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The image of the month: Association of iron overload with cardiac virus infections and inflammation


Detection of DNA from different viruses in the myocardium

Prussian blue staining

 Immunohistochemical staining for MHC class II (brown reveals activated macrophages

A 47 year old man was diagnosed for hemochromatosis (genetically confirmed) three months before he was admitted to the Department of Cardiology in our hospital. Blood tests showed high levels of ferritin (665 ug/dl) and an increased content of iron (179 ug/dl). Echocardiography revealed a reduced right and left ventricular function (LVEF 40%) and a diastolic dysfunction. In order to evaluate whether the heart is involved in hemochromatosis, endomyocardial biopsies were taken. As expected, prussian blue staining showed iron deposits in numerous myocytes and macrophages. In addition, we found a mild increase of inflammatory cells in the myocardium, which were mainly activated macrophages as demonstrated in the Figure above. Molecular analysis of cardiotropic agents demonstrated positivity for human herpesvirus 6B, Epstein-Barr virus and parvovirus B19 in PCR investigations. Blood investigations for virus infections/reactivations were negative.

Various mechanisms are suggested to enhance the predisposition to various bacterial and viral infections in patients with hemochromatosis. There is evidence that high iron concentrations increase the susceptibility for infections by modifying the host immune response, specifically by impairment of cell-mediated immune mechanisms. Iron loading of macrophages was found to result in the inhibition of IFN-gamma-mediated pathways. In hepatitis B infection it was found that patients with higher levels of serum iron or ferritin were less likely to achieve spontaneous recovery after acute HBV infection. It is also apparent that excess iron enhances fibrogenic pathways and worsens the clinical course of HCV infection by causing oxidative stress. Moreover, it was shown that excess iron decreases the viability of HIV-infected cells and elevates the activity of reverse transcriptase, indicating that iron overload associated with HIV infection is detrimental to host cell responses against this infection (for review see: Khan et al., Int J Inf Dis (2007) 11, 482-487). More recently, we found that iron overload in the myocardium may potentiate the effects of enterovirus infection by the NO/HO-1 pathway, thus increasing cardiac pathogenicity (Ursu et al., Cell Physiol Biochem (2014) 33: 52-66).

Notes to editor

Presented by:
Karin Klingel, MD
Department of Molecular Pathology,
University Hospital Tübingen, Germany 
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.