The herpes simplex virus 1 protein kinase U S 3 is required for protection from apoptosis induced by the virus

Abstract

An earlier report showed that a disabled mutant lacking both copies of the major regulatory gene (α4) of herpes simplex virus 1 induced DNA degradation characteristic of apoptosis in infected cells, whereas the wild-type virus protected cells from apoptosis induced by thermal shock. More extensive analyses of the disabled mutant revealed a second mutation which disabled U S 3, a viral gene encoding a protein kinase known to phosphorylate serine/threonine within a specific arginine-rich consensus sequence. Analyses of cells infected with a viral mutant carrying a wild-type α4 gene but from which the U S 3 gene had been deleted showed that it induced fragmentation of cellular DNA, whereas a recombinant virus in which the deleted sequences of the U S 3 gene had been restored did not cause the cellular DNA to fragment. These results point to the protein kinase encoded by the U S 3 gene as the principal viral product required to block apoptosis.