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Direct adverse effects of Sendai virus DI particles on virus budding and on M protein fate and stability
1Microbiology Department, University of Geneva Medical School, Switzerland.
Abstract:
Upon infections of BHK cells with a mixture of Sendai standard and defective interfering (DI) viruses (mixed virus infection), viral budding was found to be restricted by factors ranging from 5 to more than 20. The reduced viral budding correlated with a high intracellular M protein turnover. M appeared to be degraded shortly after its synthesis, and seemed not to be able to self-associate in a stable way under the plasma membrane as it did in St virus-infected cells. These data, added to the previous findings that infection with DI particles allowed infected cell survival and favored the cell-surface turnover of the hemagglutinin-neuraminidase protein, led to the hypothesis that DI genomes directly act by preventing the stable formation inside the cells of a viral structure composed of M/HN/nucleocapsids. When involved in this structure M would be protected from degradation and HN would be stably anchored in the plasma membrane. Formation of this structure would be necessary for viral budding and would be damaging for the cells. Comparison with results published by other authors shows that such a model is consistent with other data. It can integrate, as well, data obtained in the analysis of mutant viruses involved in persistence.
Insights
Defective interfering (DI) viruses restrict viral budding by preventing the stable formation of essential viral protein structures within infected cells. This mechanism explains viral persistence and cell survival during mixed virus infections.
Area of Science:
- Virology
- Cell Biology
- Molecular Virology
Background:
- Sendai virus infection of BHK cells can lead to restricted viral budding.
- Defective interfering (DI) particles influence viral replication and host cell survival.
Purpose of the Study:
- To investigate the mechanism by which DI viruses restrict viral budding in mixed infections.
- To elucidate the role of M protein and viral structure formation in viral budding and cell survival.
Main Methods:
- Infection of BHK cells with a mixture of Sendai standard and DI viruses.
- Analysis of viral budding rates and intracellular M protein turnover.
- Comparison of M protein behavior in standard and DI virus-infected cells.
Main Results:
- Mixed virus infection significantly restricted viral budding.
- High intracellular M protein turnover correlated with reduced budding.
- M protein degradation and failure to self-associate were observed in DI virus-infected cells.
- DI particle infection promoted infected cell survival and hemagglutinin-neuraminidase protein turnover.
Conclusions:
- DI genomes likely prevent the stable formation of a M/HN/nucleocapsid viral structure.
- This structure is proposed to be necessary for viral budding and potentially damaging to cells.
- The model integrates findings on viral persistence and mutant virus analysis.