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Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U_S3 Protein Kinase

Marjorie B. Kovler Viral Oncology Laboratories, The University of Chicago, 910 East 58th Street, Chicago, Illinois 60637

Received 30 December 2007/ Accepted 28 February 2008

Gamma interferon receptor (IFN-R) is stable but posttranslationally modified in herpes simplex virus 1(F) [HSV-1(F)]-infected cells. Studies with antibody directed to the phosphorylation site indicate that IFN-R is phosphorylated by the U_S3 kinase. The modification is abolished in cells infected with U_S3, U_L13, or (U_S3/U_L13) mutant virus. Transcripts of the IFN--dependent genes do not accumulate in cells transduced with the U_S3 protein kinase and treated with IFN-. In contrast, the accumulation of IFN--dependent gene transcripts is suppressed in cells infected with the wild-type virus, in cells infected with the U_S3 mutant virus, and to a lesser extent in the U_L41 virus-infected cells. The accumulation of IFN--dependent gene transcripts in U_L41-infected cells could be due at least in part to a significant delay and reduction in the accumulation of the U_S3 protein. The results suggest that the expression of IFN--dependent genes is blocked independently by the degradation of IFN--dependent gene transcripts—a function of the virion host shutoff RNase—and by posttranslational modification of the IFN-R protein.

Published ahead of print on 5 March 2008.