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Coxsackievirus B3-induced chronic myocarditis in outbred NMRI mice
1Institute of Virology, Clinical Center of the Friedrich Schiller University, Jena, Germany. I8MEIN@pop3.uni-jena.de
Objectives:
The pathogenesis of coxsackievirus B3 (CVB3)-induced myocarditis was investigated in adult Han:NMRI mice. The outbred model, in comparison with inbred models, represents better the natural variable susceptibility of the human population.
Study Design/Methods:
We analyzed the replicating virus titer, the antibody response in the acute and chronic phase of disease, the histology of myocardial injury, and the persistence of viral RNA.
Results:
NMRI mice infected with 5000 plaque-forming units (PFU) of the CVB3 variant "P"D, a lytic variant to human fibroblast lines, showed a peak of virus replication at day 14 and developed a severe acute myocarditis. The chronic myocarditis was characterized by progressive fibrosis, small foci of infiltrates, persistent viral RNA in the heart, and detectable anti-CVB3 IgG production and neutralizing antibody response up to day 98 postinfection.
Conclusions:
CVB3"P"D is able to induce chronic myocarditis in NMRI mice. This model provides a method for examining and proving the mechanisms of myocardial pathogenesis and of developing therapeutic strategies.
Insights
This study shows that coxsackievirus B3 (CVB3) can cause chronic myocarditis in NMRI mice. This model helps investigate viral heart disease mechanisms and develop new treatments.
Area of Science:
- Virology
- Immunology
- Pathology
Background:
- Myocarditis is inflammation of the heart muscle.
- Coxsackievirus B3 (CVB3) is a common cause of viral myocarditis.
- Understanding CVB3 pathogenesis is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the pathogenesis of CVB3-induced myocarditis in adult Han:NMRI mice.
- To establish a suitable animal model for studying chronic viral heart disease.
- To analyze the immune response and viral persistence in a susceptible mouse model.
Main Methods:
- Infection of NMRI mice with CVB3 variant "P"D.
- Analysis of viral replication, antibody response (IgG, neutralizing), and viral RNA persistence.
- Histological examination of myocardial injury and fibrosis.
Main Results:
- CVB3 infection led to severe acute myocarditis peaking at day 14.
- Chronic myocarditis was characterized by progressive fibrosis and persistent viral RNA.
- Detectable anti-CVB3 IgG and neutralizing antibodies persisted up to 98 days postinfection.
Conclusions:
- CVB3 variant "P"D successfully induces chronic myocarditis in NMRI mice.
- This model is valuable for studying myocardial pathogenesis mechanisms.
- The model facilitates the development and testing of therapeutic strategies for viral myocarditis.