Abstract
The bovine herpesvirus type 4 (BHV-4) group has a slow replication cycle, a narrow host range, and cytopathogenic effects characteristic of cytomegaloviruses (CMV), but a Group B genome structure similar to that of lymphotropic Herpesvirus saimiri (HVS). Reference BHV-4 strain DN599 and BHV-4 strains N124 and FHV-2 induced in the cytosol fraction of thymidine kinase-negative (TK −) rabbit skin (RAB-BU) cell mutants a novel TK activity. The BHV-4-induced thymidine kinase (TK) differed from the principal cytosol TK of mock-infected cells in PAGE mobility ( R m) under non-denaturing conditions and in the capacity to efficiently substitute CTP for ATP as a phosphate donor. The BHV-4 thymidine phosphorylating activity could also be distinguished from many common herpesvirus-induced TKs because it lacked iododeoxycytidine phosphorylating activity. lododeoxyuridine, trifluorothymidine and bromovinyldeoxyuridine inhibited [ 3H]thymidine (0.01 mM) phosphorylation by the BHV-4 enzyme in a dose-dependent manner, but arabinosylthymine and 2′-fluoro-5-methyl-arabinosyluracil (FMAU) were poor inhibitors of [ 3H]thymidine phosphorylation, and acyclovir and (dihydroxy-2-pro-poxymethyl)guanine (DHPG) did not inhibit at all at 60 and 40 times the concentrations of [ 3H]thymidine, respectively.
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