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Published on: October 7, 2011
Coxsackievirus B 1 induced murine polymyositis: acute infection with active virus is required for myositis
Abstract:
Although the etiology of human polymyositis (PM) remains obscure, group B coxsackieviruses (CVB) have been implicated in disease pathogenesis and a particular strain of type 1 CVB (CVB 1) has been shown to cause in mice an inflammatory myositis which is similar to human PM. After infection of neonatal Swiss mice with active CVB 1, virus replicated to high titers in muscle and produced acute myonecrosis. Viral titers peaked in muscle at Day 7 and virus was undetectable after Day 14. Myocytes regenerated, but a chronic inflammatory myositis, involving principally proximal muscle groups of the hind limbs, was observed by Day 14 and persisted through at least Day 70. Injection of inactivated virus resulted in no clinical or histological disease. Anti-CVB 1 antibody was demonstrated in mice injected with inactivated or active virus pools. This report establishes the need for active virus in the pathogenesis of CVB 1 induced murine PM.
Insights
Active coxsackievirus type 1 (CVB 1) infection causes chronic inflammatory myositis in mice, mimicking human polymyositis (PM). Inactivated virus did not induce disease, confirming active virus is necessary for CVB 1-induced PM.
Area of Science:
- Virology
- Immunology
- Neurology
Background:
- The cause of human polymyositis (PM) is unknown.
- Group B coxsackieviruses (CVB) are suspected contributors to PM pathogenesis.
- A specific strain, coxsackievirus type 1 (CVB 1), induces a PM-like condition in mice.
Purpose of the Study:
- To investigate the role of active coxsackievirus type 1 (CVB 1) in inducing inflammatory myositis.
- To establish the necessity of active virus in the pathogenesis of CVB 1-induced murine polymyositis (PM).
Main Methods:
- Neonatal Swiss mice were infected with active or inactivated CVB 1.
- Viral replication and titers in muscle tissue were monitored.
- Histological examination assessed myonecrosis and chronic inflammation.
- Antibody responses to CVB 1 were analyzed.
Main Results:
- Active CVB 1 replicated to high titers in muscle, causing acute myonecrosis.
- Viral presence peaked at Day 7 and became undetectable after Day 14.
- Despite myocyte regeneration, chronic inflammatory myositis developed by Day 14 and persisted.
- Inactivated virus did not cause disease, but induced anti-CVB 1 antibodies.
- Anti-CVB 1 antibodies were present in both active and inactivated virus groups.
Conclusions:
- Active CVB 1 infection is essential for inducing inflammatory myositis in mice.
- This murine model closely resembles human polymyositis (PM).
- The findings highlight the etiological role of active CVB 1 in PM pathogenesis.
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