“…As expected, the VZV gene is able to complement HSV-1 mutants with temperature-sensitive lesions in Vmw175 (Felser et al, 1987(Felser et al, , 1988 and, moreover, may replace the Vmw175 gene in a recombinant HSV-1 genome (Disney & Everett, 1990). In vitro transfection experiments have also implicated gene 4 in trans-activation (Inchauspe et al, 1989 The VZV dPyK has been characterized enzymologically and is thought to consist of a dimer with a subunit Mr of approximately 35000 (Doberson et al, 1976;Hackstadt & Mallavia, 1978;Lopetegui et al, 1983;Shiraki et at., 1985). The dPyK gene (gene 36) was identified on the basis of the homology of its product to HSV-1 thymidine kinase (TK) and was also mapped by biochemical transformation (Sawyer et al, 1986).…”