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Protective effect of recombinant alpha interferon on coxsackievirus B3 myocarditis in mice
A Matsumori1, N Tomioka, C Kawai
1Department of Internal Medicine, Kyoto University, Japan.
Abstract:
The effects of recombinant human leukocyte interferon alpha-A/D on experimental myocarditis caused by coxsackievirus B3 were investigated. Four-week-old male C3H/He mice were inoculated intraperitoneally with 10(5.5) 50% tissue culture infective dose (TCD50) in 0.1 ml of coxsackievirus B3 (Nancy strain). Interferon alpha-A/D, 10(4) U/gm/day, was administered subcutaneously daily, starting 1 day before (group 1) or on the day of (group 2) infection. Animals were killed on day 7. The infectivity of myocardial virus was significantly lower in group 1 (0.7 +/- 0.1 log10TCD50/mg, p less than 0.005) and in group 2 (2.5 +/- 1.2 log10TCD50/mg, p less than 0.005) than in control mice (4.4 +/- 0.9 log10TCD50/mg). Results of histologic examination showed extensive myocardial necrosis and cellular infiltration in all mice in the untreated group, but significantly less severe necrosis and infiltration in the treated groups. Thus, interferon alpha-A/D, when given before and simultaneously with virus, effectively inhibited replication of myocardial virus and reduced the inflammatory response and myocardial damage in an experimental model of viral myocarditis.
Insights
Recombinant human leukocyte interferon alpha-A/D effectively treated experimental viral myocarditis. Treatment significantly reduced coxsackievirus B3 replication and myocardial damage in mice.
Area of Science:
- Virology
- Immunology
- Cardiology
Background:
- Viral myocarditis is a serious condition often caused by coxsackievirus B3.
- Current treatments for viral myocarditis are limited, necessitating research into novel therapeutic agents.
Purpose of the Study:
- To investigate the efficacy of recombinant human leukocyte interferon alpha-A/D in an experimental model of coxsackievirus B3-induced myocarditis.
Main Methods:
- Four-week-old male C3H/He mice were infected with coxsackievirus B3.
- Interferon alpha-A/D was administered subcutaneously either one day before or on the day of infection.
- Viral infectivity and histological changes in the myocardium were assessed on day 7.
Main Results:
- Interferon alpha-A/D treatment significantly reduced myocardial coxsackievirus B3 infectivity compared to controls.
- Histological examination revealed significantly less severe myocardial necrosis and cellular infiltration in treated mice.
- Both prophylactic and simultaneous administration of interferon demonstrated protective effects.
Conclusions:
- Recombinant human leukocyte interferon alpha-A/D is a promising therapeutic agent for viral myocarditis.
- Interferon alpha-A/D effectively inhibits viral replication and mitigates the inflammatory response and myocardial damage.
- Early intervention with interferon alpha-A/D is crucial for optimal outcomes in experimental viral myocarditis.