Herpes viruses stimulate the activity of thymidine kinase (E.C. in a number of cell types (Kit & Dubbs, 1969) and a mutant virus which fails to produce the enzyme has been isolated (Dubbs & Kit, 1964). Simultaneous infection of cells with wild-type and mutant virus results in the inhibition of thymidine kinase activity (Munyon & Kit, 1965). A possible explanation of this inhibition is that thymidine kinase is composed of subunits and the mutant virus synthesizes an inactive subunit which competes with the active units (Kit & Dubbs, 1969; McAuslan, 1969). The postulated inactive subunit may be antigenically similar to or different from the active enzyme subunit. We have examined this possibility immunologically.

Wild-type herpes virus and the mutant (2006) (Dubbs & Kit, 1964) were grown in BHK 21 cells or RK13 cells (Watson 1966). Antisera to RK13 cells infected with each virus were produced by the method of Watson (1969).


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