Related Experiment Videos
The cell-growth inhibitory effect of interferon. Studies of a resistant cell-subline
Abstract:
Studies performed in the CSV subline of mouse L-cells suggest that activated endogenous and/or exogenous viral infection might be the factor that modifies the cell surface and, in consequence, the sensitivity of the cell to the cell-growth inhibitory action of interferon. In contrast with the parental L-cells, the CSV subline obtained by prolonged passage of L-cells in the presence of interferon shows an altered electron microscopic morphology, absence of C type particles and a decreased agglutinability with Concanavalin A. It is resistant to the cell-growth inhibitory effect of interferon but retains the sensitivity toward its antiviral effect. However, the sensitivity of the CSV subline toward the cell-growth inhibitory effect of interferon increased significantly after treatment with 5-iododexyuridine, infection with the Harvey strain of mouse sarcoma virus and/or prolonged passages in vitro. In this respect, the CSV subline resembles the primary mouse embryonic cells. Since sensitivity of CSV cells increased also after treatment with cyclic 3'-5' adenosine monophosphate and/or prostaglandin E2, it is possible that the cell-growth inhibitory effect of interferon is mediated through the "second messenger" system.
Insights
Viral infection modifies mouse L-cell surface, impacting interferon sensitivity. CSV cells, resistant to growth inhibition by interferon, showed increased sensitivity after viral infection or specific treatments, suggesting a second messenger system role.
Area of Science:
- Cell Biology
- Virology
- Immunology
Background:
- Mouse L-cells, specifically the CSV subline, exhibit altered characteristics compared to parental cells.
- CSV subline is derived from prolonged passage of L-cells in the presence of interferon.
- CSV subline shows altered morphology, lacks C-type particles, and has reduced Concanavalin A agglutinability.
Purpose of the Study:
- To investigate the role of viral infection in modifying cell surface properties.
- To understand the altered sensitivity of CSV subline cells to interferon's growth-inhibitory effects.
- To explore the potential involvement of the second messenger system in interferon's action.
Main Methods:
- Comparative analysis of parental L-cells and CSV subline.
- Electron microscopy for morphological assessment.
- Assays for cell agglutinability and sensitivity to interferon's antiviral and growth-inhibitory effects.
- Treatment of CSV cells with 5-iododeoxyuridine, Harvey strain of mouse sarcoma virus, cyclic AMP, and prostaglandin E2.
Main Results:
- CSV subline is resistant to interferon's cell-growth inhibitory effect but retains sensitivity to its antiviral effect.
- Sensitivity of CSV subline to interferon's growth inhibition increased significantly after 5-iododeoxyuridine treatment, viral infection, or prolonged in vitro passage.
- CSV subline treated with cyclic 3 -5 adenosine monophosphate and/or prostaglandin E2 also showed increased sensitivity.
Conclusions:
- Activated viral infection may alter cell surface and influence sensitivity to interferon's growth inhibition.
- The CSV subline's response to interferon, particularly after specific treatments, resembles primary mouse embryonic cells.
- Interferon's cell-growth inhibitory effect might be mediated through the second messenger system.