期刊
CLINICAL AND VACCINE IMMUNOLOGY
卷 19, 期 8, 页码 1182-1187出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/CVI.00281-12
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资金
- Netherlands Heart Foundation (NHS) [2005B082, 2007B036]
- VIDI grant from the Netherlands Organization for Scientific Research (NWO)
Infections with cardiotrophic viruses and immune-mediated responses against the heart have been suggested to play a dominant role in the pathogenesis of idiopathic dilated cardiomyopathy (DCM). Furthermore, immune-mediated inflammatory diseases (IMIDs) may result in DCM. It has not previously been assessed whether DCM patients with and without an IMID have different prevalences and quantities of cardiotrophic viruses in the heart. Therefore, we compared the profiles of cardiotrophic viruses in heart tissue of DCM patients with and without an IMID. Serum and myocardial tissue samples were obtained from 159 consecutive patients with DCM and 20 controls. Patients were subdivided into three groups, the first two based on the presence (n = 34) or absence (n = 125) of an IMID and the third being a control group. The parvovirus B19 virus genome was detected in equal quantities in the non-IMID DCM patients (100/125) and the control group (15/20) but in lower quantities in the IMID patients (21/34, P = 0.02). Both the non-IMID and IMID DCM patients demonstrated increased myocardial inflammation compared to controls: 12.5 +/- 1.8 and 14.0 +/- 3.2 CD45-positive inflammatory cells, respectively, versus 5.1 +/- 0.7 for the controls (P<0.05 for both). Importantly, significantly higher parvovirus B19 copy numbers could be amplified in non-IMID than in IMID patients (561 +/- 97 versus 191 +/- 92 copies/mu g DNA, P<0.001) and control subjects (103 +/- 47 copies/mu g DNA, P<0.001). The present study shows decreased parvovirus B19 prevalence and copy numbers in hearts of DCM patients with an IMID compared to those without an IMID. These findings may suggest that DCM patients with an IMID have a different pathophysiologic mechanism from that which is present in the virus-induced form of DCM.
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