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Interferon-induced disease in mice and rats
Abstract:
Treatment of newborn mice with potent mouse interferon preparations resulted in an acute "early" syndrome characterized by inhibition of growth, delay in maturation of several organs, diffuse liver cell necrosis and death. When interferon treatment was discontinued at 1 week of life, mice appeared to recover, but subsequently developed a progressive glomerulonephritis ("late syndrome"). Treatment of newborn rats with potent rat interferon preparations also resulted in inhibition of growth, delay in maturation, and the subsequent development of glomerulonephritis. After infection at birth with lymphocyte choriomeningitis (LCM) virus, most strains of mice developed a similar acute early syndrome and surviving mice subsequently developed glomerulonephritis. We postulated that the endogenous interferon induced by LCM virus early in life was partially responsible for these syndromes. Administration of a potent anti-mouse interferon serum to LCM virus-infected mice neutralized the circulating endogenous interferon and inhibited the development of both the early and late syndromes. Our results suggest that large amounts of exogenous or endogenous interferon at a crucial stage of rapid growth or development of mice and rats can induce lesions in several different organs. Some lesions (i.e. the kidney) only become apparent weeks or even months after exposure to interferon.
Insights
High-dose interferon (IFN) administration in newborn mice and rats can cause acute illness and delayed kidney damage. Endogenous IFN from viral infections also triggers similar syndromes, preventable with anti-IFN serum.
Area of Science:
- Immunology
- Virology
- Toxicology
Background:
- Interferon (IFN) is crucial for antiviral immunity.
- Neonatal exposure to potent IFN preparations can lead to adverse effects.
- Viral infections in newborns can induce endogenous IFN production.
Purpose of the Study:
- To investigate the effects of exogenous and endogenous interferon on neonatal development.
- To determine the role of interferon in post-viral syndromes in newborns.
- To explore potential therapeutic interventions for interferon-induced pathologies.
Main Methods:
- Treatment of newborn mice and rats with exogenous interferon preparations.
- Infection of mice with Lymphocyte Choriomeningitis (LCM) virus.
- Administration of anti-mouse interferon serum to infected mice.
Main Results:
- Exogenous interferon induced acute syndromes (growth inhibition, organ damage, mortality) and delayed glomerulonephritis in mice and rats.
- LCM virus infection in mice caused similar acute and late syndromes.
- Anti-interferon serum neutralized endogenous interferon and prevented syndrome development.
Conclusions:
- Large amounts of interferon, whether exogenous or endogenous, can induce organ lesions during critical developmental stages.
- Kidney damage (glomerulonephritis) may manifest weeks or months after initial interferon exposure.
- Interferon plays a significant role in the pathogenesis of early and late syndromes following viral infections in newborns.