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[Electron microscopic study of a tick-borne encephalitis virus-infected cell culture exposed to tunicamycin]
Abstract:
Ultrastructural features of tick-borne encephalitis virus-infected pig embryo cell culture treated with different concentrations of tunicamycin at various intervals after infection were studied electron microscopically. The inhibition of glycosylation did not prevent virion formation in the infected cells. At the same time, treatment with tunicamycin led to marked accumulation of virus particles in cisterns and vacuoles of the Golgi complex and to a decrease in the number of virions released into the extracellular space. It is assumed that inhibition of glycosylation leads to disorders in the regulation of the final stages of virus particles transportation and release from the infected cell. The results of the study indicate an important role of the Golgi complex in realization of the final stages of flavivirus morphogenesis.
Insights
Inhibiting glycosylation in tick-borne encephalitis virus-infected cells did not stop virion formation but disrupted virus release. This suggests the Golgi complex is crucial for flavivirus particle transport and final assembly.
Area of Science:
- Virology
- Cell Biology
- Microbiology
Background:
- Tick-borne encephalitis virus (TBEV) is a significant flavivirus pathogen.
- Understanding flavivirus morphogenesis is key to developing antiviral strategies.
- The role of glycosylation in TBEV replication requires further elucidation.
Purpose of the Study:
- To investigate the ultrastructural effects of glycosylation inhibition on TBEV-infected cells.
- To determine the impact of tunicamycin on TBEV virion formation and release.
- To explore the involvement of the Golgi complex in flavivirus particle assembly.
Main Methods:
- Electron microscopy was used to examine TBEV-infected pig embryo cells.
- Cells were treated with varying concentrations of tunicamycin at different post-infection times.
- Ultrastructural changes and virus particle localization were analyzed.
Main Results:
- Glycosylation inhibition by tunicamycin did not impede TBEV virion formation.
- Tunicamycin treatment caused significant accumulation of virus particles within Golgi cisterns and vacuoles.
- A notable decrease in extracellular TBEV virion release was observed.
Conclusions:
- Disrupting glycosylation interferes with the final stages of TBEV transport and release.
- The Golgi complex plays a critical role in the morphogenesis and release of flaviviruses.
- Targeting glycosylation pathways may offer a novel approach to controlling TBEV infection.