of the enteroviral VP1 capsid protein (1). Previous extensive investigations regarding immunohistochemical stainings for the detection of enteroviral proteins in cardiac tissue by applying the antibody from clone 5-D8/1 (Dako, Glostrup, Denmark), which was also applied in this study, revealed a considerable unspecific cross-reaction with uninfected necrotic or apoptotic human cardiomyocytes (2). In fact, using this antibody, we found that false positive staining of cardiomyocytes can be detected in all kinds of cardiac diseases where affected cardiomyocytes are present including patients with myocardial infarction and coronary artery disease. Therefore, the suitability of this antibody for the visualization of CV-B capsid proteins is questionable at least in diseased hearts.
In addition, it is surprising that Andréoletti et al. (1) found enteroviruses to be the only cardiotropic viral agents active in France. In contrast, endomyocardial biopsies in Germany consistently and almost exclusively contain parvovirus B19 (PVB19) and human herpes virus type 6 whereas CV-B is a rare finding (3–7). As PVB19 may lead to endothelial dysfunction (8,9) and is found in the majority of patients with a clinical picture of acute myocardial infarction despite a normal coronary anatomy (10), one might expect to find also PVB19 genomes in French patients dying of acute myocardial infarction. Of course, there are very little data on endomyocardial biopsy findings in German patients with acute myocardial infarction, and it cannot be excluded that one would find CV-B in such a cohort.
How can this astonishing difference between endomyocardial biopsy findings in French and German people be explained? Is viral disease of the heart a locally restricted phenomenon? Does CV-B show a tropism for wine-drinking humans while PVB19 is mainly attracted to beer drinkers? Is there a mechanism preventing viruses from crossing the French-German border? Or is the difference not a real one, but is due to methodological differences (polymerase chain reaction primers?) in identifying small amounts of viral genome. Whatever the reason for this discrepancy, it is important to verify the findings of Andréoletti et al. (1) in other labs with experience in identifying very small amounts of viral genomes in human myocardium.
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1. Andréoletti L, Venteo L, Douche-Aourik F, et al. Active coxsackieviral B infection is associated with disruption of dystrophin in endomyocardial tissue of patients who died suddenly of acute myocardial infarction J Am Coll Cardiol 2007;50:2207-2214.[Abstract/Free Full Text]2. Klingel K, Sauter M, Bock CT, Szalay G, Schnorr JJ, Kandolf R. Molecular pathology of inflammatory cardiomyopathy Med Microbiol Immunol 2004;193:101-107.[CrossRef][Medline] 3. Kuhl U, Pauschinger M, Noutsias M, et al. High prevalence of viral genomes and multiple viral infections in the myocardium of adults with "idiopathic" left ventricular dysfunction Circulation 2005;111:887-893.[Abstract/Free Full Text] 4. Mahrholdt H, Wagner A, Deluigi CC, et al. Presentation, patterns of myocardial damage, and clinical course of viral myocarditis Circulation 2006;114:1581-1590.[Abstract/Free Full Text] 5. Pankuweit S, Moll R, Baandrup U, Portig I, Hufnagel G, Maisch B. Prevalence of the parvovirus B19 genome in endomyocardial biopsy specimens Hum Pathol 2003;34:497-503.[CrossRef][Web of Science][Medline] 6. Pankuweit S, Lamparter S, Schoppet M, Maisch B. Parvovirus B19 genome in endomyocardial biopsy specimen Circulation 2004;109:e179.[Free Full Text] 7. Tschope C, Bock CT, Kasner M, et al. High prevalence of cardiac parvovirus B19 infection in patients with isolated left ventricular diastolic dysfunction Circulation 2005;111:879-886.[Abstract/Free Full Text] 8. Vallbracht KB, Schwimmbeck PL, Kuhl U, Seeberg B, Schultheiss HP. Endothelium-dependent flow-mediated vasodilation of systemic arteries is impaired in patients with myocardial virus persistence Circulation 2004;110:2938-2945.[Abstract/Free Full Text] 9. Vallbracht KB, Schwimmbeck PL, Kuhl U, Rauch U, Seeberg B, Schultheiss HP. Differential aspects of endothelial function of the coronary microcirculation considering myocardial virus persistence, endothelial activation, and myocardial leukocyte infiltrates Circulation 2005;111:1784-1791.[Abstract/Free Full Text] 10. Kuhl U, Pauschinger M, Bock T, et al. Parvovirus B19 infection mimicking acute myocardial infarction Circulation 2003;108:945-950.[Abstract/Free Full Text]
Related Article
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- Laurent Andréoletti
J. Am. Coll. Cardiol. 2008 52: 82-83.
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