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首页> 外文期刊>Clinical and vaccine immunology: CVI >Differences in virus prevalence and load in the hearts of patients with idiopathic dilated cardiomyopathy with and without immune-mediated inflammatory diseases
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Differences in virus prevalence and load in the hearts of patients with idiopathic dilated cardiomyopathy with and without immune-mediated inflammatory diseases

机译:不同的病毒患病率和加载的特发性扩张型患者的心没有免疫介导性心肌病和炎性疾病

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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/μg DNA, P < 0.001) and control subjects (103 ± 47 copies/μg 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.
机译:cardiotrophic病毒和感染免疫介导的反应对心脏建议中发挥主导作用特发性扩张型心肌病的发病机制(DCM)。疾病(醯亚氨)可能会导致扩张型心肌病。此前是否DCM患者有或没有一个醯亚氨有不同cardiotrophic肥胖盛行程度和数量病毒的心。概要cardiotrophic病毒在心脏组织扩张型心肌病患者和没有醯亚氨。和心肌组织样本被获得159年连续DCM患者和20名控制。组,前两个的基础上(n =34)与否(n = 125)醯亚氨和第三作为一个对照组。基因组中发现数量相等non-IMID DCM患者(100/125)和控制组(15/20),但在低量醯亚氨患者(21/34,P = 0.02)。醯亚氨DCM患者表现出增加心肌炎症与控制:12.5±1.8,14.0±3.2 CD45-positive炎症细胞,分别与5.1±0.7的控制(P < 0.05)。重要的是,明显高于细小病毒B19复制数字可能被放大在non-IMID比in IMID角力191个病人(561±97±92拷贝/μg DNA, P < 0.001),对照组(103±47份/μg DNA, P < 0.001)。研究显示细小病毒B19感染率下降和复制数量扩张型心肌病患者的心一个醯亚氨比那些没有一个醯亚氨。发现可能表明DCM患者醯亚氨有不同的病理生理机制它存在于病毒诱导DCM的形式。

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