Abstract
Stress granules are induced in many different viral infections, and in turn are inhibited by the expression of viral proteins or RNAs. It is therefore evident that these bodies are not compatible with efficient viral replication, but the mechanism by which they act to restrict viral gene expression or genome replication is not yet understood. This article discusses a number of methods that can be employed to gain a more complete understanding of the relationship between cellular SGs and viral RNA and protein synthesis in cells infected with diverse viruses.