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Interferon has no protective effect during acute or persistent reovirus infection of mouse SC1 fibroblasts
1Département de Microbiologie et Immunologie, Université de Montréal, Quebec, Canada.
Abstract:
Mouse SC1 fibroblasts can support reovirus multiplication although they exhibit a partial resistance to viral-induced cytopathology; a significant percentage of infected SC1 cells can remain viable while becoming persistently infected by the virus. In the present study, the possible role of interferon on the fate of reovirus-infected cells was investigated. Treatment of mouse L fibroblasts with beta-interferon resulted in a reduced viral efficiency of plating while essentially no effect was observed on SC1 cells; the results were similar with the unrelated encephalomyocarditis virus. This suggests that the interferon-regulated pathways are somehow deficient in SC1 cells even though these cells do respond to interferon treatment, as evidenced by an increase in the level of active interferon-inducible protein kinase double-stranded RNA-dependent (PKR) enzyme. Persistently infected SC1 cells constitutively release interferon even though treatment with anti-interferon antiserum suggests that interferon presence is unrelated to maintenance of the persistent state. The possible significance of the correlation between the lack of interferon-induced antiviral effect and relative resistance of SC1 cells to viral-induced cytopathology is briefly discussed.
Insights
SC1 fibroblasts resist reovirus-induced cell damage and establish persistent infections, suggesting a deficiency in their interferon antiviral pathways despite some response. This impacts viral fate and cell survival.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Mouse SC1 fibroblasts support reovirus replication but show partial resistance to viral cytopathology.
- A significant proportion of SC1 cells can remain viable during persistent reovirus infection.
Purpose of the Study:
- To investigate the role of interferon in the fate of reovirus-infected SC1 cells.
- To determine if interferon-regulated pathways are functional in SC1 cells.
Main Methods:
- Treatment of mouse L fibroblasts and SC1 cells with beta-interferon.
- Assessment of viral efficiency of plating for encephalomyocarditis virus and reovirus.
- Measurement of active interferon-inducible protein kinase double-stranded RNA-dependent (PKR) enzyme levels.
- Analysis of interferon release from persistently infected SC1 cells using anti-interferon antiserum.
Main Results:
- Beta-interferon reduced viral efficiency of plating in L fibroblasts but not in SC1 cells.
- SC1 cells showed increased active PKR levels upon interferon treatment, indicating a partial response.
- Persistently infected SC1 cells constitutively released interferon, but this was not linked to maintaining the persistent state.
Conclusions:
- SC1 cells possess deficient interferon-regulated antiviral pathways, contributing to their relative resistance to viral cytopathology.
- The lack of a strong interferon-induced antiviral effect in SC1 cells correlates with their ability to sustain persistent reovirus infections.
- Interferon release by SC1 cells does not appear to be essential for maintaining the persistent infection state.