SynthesisInternational journal of molecular sciences2024
Viral Myocarditis as a Factor Leading to the Development of Heart Failure Symptoms, Including the Role of Parvovirus B19 Infection-Systematic Review.
Synthesis in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Human parvovirus B19 infection in a Spanish healthcare area: epidemiology, clinical spectrum, and factors associated with hospitalization.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Article
- Clinical and virological impacts of human parvovirus B19 epidemics on fulminant myocarditis in childhood.BMC pediatrics · 2026Article
- Parvoviruses at the Heart: Endothelial Injury and Myocyte Lysis in Human B19V and Canine CPV-2 Infections.Current issues in molecular biology · 2025Review
- Immunometabolism in heart failure.Nature reviews. Cardiology · 2025Review
- Fulminant parvovirus B19 myocarditis in infants -report of three post-pandemic cases.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025Article
- Fulminant Influenza Myocarditis Requiring Extracorporeal Membrane Oxygenation (ECMO) Support.Cureus · 2025Article
- Autoimmunity in Cardiomyopathy-Induced Heart Failure and Cardiac Autoantibody Removal by Immunoadsorption.Journal of clinical medicine · 2025Review
- Outbreak of paediatric myocarditis associated with parvovirus B19 infection in Italy, January to October 2024.Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2024Article
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Authors and funding
8 authors.
Funding
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Abstract
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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