Direct adverse effects of Sendai virus DI particles on virus budding and on M protein fate and stability.

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.