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[Virus demonstration and pathologic changes in different phases of coxsackievirus B myocarditis in mice]
I Rabausch-Starz1, N Neu, H K Müller-Hermelink
1Pathologisches Institut, Universität Würzburg.
Abstract:
A/J mice between 15 days and 10 weeks of age were infected intraperitoneally with Coxsackievirus B3 (CVB3). To search for virus in the myocardium various methods were applied: virus isolation from the myocardium, RNA extraction for dot blot hybridization and in situ hybridization. Two different RNA probes, one specific for CVB3 the other cross-reacting with other enteroviruses, were radioactively labeled with 35S or 32P by in vitro transcription. In paraffin sections histological alterations were assessed semiquantitatively. The animals developed acute myocarditis with myolysis and virus in the myocardium until 14 days after infection. The second stage of the disease was characterized by a persistent inflammatory infiltrate. At this stage no virus could be shown in the myocardium. Antibodies against cardiac myosin appeared 16 days after infection. Autoimmune mechanisms thus seem to be a most relevant factor for persistent inflammation after the acute viral phase of the disease.
Insights
Coxsackievirus B3 infection causes acute myocarditis in mice. Autoimmune responses, not persistent virus, appear to drive chronic inflammation after the initial viral phase.
Area of Science:
- Virology
- Immunology
- Pathology
Context:
- Coxsackievirus B3 (CVB3) is a known cause of viral myocarditis.
- Understanding the pathogenesis of CVB3-induced myocarditis is crucial for developing effective treatments.
Purpose:
- To investigate the presence of CVB3 in the myocardium during different stages of infection.
- To explore the role of viral persistence versus autoimmune mechanisms in chronic myocarditis.
Summary:
- A/J mice were infected with CVB3 and monitored for viral presence and histological changes.
- Virus was detected in the myocardium during the acute phase (up to 14 days post-infection).
- A persistent inflammatory infiltrate was observed in the chronic phase, with no detectable virus, but antibodies against cardiac myosin emerged, suggesting autoimmune involvement.
Impact:
- This study highlights the potential role of autoimmune mechanisms in the chronic phase of CVB3 myocarditis.
- Findings suggest that therapeutic strategies targeting the immune system may be beneficial for managing persistent inflammation.