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Prevention of viral myocarditis with recombinant human leukocyte interferon alpha A/D in a murine model
Abstract:
Effects of recombinant human leukocyte interferon alpha A/D on experimental myocarditis due to encephalomyocarditis virus were investigated. Plaque reduction assays revealed that 50% of plaque formation in vitro in human amnion (FL) cells was inhibited by interferon alpha A/D (9.7 U/ml) when it was administered 24 hours before infection with the encephalomyocarditis virus. Four week old male DBA/2 mice were inoculated intraperitoneally with 10 plaque-forming units (pfu) of encephalomyocarditis virus. Interferon alpha A/D was administered subcutaneously (10(2) U/g body weight per day in Group 1, 10(3) U/g per day in Group 2 and 10(4) U/g per day in Group 3) starting 1 day before infection. It was also administered starting the same day in Group 4 and 1 day after virus inoculation in Group 5 (10(4) U/g per day in both groups). Control mice were injected with saline solution. Each group consisted of 10 mice; they were killed on day 4 for evaluation. Myocardial virus titers were significantly lower in Group 3 (8.2 +/- 25.2 X 10(2) pfu/mg, p less than 0.05) and Group 4 (3.0 +/- 5.5 X 10(3) pfu/mg, p less than 0.05) than in control mice (5.6 +/- 4.1 X 10(4) pfu/mg). Histologic examination showed extensive myocardial necrosis and cellular infiltration in all control mice, but no myocardial necrosis or cellular infiltration in Group 3 and less severe necrosis and infiltration in Group 4. There were no significant differences in myocardial virus titers or histologic changes between control mice and Group 1, 2 or 5.(ABSTRACT TRUNCATED AT 250 WORDS)
Insights
Recombinant human leukocyte interferon alpha A/D effectively treated experimental myocarditis in mice by reducing viral load and preventing myocardial damage when administered before or on the day of encephalomyocarditis virus infection.
Area of Science:
- Virology
- Immunology
- Cardiology
Background:
- Myocarditis is an inflammation of the heart muscle, often caused by viral infections.
- Encephalomyocarditis virus (EMCV) is a known cause of experimental myocarditis.
- Interferons are cytokines with antiviral properties.
Purpose of the Study:
- To investigate the efficacy of recombinant human leukocyte interferon alpha A/D (IFN-αA/D) in treating EMCV-induced experimental myocarditis.
- To determine the optimal timing and dosage of IFN-αA/D administration for therapeutic benefit.
Main Methods:
- In vitro plaque reduction assays were performed to assess the antiviral activity of IFN-αA/D against EMCV.
- DBA/2 mice were infected with EMCV and treated with varying doses and schedules of subcutaneous IFN-αA/D.
- Myocardial viral titers and histological changes were evaluated on day 4 post-infection.
Main Results:
- IFN-αA/D demonstrated significant in vitro inhibition of EMCV plaque formation.
- Subcutaneous administration of 10^4 U/g/day of IFN-αA/D starting 1 day before or on the day of infection significantly reduced myocardial viral titers.
- Histological analysis revealed that this treatment regimen prevented myocardial necrosis and cellular infiltration in mice.
Conclusions:
- Recombinant human leukocyte interferon alpha A/D is a promising therapeutic agent for EMCV-induced myocarditis.
- Early administration of IFN-αA/D, particularly before or on the day of infection, is crucial for its efficacy.
- Further research into interferon-based therapies for viral myocarditis is warranted.