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

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.