The control mechanisms which determine whether the infection of a cell by a herpesvirus will result in a productive cycle of replication with the production of infectious progeny, an abortive cycle of replication with the production of a virus latent infection, or the transformation of the infected cell to oncogenic potential, have yet to be determined. However, in many cases it appears that the physiological state of the infected cell, especially the regulation of cellular DNA synthesis, plays an important, if not key, role in determining the susceptibility of a cell to virus infection. Therefore, experiments have been designed to investigate the role of modifications of the pattern of cellular DNA synthesis on the replication of varicella-zoster virus in human embryonic lung cells. Various systems known to change the normal pattern of cell DNA synthesis, including the pretreatment of the cells with Iododeoxyuridine, abortive infection of the human cells with SV40 virus, and serum stimulation of starved cells, will be used. The replication cycle of varicella-zoster virus will be monitored by plaque assay for the production of infectious virus, and a combination of radioautography and immunofluorescence techniques. The product of cellular factors which inhibit or enhance virus replication will be determined in extracts of cells whose pattern of cellular DNA synthesis has been modified. Attempts will be made to correlate the type of virus replication cycle with changes in the pattern of cellular DNA synthesis.