Why the study?
A small number of reports and conflicting data make it unclear whether PVB19 induces de novo myocarditis and DCM or merely accompanies these conditions.
Does parvovirus B19 infection contribute to the development of myocarditis and inflammatory dilated cardiomyopathy?
Does parvovirus B19 infection contribute to the development of myocarditis and inflammatory dilated cardiomyopathy?
Parvovirus B19 is increasingly recognized as a primary viral etiological agent capable of causing de novo myocarditis and inflammatory dilated cardiomyopathy, with evidence suggesting IFN-β therapy may improve clinical parameters in affected patients.
Answers are grounded in this paper and cite their sources.
May support PVB19 testing in DCMi; extends evidence for viral etiology in heart failure progressing to dilated cardiomyopathy.
Myocarditis (MC) is defined as an immunological inflammatory reaction with various etiologies, clinical presentations and prognoses within the myocardium. Currently, parvovirus B19 (PVB19) has become the main factor leading to this disease, replacing the previously dominant viruses A and B. In the case of chronic heart failure with subsequent dilated cardiomyopathy, approximately 67% have a viral etiology, and most of them are the result of PVB19 infection. However, the analysis showed a correlation between PVB19 infection and the risk of developing inflammatory dilated cardiomyopathy (DCMi). PVB19 is detected in 23% of patients with DCMi. Chronic infection may also contribute to progressive left ventricular failure in patients with a history of MC. The above effect suggests the active replication of PVB19 only in heart biopsies with inflammation due to MC or DCMi. Moreover, the supply of IFN-β to suppress the active transcription of PVB19 accompanied by DCMi over a period of 6 months results in the normalization of NT-proBNP and an improvement in LVEF along with NYHA performance. The small number of reports on this topic and inaccuracies resulting from constantly conducted research and ongoing changes make it impossible to clearly answer the question of whether PVB19 is a factor inducing de novo MC and DCM or only accompanies the above conditions. However, large clinical cohort studies lead to the perception of PVB19 as a viral etiological agent capable of causing de novo MC together with DCMi.
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Krych et al. (2024) studied this question.
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