Parvovirus and Myocarditis

Human parvovirus B19 has been linked to a variety of cardiac diseases. A causal association between viral infection and cardiac disease was frequently postulated following the detection of B19 DNA by PCR in endomyocardial biopsy specimens. Several authors have postulated a causative role of B19 in cardiac disease, such as acute myocarditis (Schowengerdt, et al.,1997, Dettmeyer et al., 2003, Kühl et al.,2005,), dilative cardiomyopathy or idiopathic left ventricular dysfunction (Donosoet al., Klein 2004, et al,2004 ), and peripartum cardiomyopathy (Bultmannet al., 2005, Schenk et al., 2009).
There have been two fatal cases of PB19-associated myocarditis reported. A 1 year-old child, developed cardiac insufficiency following serologically confirmed erythema infectiosum. There was a temporary response to digoxin and diuretics, but the child died two weeks later. On autopsy there was an active myocarditis with a mononuclear inflammatory infiltrate and severe myocyte necrosis. PB19 capsid proteins were detected in myocardial tissue sections. The myocardial findings were similar to those seen in fetuses infected in utero by PB19 (Saint-Martin et al., 1990). In a second case, a 3 year-old child died of myocarditis following PB19 infection. Although PB19 could be detected in liver and spleen tissues, no PB19 DNA was detected in the myocardial tissue. The role of PB19 in the pathogenesis of myocarditis needs further investigations, particularly as P antigen is found on fetal myocardial cells and PB19 appears to cause myocarditis in the fetus (Young and Brown, 2004).
Parvovirus and Hematological disorders in children
PB19-associated inflammatory cardiomyopathy is characterized by infection of intracardiac endothelial cells of small arterioles and veins, which may be associated with endothelial dysfunction, impairment of myocardial microcirculation, penetration of inflammatory cells, and secondary myocyte necrosis. Recent observations showed that B19 is involved in intracellular calcium regulation by the viral phospholipase. B19-induced caspase activation can lead to proinflammatory/proapoptotic processes through dysregulation of STAT signaling. These cellular interactions may contribute to mechanisms by which B19 establishes persistent infection in endothelial cells and play a critical role in viral pathogenesis of inflammatory cardiomyopathy (Kandolf et al., 2008).