ArticlePathogens (Basel, Switzerland)2021
Coinfection of Parvovirus B19 with Influenza A/H1N1 Causes Fulminant Myocarditis and Pneumonia. An Autopsy Case Report.
Article in Pathogens (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Viral Myocarditis as a Factor Leading to the Development of Heart Failure Symptoms, Including the Role of Parvovirus B19 Infection-Systematic Review.International journal of molecular sciences · 2024Pooled it
- Influenza-Associated Cardiac Manifestations: A Systematic Review of Case Reports and Case Series.Journal of clinical medicine · 2026Review
- Retrospective and Prospective Surveillance and Clinical Presentation of Parvovirus B19 in Veneto, Italy, 2024.Microorganisms · 2025Article
- Review
- Encephalopathy Caused by Human Parvovirus B19 Genotype 1 Associated withCurrent issues in molecular biology · 2023Article
- Advancing Precision Medicine in Myocarditis: Current Status and Future Perspectives in Endomyocardial Biopsy-Based Diagnostics and Therapeutic Approaches.Journal of clinical medicine · 2023Review
- RKIP suppresses the influenza A virus‑induced airway inflammatory response via the ERK/MAPK pathway.International journal of molecular medicine · 2023Article
- Research focus and theme trend on fulminant myocarditis: A bibliometric analysis.Frontiers in cardiovascular medicine · 2022Article
- Viral Myocarditis-From Pathophysiology to Treatment.Journal of clinical medicine · 2021Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parvovirus-B19 (PVB19) is a frequent causative agent of myocarditis. For unclear reasons, viral reactivation can cause acute myocarditis, a leading cause of sudden death in the young. Influenza A/H1N1(2009) virus (IAV/H1N1) is known for causing flu/pneumonia, but the heart is rarely involved. Co-infections of cardiotropic viruses are rarely reported and the mechanisms of viral interactions remain unknown. A 5-year old girl had a flu-like syndrome, when she suddenly presented with a respiratory distress and cardiac arrest. At autopsy, the lungs were found haemorrhagic. Lungs' histology showed severe bronchiolitis, diffuse haemorrhagic necrosis, and mononuclear inflammation. In the heart, a moderate inflammation was found with no necrosis. IAV/H1N1 was detected in nasal and tracheal swabs, lungs, and the heart. The viral load was high in the lungs, but low in the heart. PVB19 was detected in the heart with a high viral load. Viral co-infection increases the risk of severe outcome but the mechanisms of interaction between viruses are poorly understood. In our case, viral loads suggested a reactivated PVB19-induced acute myocarditis during an IAV/H1N1 pneumonia. Viral interactions may involve an IAV/H1N1-induced cytokine storm, with a fulminant fatal outcome. Clinically, our case shows the importance of investigating inflammatory pathways as therapeutic targets.
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