Target for Inhibition of Protein Synthesis

Most of the circumstantial evidence indicates that inhibition of protein synthesis in VSV-infected cells takes place at the level of 

Most of the early studies of VSV effects on cellular macromo-lecular synthesis were done by measuring cell protein synthesis. We now focus our attention on the effect of VSV on cellular nucleic acids, a field which has gained momentum in recent years. There is now reasonable evidence to indicate that VSV inhibits protein and nucleic acid synthesis by two different mechanisms. Although the problems are related, we shall also examine separately (1) the viral functions required to inhibit cellular nucleic acid synthesis, and (2) the cellular 

The importance of cell type in susceptibility to VSV inhibition of cellular RNA synthesis was also demonstrated much later by Rob- 

In the previous section, we dealt with the question whether VSV inhibition of cellular protein synthesis was a primary effect of the virus or was secondary to its effect on cellular RNA synthesis. We came to the conclusion, based on kinetics of the reactions and UV sensitivity, that inhibition of cellular protein synthesis was largely, if not entirely, due to a primary effect of the virus and not secondary to inhibition of cellular RNA synthesis. 

This statement still applies despite the recent elegant study of Dunigan and Lucas-Lenard (1983) which provides evidence for two sites of UV inactivation of protein synthesis inhibition, one of which may be identical to the leader sequence presumably responsible for inhibiting cellular RNA synthesis (Week et al., 1979 McGowan et al., 1982). In any case, the kinetic data and UV inactivation data seem to implicate the same or closely-related viral functions for inhibiting both cellular RNA and DNA synthesis and not inhibition of cellular protein synthesis, at least not entirely. 

---