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Protein synthesis in VSV infected CNS, neuroblastoma and BHK cell lines
Abstract:
The protein synthesis of VSV infected CNS of mice was analysed by SDS-PAGE. Cellular and viral protein synthesis in the CNS were also compared to VSV infected neuroblastoma cells (clone NS 20) and fibroblasts (BHK21). Inhibition of host protein synthesis was observed in the three systems tested. However, this inhibition was shown to occur faster in neuroblastoma cells than in BHK cells, whereas it proceeded progressively in the brain. Thus the shut off of host cell protein synthesis by VSV seems to be a general phenomenon that occurs in vivo as well as in vitro. VSV protein from the CNS, or from neuroblastoma cells and fibroblasts were found to migrate similarly in SDS-PAGE. The viral L protein synthesis was found to be particularly active in the CNS, with respect to that observed in NS20 and BHK cells. The viral glycoprotein failed to be detected in the VSV infected mouse brain in our experimental conditions. The results show that VSV infection in vivo occurs with some difference with that of non neuronal cells, and that in vivo studies suggest the existence of cellular modulation that should be taken in account in the pathogenesis of this rhabdovirus.
Insights
Vesicular stomatitis virus (VSV) infection inhibits host protein synthesis in mouse central nervous system (CNS) and cultured cells. Viral L protein synthesis is highly active in the CNS, differing from non-neuronal cells.
Area of Science:
- Virology
- Neuroscience
- Molecular Biology
Background:
- Vesicular stomatitis virus (VSV) is a rhabdovirus known to infect various cell types.
- Understanding host-pathogen interactions is crucial for elucidating viral pathogenesis.
Purpose of the Study:
- To analyze protein synthesis in the mouse central nervous system (CNS) following VSV infection.
- To compare VSV infection dynamics and protein synthesis in vivo (CNS) versus in vitro (neuroblastoma and fibroblast cells).
Main Methods:
- Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) was used to analyze protein synthesis.
- Comparison of cellular and viral protein synthesis in mouse CNS, neuroblastoma cells (clone NS 20), and fibroblasts (BHK21) infected with VSV.
Main Results:
- VSV infection inhibited host protein synthesis in all three systems (CNS, neuroblastoma, fibroblasts).
- Inhibition occurred faster in neuroblastoma cells than in BHK cells; it was progressive in the brain.
- Viral L protein synthesis was particularly active in the CNS compared to cell cultures.
- Viral glycoprotein was not detected in VSV-infected mouse brain under experimental conditions.
Conclusions:
- VSV-induced shut-off of host protein synthesis is a general phenomenon, occurring both in vivo and in vitro.
- VSV infection in vivo exhibits differences compared to non-neuronal cells, suggesting cellular modulation in pathogenesis.
- In vivo studies are essential for understanding the complete picture of VSV pathogenesis.